Iranian Journal Of Allergy, Asthma, And Immunology[JOURNAL]
Sun
200 papers
Integration of Cervical Length, Inflammatory Marker, and Vaginal Biomarkers (PAMG-1 and fFN) in the Diagnosis of Threatened Preterm Labor.
Lu J, Lu J, Zhang X … +2 more , Mu L, Luo W
Iran J Allergy Asthma Immunol · 2026 Feb · PMID 42113495 · Publisher ↗
The aim of this research was to evaluate the diagnostic efficacy of integrating cervical length (CL), interleukin-6 (IL-6), placental alpha microglobulin-1 (PAMG-1), and fetal fibronectin (fFN) in predicting preterm birt...
The aim of this research was to evaluate the diagnostic efficacy of integrating cervical length (CL), interleukin-6 (IL-6), placental alpha microglobulin-1 (PAMG-1), and fetal fibronectin (fFN) in predicting preterm birth among pregnant women with threatened preterm labor (TPL). This study retrospectively analyzed clinical data from 150 pregnant women admitted for TPL between January 2021 and December 2024. Participants were divided into two groups based on pregnancy outcome: full-term delivery (n=85) and preterm birth (n=65). Additionally, 100 healthy pregnant women with no history of adverse pregnancy outcomes who underwent routine prenatal examinations during the same period were selected as the healthy control group. All participants underwent transvaginal ultrasound to measure CL, and venous blood samples were collected to assess serum IL-6 levels. PAMG-1 and fFN levels were measured in vaginal secretions. There were no significant differences in baseline characteristics among the three groups. However, significant differences in CL, serum IL-6 levels, and positive rates of PAMG-1 and fFN were detected. Pearson correlation analysis showed significant associations between CL, IL-6, PAMG-1, fFN, and preterm birth. ROC curve analysis indicated that the AUC values for CL, IL-6, PAMG-1, and fFN alone were 0.798, 0.803, 0.753, and 0.754, respectively. The combined application of these markers yielded an AUC of 0.920, significantly higher than any single marker. The combined use of CL, IL-6, PAMG-1, and fFN significantly enhances the diagnostic accuracy of preterm birth in patients with TPL.
Analysis of the Diagnostic Value of Peripheral Blood Indicators for Acute Pyelonephritis and the Influencing Factors of Poor Prognosis.
Qian H, Zhou D, Wang H
Iran J Allergy Asthma Immunol · 2026 Feb · PMID 42113494 · Publisher ↗
This study explored the diagnostic value of peripheral blood indices for acute pyelonephritis (APN) and the factors influencing poor prognosis. A total of 118 patients with APN admitted to our hospital from January 2022...
This study explored the diagnostic value of peripheral blood indices for acute pyelonephritis (APN) and the factors influencing poor prognosis. A total of 118 patients with APN admitted to our hospital from January 2022 to June 2024 were retrospectively included as the observation group. Another 62 healthy volunteers were selected as the control group. Clinical data from the two groups were collected, and the diagnostic value of peripheral blood indices for APN was analyzed. The patients were divided according to their prognoses into good-prognosis group and poor-prognosis group, and the influencing factors of poor prognosis were identified by multivariate logistic regression analysis. Compared to the control group, the white blood cell count (WBC) and C-reactive protein (CRP) were higher in the observation group, while IgG and C3 were lower. The areas under the curves (AUCs) of WBC, CRP, IgG, and C3 in the diagnosis of APN were 0.857, 0.846, 0.902, and 0.893, respectively, and their combined AUC was 0.981. After 3 months of follow-up, there were 43 cases of recurrence (36.44%). The multivariate logistic analysis showed that serum albumin< 35 g/L and a decrease of the IgG level were the influencing factors of poor prognosis in patients with APN. In conclusion, WBC, CRP, IgG, and C3 had high value for the diagnosis of APN, and serum albumin< 35 g/L and the decrease of IgG level were the i factors influencing prognosis.
Association of Systemic Immune Inflammation Index and Pan-immune Inflammation Value with Prognosis in Idiopathic Membranous Nephropathy.
Liang F, Yang Y, Sun Y … +4 more , Xing L, Yu X, Xia J, Gao J
Iran J Allergy Asthma Immunol · 2026 Feb · PMID 42113493 · Publisher ↗
Idiopathic membranous nephropathy (IMN) presents a heterogeneous clinical course, with approximately 30% to 40% of patients experiencing spontaneous remission, while others respond poorly to treatment. This study aims to...
Idiopathic membranous nephropathy (IMN) presents a heterogeneous clinical course, with approximately 30% to 40% of patients experiencing spontaneous remission, while others respond poorly to treatment. This study aims to identify reliable biomarkers for risk stratification in IMN patients. We conducted a prospective observational study involving 187 patients with IMN from February 2022 to February 2024. Patients were categorized into remission and non-remission groups based on clinical outcomes one year post-treatment. Comparative analyses revealed that the non-remission group exhibited significantly higher incidences of hypertension, elevated 24-hour urinary protein, higher serum creatinine levels, and increased inflammatory markers, including the systemic immune inflammation index (SII), systemic inflammation response index (SIRI), and pan-immune inflammation value (PIV). Conversely, the estimated glomerular filtration rate (eGFR) and lymphocyte-to-monocyte ratio (LMR) were lower in non-remission patients. Spearman correlation identified hypertension, 24-hour urinary protein, and inflammatory indexes as positive correlates with non-remission, while eGFR showed a negative correlation. Multivariate logistic regression confirmed hypertension, high 24-hour urinary protein, SII, SIRI, and PIV as independent risk factors for non-remission; eGFR was a protective factor. Receiver operating characteristic analysis revealed that SII and PIV effectively predicted non-remission (AUC=0.743 and 0.759, respectively). These findings underscore the potential of these indicators in assessing disease severity and guiding personalized treatment strategies.
Assessment of Rigid Nasopharyngoscopy Beyond the Nasal Cavity in Diagnosis of Immune-mediated Nasopharyngeal Allergic Diseases.
Wang H, Zhu P, Geng J … +2 more , Yu P, Dong J
Iran J Allergy Asthma Immunol · 2026 Feb · PMID 42113492 · Publisher ↗
Rigid nasopharyngoscopy is a valuable diagnostic method for immune-mediated allergy conditions, particularly for children aged≤6 years. In addition to evaluating the structural characteristics of the nasal cavity, the pr...
Rigid nasopharyngoscopy is a valuable diagnostic method for immune-mediated allergy conditions, particularly for children aged≤6 years. In addition to evaluating the structural characteristics of the nasal cavity, the procedure also reveals inflammatory activity in the nasopharyngeal framework. This study assessed 110 pediatric patients between 2 and 6 years old who presented with suspected allergic conditions. Rigid nasopharyngoscopy was performed, and its diagnostic performance was high with 85.45% sensitivity, 78.18% specificity, and an overall diagnostic accuracy of 83.00%, which supports its role in diagnosing and ruling out allergic disorders. The findings revealed strong associations between mucosal erythema, cobblestoning, and mucosal secretions with symptoms like nasal obstruction and postnasal drip. These signs have proven to be reliable indicators of inflammation and chronic irritation in this age group. The procedure was well tolerated, and over 85% of children experienced no adverse effects. Minor discomfort and nasal bleeding were reported in a small number of cases. Taken together, the results show that rigid nasopharyngoscopy is an essential diagnostic modality for early detection of allergy conditions in the pediatric population.
Evaluating the Efficacy of Intranasal Montelukast in Pediatric Acute Asthma Attacks: A Single-blinded, Placebo-controlled Clinical Trial.
Sadinejad M, Amini N, Tavakoli E … +1 more , Sabzghabaee AM
Iran J Allergy Asthma Immunol · 2026 Feb · PMID 42113491 · Publisher ↗
Asthma is a common chronic respiratory disease in children, often leading to acute exacerbations marked by dyspnea, cough, and wheezing, which frequently necessitate emergency medical care. While standard therapies are e...
Asthma is a common chronic respiratory disease in children, often leading to acute exacerbations marked by dyspnea, cough, and wheezing, which frequently necessitate emergency medical care. While standard therapies are effective, the exploration of novel drug delivery routes continues. Oral montelukast is a recognized treatment, but the efficacy of its intranasal formulation for acute attacks remains underexplored. This study aimed to evaluate the clinical effectiveness of intranasal montelukast as an adjunct therapy for pediatric asthma exacerbations. A single-blinded, placebo-controlled, single-center trial was conducted involving children aged 2-12 years hospitalized with moderate to severe acute asthma. Participants were randomized to receive either intranasal montelukast or a placebo alongside standard care. Key outcomes, including the Pulmonary Index Score (PIS), respiratory rate, oxygen saturation, and length of hospital stay, were systematically assessed. The analysis of 25 patients in each group revealed no significant baseline differences. The intranasal montelukast group demonstrated a statistically significant and sustained reduction in PIS scores at critical intervals (8, 12, and 24 hours) compared to the placebo group. Improvements in respiratory rate and oxygen saturation were also more pronounced with the active treatment. Notably, the mean hospital stay was significantly shorter for the montelukast group (2.16 days) than the placebo group (3.12 days). In conclusion, intranasal montelukast shows significant promise as an effective adjunct therapy for acute pediatric asthma, correlating with accelerated clinical improvement and a reduced duration of hospitalization. These encouraging results justify further investigation through larger, multicenter trials to definitively establish its efficacy and safety profile.
Allergic Diseases and Head and Neck Cancer: A Systematic Review and Meta-analysis.
Karlsson D, Saber A
Iran J Allergy Asthma Immunol · 2026 Feb · PMID 42113490 · Publisher ↗
Allergic disorders such as asthma, atopic dermatitis, and allergic rhinitis affect a large portion of the global population. The relationship between allergies and cancer has been studied extensively, but results remain...
Allergic disorders such as asthma, atopic dermatitis, and allergic rhinitis affect a large portion of the global population. The relationship between allergies and cancer has been studied extensively, but results remain inconsistent for head and neck cancer. The aim of this meta-analysis is to evaluate whether there is a negative association between allergic disorders and head and neck cancer. A systematic search of five databases was conducted based on Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Cohort- and case-control studies examining allergies and head and neck cancer were included. Random-effect and fixed-effect models were used to calculate pooled relative risk, with heterogeneity assessed via the I2 and Cochrane's Q-test. Subgroup and sensitivity analyses were performed to explore variations by study design, allergy type, and cancer site. Twenty-five studies with 3.6 million participants were included. No significant overall association was found between allergic diseases and head and neck cancer (meta-RR: 0.89; 95% confidence intervals (CI): 0.76-1.05). Subgroup analyses revealed protective effects for asthma (meta-RR: 0.81; 95% CI: 0.70-0.95) and food allergies (meta-RR: 0.73; 95% CI: 0.54-0.99). Allergic rhinitis showed negative associations with oropharyngeal cancer (meta-RR: 0.76; 95% CI: 0.69-0.84) and hypopharyngeal cancer (meta-RR: 0.65; 95% CI: 0.55-0.78), but a positive association with nasopharyngeal cancer (meta-RR: 1.67; 95% CI: 1.15-2.43). These findings suggest complex relationships between allergies and head and neck cancer, with negative and positive associations varying by allergy type and cancer site. Further research is needed to clarify these associations.
Development and Validation of a Manganese-metabolism and Immune-integrated Gene Signature for Prognosis and Immune Contexture in Patients with Colorectal Cancer.
He L, Chen Z, Zhang C … +2 more , Zhu P, Dai S
Iran J Allergy Asthma Immunol · 2026 Jan · PMID 41674176 · Publisher ↗
Colorectal cancer (CRC) is the third most frequently diagnosed cancer and the second leading cause of cancer-related mortality globally. Emerging evidence identifies manganese as an important trigger for the cyclic GMP-A...
Colorectal cancer (CRC) is the third most frequently diagnosed cancer and the second leading cause of cancer-related mortality globally. Emerging evidence identifies manganese as an important trigger for the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, but prognostic signatures integrating manganese metabolism and immune pathways remain unexplored in CRC. Through analysis of transcriptomic and clinical data from TCGA-CRC and GSE17538 cohorts, we established and validated an eleven-gene manganese metabolism and immune-related signature that robustly stratified CRC patients into distinct risk groups with significant survival differences. High-risk patients exhibited suppressed immune microenvironments with enriched M2 macrophages and Tregs and activation of oncogenic pathways. Quantitative real-time polymerase chain reaction (qRT-PCR) validation confirmed dysregulation of eight signature genes in clinical CRC samples, indicating the model's potential for prognostic prediction and immunotherapeutic stratification. We established a novel MIRGs signature that accurately predicts CRC clinical outcome. Integration of manganese-based agents with immune checkpoint inhibitors (ICIs) represents a potential therapeutic strategy for immunotherapy-resistant CRC.
Molecular Mechanisms of Pulmonary Fibrosis: The Interaction of Epithelial-mesenchymal Transition and AMPK Pathways in a Bleomycin-induced Model.
Sadatpour O, Kavosi H, Mahmoudi M … +4 more , Mohammadi M, Saffar H, Farhadi E, Vodjgani M
Iran J Allergy Asthma Immunol · 2026 Jan · PMID 41674175 · Publisher ↗
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease marked by excessive extracellular matrix (ECM) deposition, largely mediated by activated fibroblasts. Epithelial-mesenchymal transition (EMT), regulated b...
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease marked by excessive extracellular matrix (ECM) deposition, largely mediated by activated fibroblasts. Epithelial-mesenchymal transition (EMT), regulated by transcription factors such as TGF-β, Twist1, and Snail, is a critical mechanism in fibrosis progression. AMP-activated protein kinase (AMPK) has been implicated in modulating fibrotic pathways, but its role in EMT remains unclear. This study aimed to explore the interaction between EMT and AMPK signaling in pulmonary fibrosis. A bleomycin-induced pulmonary fibrosis mouse model was used. Histological analysis assessed fibrosis and inflammation, while gene expression (TGF-β, Twist1, Snail) was measured by qPCR. Protein levels of E-cadherin, α-SMA, and phosphorylated AMPK were analyzed using Western blotting to evaluate EMT and AMPK activity. Bleomycin-treated mice showed significant lung inflammation and fibrosis, particularly in the lower region of the left lung. Gene expression analysis revealed elevated TGF-β, Twist1, and Snail in fibrotic areas. Protein analysis demonstrated increased α-SMA and decreased E-cadherin, confirming EMT induction. Notably, AMPK phosphorylation was significantly reduced in fibrotic regions, occurring concurrently with EMT activation. These findings indicate an inverse relationship between AMPK signaling and EMT in pulmonary fibrosis. EMT may serve as a direct therapeutic target, either by inhibiting transcription factors such as Snail and Twist1 or by modulating upstream metabolic regulators including AMPK.
Evaluation of the Effects of Newcastle Disease Virus as an Oncolytic Virus on the Expression of Apoptosis-related Genes in TC-1 Cell Line.
Ali Akbar Esfahani M, Dorostkar R, Esmaeili Gouvarchin Ghaleh H … +5 more , Ramezani R, Ramezani R, Mir Mohammad Sadeghi SM, Ghorbani Alvanegh A, Aghayan SK
Iran J Allergy Asthma Immunol · 2026 Jan · PMID 41674174 · Publisher ↗
TC-1 is a recognized cancer cell line derived from lung epithelial cells that have been altered using the oncogenic E6 and E7 genes of human papillomavirus (HPV). These TC-1 cells are frequently utilized in preclinical r...
TC-1 is a recognized cancer cell line derived from lung epithelial cells that have been altered using the oncogenic E6 and E7 genes of human papillomavirus (HPV). These TC-1 cells are frequently utilized in preclinical research focused on lung cancer and HPV-associated tumors. The incidence of lung cancer and HPV-related cancers is significantly increasing. Drug resistance and the lack of selectivity in current treatments reduce their effectiveness. Researchers are seeking new therapeutic methods, including targeted therapies, immunotherapy, and oncolytic virus and bacterial therapies, to improve treatment outcomes and decrease mortality associated with these diseases. In this context, the present original study aimed to evaluate the potency of wild-type Newcastle disease virus (NDV-WTS) on lactate dehydrogenase (LDH) secretion and the induction of apoptosis in TC-1 cells. In this experimental study, the TC-1 cell lines were cultured under laboratory conditions. Subsequently, they were treated with different multiplicities of infection (MOIs) of NDV-WTS (1, 2, and 4). Finally, the oncolytic effects of the virus were evaluated using laboratory assays, including MTT (cell viability), reactive oxygen species (ROS), LDH, survival rates, and the activities of Caspases 8 and 9. The results indicated that NDV-WTS significantly decreased cell viability while increasing apoptosis, ROS levels, LDH release, and Caspase 8 and 9 activities compared to the control group. Molecular analyses further revealed that treatment of TC-1 cells with NDV significantly increased the expression of Bax, Casp8, and Casp9, while significantly decreasing Bcl2 expression relative to the control group. NDV-WTS demonstrated remarkable efficacy in treating lung cancer and HPV-associated tumors. Based on the results of the present study, the use of Newcastle disease virus in the treatment of lung cancer and HPV-associated tumors may be beneficial, which requires further studies and clinical trials.
TREM1 Enhances Macrophage Proinflammatory Response to LPS by Promoting NF-κB Activation via an IL-26-mediated JAK/STAT Signaling Pathway.
Xie L, Gao F, Xu J … +3 more , Xiong W, Yin J, Sun W
Iran J Allergy Asthma Immunol · 2026 Jan · PMID 41674173 · Publisher ↗
Lipopolysaccharide (LPS)-induced inflammation in macrophages involves complex signaling pathways. This investigation explored the regulatory roles of triggering receptor expressed on myeloid cells-1 (TREM1) and interleuk...
Lipopolysaccharide (LPS)-induced inflammation in macrophages involves complex signaling pathways. This investigation explored the regulatory roles of triggering receptor expressed on myeloid cells-1 (TREM1) and interleukin (IL)-26 in the Janus kinase/signal transducer and activator of transcription (JAK/STAT) and nuclear factor-kappa B (NF-κB) p65 pathways in LPS-stimulated RAW 264.7 macrophages. RAW 264.7 cells were treated with LPS to assess TREM1 expression. TREM1 or IL-26 was silenced using short hairpin RNA (shRNA), while IL-26 was overexpressed via plasmid transfection. The JAK2 inhibitor AG490 was used to block JAK/STAT signaling. Western blot, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and enzyme-linked immunosorbent assay (ELISA) were employed to analyze the protein and mRNA levels of inflammatory markers and signaling molecules. Results showed that LPS upregulated TREM1 expression. In addition, TREM1 knockdown suppressed p65 activation and reduced inflammatory cytokine levels. Moreover, silencing TREM1 inhibited IL-26 and JAK/STAT phosphorylation (p-JAK1, p-JAK2, p-STAT1, and p-STAT3). Similarly, IL-26 knockdown or AG490 treatment attenuated p65 activation and inflammation. Furthermore, IL-26 overexpression reversed the anti-inflammatory effects of TREM1 silencing. Overall, TREM1 promoted LPS-induced macrophage inflammation via IL-26-mediated JAK/STAT and NF-κB pathway activation, suggesting that TREM1 and IL-26 are potential therapeutic targets.
In vitro Safety and Immunotoxicity Assessment of a Novel mRNA-LNP Vaccine against Cytomegalovirus: Insights into Safety and Immunomodulatory Profiles.
Mami S, Shekarchian S, Naderi Sohi A … +3 more , Kiani J, Soleimani M, Nicknam MH
Iran J Allergy Asthma Immunol · 2026 Jan · PMID 41674172 · Publisher ↗
Predominantly a widespread beta herpesvirus, human cytomegalovirus (HCMV) triggers lifelong latent infection in most of the people, and HCMV vaccine development has been designated a high public health priority. In the c...
Predominantly a widespread beta herpesvirus, human cytomegalovirus (HCMV) triggers lifelong latent infection in most of the people, and HCMV vaccine development has been designated a high public health priority. In the current study, the in vitro safety profile and potential immunotoxic effects of a novel messenger RNA (mRNA)-lipid nanoparticle (LNP) vaccine designed against human cytomegalovirus (HCMV) were assessed. The aim was to measure inflammation, allergic reactions, complement activation, cytotoxicity, and hemolytic effects of the mRNA-LNP vaccine. Proinflammatory cytokine secretion, evident in human peripheral blood mononuclear cells (hPBMCs) treated with unmodified mRNA-LNP, was markedly attenuated by incorporating modified nucleotides. The vaccine appeared incapable of sparking allergic cytokine production or complement activation. Cell viability assays indicated no pronounced cytotoxicity, and hemolysis assays showed no notable hemolytic activity. The findings suggest that the modified mRNA-LNP vaccine exhibits a promising in vitro safety profile, supporting further development of this vaccine candidate.
Investigating the Interplay between the Gut Microbiota and Host Immunity in Gastroenteric Disorders: The Potential of Combined Drug Therapies to Restore Microbial-immune Homeostasis.
Qiao Y, Gao X
Iran J Allergy Asthma Immunol · 2026 Jan · PMID 41674171 · Publisher ↗
This study examines the interaction between the microbiota and the immune system in diseases of the gastrointestinal tract, with a special emphasis on the synergistic use of pharmacological agents. This was a retrospecti...
This study examines the interaction between the microbiota and the immune system in diseases of the gastrointestinal tract, with a special emphasis on the synergistic use of pharmacological agents. This was a retrospective, observational study of 100 patients with moderate to severe gastrointestinal disorders, including irritable bowel syndrome and inflammatory bowel disease, receiving control, monotherapy, or combination therapy. Over 12 weeks, combination therapy demonstrated superior efficacy in enhancing gut microbial diversity. Improvements were achieved in alpha diversity, and a decrease in inflammatory indices and a shift in the immune phenotype were observed. Patients experienced significant improvements in symptom severity, pain, and general health. In addition, the general health of patients also improved. Importantly, the combination therapy group had better responses compared with the other groups. With respect to the identified factors, regression analysis revealed that microbial diversity, immune system regulation, and inflammation had positive effects on disease symptom alleviation. These findings therefore help support the perspective of combination therapy as a more comprehensive mode of approaching and treating gastroenteric diseases.
Evaluation of Salivary sIgA Levels in Hospitalized COVID-19 Patients with COVID-19 Disease Severity: A Cross-sectional Study.
Valizadeh Z, Ghaderkhani S, Eshraghi S … +4 more , Abbasian L, Abdollahi A, Soori T, Roozbahani MM
Iran J Allergy Asthma Immunol · 2026 Jan · PMID 41674170 · Publisher ↗
Since late 2019, the severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) pandemic has dramatically affected public health worldwide. Although systemic antibodies like Immunoglobulin G (IgG) and Immunoglobulin M...
Since late 2019, the severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) pandemic has dramatically affected public health worldwide. Although systemic antibodies like Immunoglobulin G (IgG) and Immunoglobulin M (IgM)have been widely studied in Coronavirus disease 2019 (COVID-19), the role of Immunoglobulin A (IgA) in mucosal immunity remains less understood. This study evaluated whether salivary IgA levels could serve as prognostic markers for disease severity, progression, and outcomes in hospitalized patients with COVID-19. In this cross-sectional study, 61 hospitalized patients with COVID-19 were enrolled. After obtaining informed consent, saliva samples were collected at admission to measure IgA levels using an ELISA-based assay. Comprehensive clinical and laboratory data, including chest CT results, oxygen saturation, inflammatory markers, and clinical outcomes, were also recorded. Statistical tests were used to examine the association between salivary IgA levels and disease severity, progression, and outcomes. We enrolled 61 hospitalized patients with COVID-19 (30 females, 31 males; mean age: 56.20 ± 17.45 years; mean admission oxygen saturation: 89.98 ± 5.77%). At admission, 39.3% of patients reported dyspnea, and 40% demonstrated severe lung involvement on chest CT scans. The mean salivary IgA level was 1729.69 ± 391.35 mg/dL. No significant associations were found between salivary IgA levels and COVID-19 severity, disease progression, or clinical outcomes, including mortality. Our findings show that salivary IgA levels did not significantly correlate with COVID-19 severity, disease progression, or clinical outcomes in hospitalized patients. Therefore, salivary IgA alone cannot be recommended as a prognostic biomarker for COVID-19. Further research is needed to identify more reliable immunological indicators for predicting COVID-19 severity and outcomes.
Correlation between Component-resolved Diagnostics (CRD) and Clinical Symptoms in Allergic Children: A One-year Study at the Children's Medical Center (April 2023-March 2024).
Khoshkam M, Movahedi M, Gharagozlou M … +2 more , Farokhzadeh Soltani M, Movahedi M
Iran J Allergy Asthma Immunol · 2026 Jan · PMID 41674169 · Publisher ↗
Component- Resolved Diagnosis (CRD) is an effective tool in allergy diagnosis, that detects specific IgE to allergenic molecules. The ALEX (Allergy Explorer) test, commercially available since 2019, measures specific IgE...
Component- Resolved Diagnosis (CRD) is an effective tool in allergy diagnosis, that detects specific IgE to allergenic molecules. The ALEX (Allergy Explorer) test, commercially available since 2019, measures specific IgE to allergenic extracts and components associated with inhalant, food, animal, latex, and insect allergens. CRD results should be interpreted based on the patient's clinical history. Since Children's Medical Center Hospital is one of the largest referral centers for allergic patients, we evaluated the results of the ALEX2 test in patients referred to this center and compared them with the patients' clinical symptoms. Clinical symptoms were concordant with positive CRD (ALEX2) test in 76.7% of cases. The overall agreement between positive allergen components and clinical symptoms was 58%. These findings indicate that the ALEX2 test can improve diagnostic accuracy in allergic patients; however, positive test results should be interpreted in the context of the patient's clinical history.
miR-10a Delivered via MSC-derived Extracellular Vesicles Modulates Inflammation in a CCl4-induced Liver Fibrosis Model.
Wang L, Ni Y
Iran J Allergy Asthma Immunol · 2026 Jan · PMID 41674168 · Publisher ↗
Liver fibrosis is a significant global health issue characterized by an abnormal accumulation of extracellular matrix proteins, that disrupts normal liver architecture and function. Mesenchymal stem cells (MSCs) show the...
Liver fibrosis is a significant global health issue characterized by an abnormal accumulation of extracellular matrix proteins, that disrupts normal liver architecture and function. Mesenchymal stem cells (MSCs) show therapeutic potential by releasing extracellular vesicles (EVs) containing regulatory microRNAs like miR-10a. This study evaluates miR-10a-enriched human umbilical cord MSC (hUCMSC)-EVs in a CCl4-induced model of liver fibrosis, focusing on inflammatory marker modulation. Liver fibrosis was induced in experimental animals using CCl4 administration. MSCs were isolated from the human umbilical cord and loaded with either a miR-10a mimic or a control sequence through Lipofectamine 3000. EVs were then isolated from the culture media of both miR-control and miR-10a-modified MSCs. The therapeutic potential of these miR-10a-loaded EVs was assessed by treating the CCl4-induced fibrosis model with these vesicles. The efficacy of the treatment was evaluated by measuring two anti-inflammatory markers interleukin (IL)-10 and IL-4) and three pro-inflammatory markers (tumor necrosis factor-α (TNF-α), IL-6, and interferon-γ (IFN-γ)) using enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR) techniques. The administration of miR-10a-loaded MSC-EVs resulted in a significant modulation of inflammatory markers. Our results revealed an increase in the levels of anti-inflammatory cytokines (IL-10 and IL-4) and a concurrent decrease in pro-inflammatory cytokines (TNF-α, IL-6, and IFN-γ) in the treated group compared to the control group. The study demonstrates the therapeutic potential of MSC-EVs encapsulating miR-10a in ameliorating CCl4-induced liver fibrosis. By modulating the balance between pro-inflammatory and anti-inflammatory cytokines, miR-10a-loaded EVs show promise as a targeted treatment approach for liver fibrosis.
A Mendelian Randomization Study of Cardiovascular Proteins, Immune Cell Traits, and Lifestyle Factors.
Deng H, Wang Q, Wang Y … +2 more , Zheng W, Dai Y
Iran J Allergy Asthma Immunol · 2026 Jan · PMID 41674167 · Publisher ↗
We aimed to investigate the causal relationship between cardiovascular-related proteins and osteoporosis and to assess the influence of immune cell traits and lifestyle factors such as smoking and alcohol consumption on...
We aimed to investigate the causal relationship between cardiovascular-related proteins and osteoporosis and to assess the influence of immune cell traits and lifestyle factors such as smoking and alcohol consumption on osteoporosis risk. A two-sample Mendelian randomization (MR) approach was employed using publicly available genome-wide association study (GWAS) data. Univariable and multivariable MR analyses were conducted using the inverse variance weighted (IVW) method to evaluate causal effects. Additional sensitivity analyses were performed to validate findings. Three cardiovascular proteins showed significant associations with osteoporosis and pathological fractures: TNF-related apoptosis-inducing ligand receptor 2 (OR=0.10), TNF-related activation-induced cytokine (OR=2.90), and C-C motif chemokine 4 (OR=1.12). Lifestyle factors, including household tobacco smoke exposure, daily smoking quantity, and alcohol consumption, were also significantly associated with increased osteoporosis risk. Immune cell traits were identified as potential mediators in the relationship between cardiovascular proteins and osteoporosis. This study highlights a novel link between cardiovascular health and osteoporosis, suggesting that specific proteins increase risk, while immune traits mediate this effect, and lifestyle factors are independent risk factors. These findings underscore the importance of integrated strategies addressing inflammation and lifestyle in osteoporosis prevention and management.
A Safer Lytic Alternative: Multi-omics and Immunoinformatics Reveal Reduced Inflammatory Impact of a Chimeric Endolysin Against Antibiotic-induced Immune Dysregulation.
Noori A, Amini-Bayat Z, Mirdamadi S … +2 more , Azizmohseni F, Borhani S
Iran J Allergy Asthma Immunol · 2026 Jan · PMID 41674166 · Publisher ↗
Natural killer (NK) cells contribute to the development of Rheumatoid Arthritis (RA). Increased expression of programmed cell death protein 1 (PD-1), encoded by the PDCD1 gene, indicates NK cell exhaustion, a process tha...
Natural killer (NK) cells contribute to the development of Rheumatoid Arthritis (RA). Increased expression of programmed cell death protein 1 (PD-1), encoded by the PDCD1 gene, indicates NK cell exhaustion, a process that may be influenced by microRNAs (miRNAs). In this study, we examined PD-1 expression on NK cells from RA patients and evaluated whether miRNAs modulate this pathway. Although antibiotics are critical for treating infections, they can provoke harmful immune responses by releasing bacterial components that overstimulate the immune system. Such responses may lead to excessive inflammation or cytokine storms. To address this risk, we assessed the immune safety of a newly designed chimeric endolysin, ZAM-MSC, and compared its effects with traditional antibiotics using transcriptomic, proteomic, and computational analyses. We analyzed public gene and protein expression datasets from antibiotic-treated human cells and performed in silico studies on ZAM-MSC. Differential expression analysis and pathway enrichment were conducted, alongside structural modeling of the endolysin and its predicted interactions with immune receptors. Antibiotic treatment strongly activated inflammatory genes and pathways, including nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK). In contrast, ZAM-MSC minimally affected immune-related gene expression, with downregulation of interleukin-6 receptor (IL6R) and tumor necrosis factor receptor 1A (TNFRSF1A). Structural modeling showed weak interactions with Toll-like receptors, and epitope analysis predicted low immunogenicity. These results suggest ZAM-MSC may offer a safer antimicrobial alternative, though all protein-level findings are based on computational predictions and require experimental validation.
Metformin in Diabetes Management and Immune Modulation: A Comprehensive Review.
Ghafari M, Poursamimi J, Asli F
Iran J Allergy Asthma Immunol · 2026 Jan · PMID 41674165 · Publisher ↗
Metformin is a primary treatment for type 2 diabetes (T2D), well-known for its ability to lower blood glucose levels through both AMP-activated protein kinase (AMPK)-dependent and -independent pathways. Recent evidence s...
Metformin is a primary treatment for type 2 diabetes (T2D), well-known for its ability to lower blood glucose levels through both AMP-activated protein kinase (AMPK)-dependent and -independent pathways. Recent evidence suggests that metformin also possesses immunomodulatory properties, indicating its potential as a therapeutic agent that extends beyond metabolic regulation. This review summarizes the current understanding of metformin's dual roles in managing diabetes and modulating the immune system. It also explores the underlying mechanisms, clinical implications, and potential directions for future research.
Diverse Phenotypic Expressions of ADA2 Deficiency: Two Case Studies.
Razaghian A, Alizadeh Z, Meyts I … +4 more , Kalantari A, Rostami Hir S, Wouters M, Fazlollahi MR
Iran J Allergy Asthma Immunol · 2025 Oct · PMID 41266270 · Publisher ↗
Adenosine deaminase 2 (ADA2) deficiency is an autosomal recessive disease with varying degrees of clinical phenotypes and disease severity. The phenotypic spectrum of the disorder has expanded from vasculitis with stroke...
Adenosine deaminase 2 (ADA2) deficiency is an autosomal recessive disease with varying degrees of clinical phenotypes and disease severity. The phenotypic spectrum of the disorder has expanded from vasculitis with stroke to include pure red cell aplasia, bone marrow failure, autoimmune cytopenia, lymphoproliferation, and variable degrees of immunodeficiency. Here, we describe two cases of ADA2 deficiency: one presented with an early-onset stroke that resembled an early-onset polyarteritis nodosa (PAN), and the other as an adult-onset vasculitis that progressed to severe neutropenia with recurrent infection and lymphoproliferation. Patient 1, a 10-year-old male, had a reported pathogenic ADA2 homozygote variant; c.139G˃C (p.Gly47Arg), and patient 2, a 34-year-old male, had a reported likely pathogenic homozygous ADA2 variant; c.578C>T (p.Pro193Lys). Our second patient was the first DADA2 patient who showed that DADA2 is not a static disease and can progress from vasculitis to bone marrow failure in the course of the disease. Therefore, the previous recommendation introducing anti-TNF-α as a preferred treatment for vasculitis manifestations and hematopoietic stem cell transplantation as the preferred treatment for bone marrow failure can no longer apply. We should consider HSCT for DADA2 patients from the very beginning. The Physician has to be aware of this monogenic disorder's varied presentation and multi-organ involvement. Early recognition and proper treatment are crucial for this potentially fatal disease.
The Mechanism of Notopterol Alleviating LPS-induced Endometritis by Inhibiting the TLR4/NF-κB Signaling Pathway.
Xu Z, Zhang Y, Pang J … +4 more , Chen X, Chen Y, Chen Y, Wang Y
Iran J Allergy Asthma Immunol · 2025 Oct · PMID 41266269 · Publisher ↗
This study aims to investigate the role of notopterol in alleviating endometritis induced by lipopolysaccharide (LPS) and to explore its underlying mechanisms.Human endometrial epithelial cells (hEECs) were treated with...
This study aims to investigate the role of notopterol in alleviating endometritis induced by lipopolysaccharide (LPS) and to explore its underlying mechanisms.Human endometrial epithelial cells (hEECs) were treated with LPS to establish an in vitro model of endometritis, and the cells were divided into five groups: control, LPS, LPS+notopterol(15 mol/L), LPS+notopterol(305 mol/L) and LPS+notopterol(45 mol/L) groups. The expression levels of inflammatory factors were determined by Enzyme-Linked ImmunoSorbent Assay (ELISA). Apoptosis was detected by TdT-mediated dUTP Nick-End Labeling (TUNEL) method. Cell viability was determined by Cell Counting Kit-8 (CCK-8) test. Western blot was used to detect the expression levels of nuclear factor κB(NF-κB) p65, NF-κB inhibitor (IκBα), p-NF-κB p65 and p-IκBα. Following LPS treatment, cytokine levels significantly increased compared to the control group.; moreover, cell proliferation decreased, apoptosis increased, and the expression level of p-NF-κB p65 was increased. Subsequently, the LPS-treated hEECs were exposed to notopterygium. Compared to the LPS group. Treatment with LPS + notopterol resulted in a dose-dependent reduction in inflammatory cytokines, increased cell proliferation, and a significant reduction in apoptosis. Furthermore, the expression levels of p-NF-κB p65 and p-IκBα were downregulated. These findings suggest that notopterol alleviates LPS-induced endometritis by inhibiting the TLR4/NF-κB signaling pathway.
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