Allergologia et immunopathologia最新文献

Background: Molecular diagnosis in allergology helps to identify multiple allergenic molecules simultaneously. The use of purified and/or recombinant allergens increases the accuracy of individual sensitization profiles in allergic patients.

Objective: To assess the impact of molecular diagnosis through the ImmunoCAP^TM ISAC 112 microarray on etiological diagnosis and specific immunotherapy (SIT) prescription. This was compared to the use of conventional diagnoses in pediatric, adolescent, and young adult patients with rhinitis or rhinoconjunctivitis and/or allergic asthma, sensitized to three or more pollen allergens of different botanical species.

Methods: A multicenter, prospective, observational study was conducted in patients aged 3-25 years who received care at the Allergology service of 14 hospitals in Catalonia from 2017 to 2020. Allergology diagnosis was established based on the patient's clinical assessment and the results of the skin prick test and specific immunoglobulin E assays. Subsequently, molecular diagnosis was conducted using ImmunoCAP^TM ISAC^® 112 to recombinant and/or purified allergen components.

Results: A total of 109 patients were included; 35 (32.1%) were pediatric patients and 74 (67.9%) were adolescents or young adults (mean age: 18 years), with 58.0% being females. A change of 51.0% was observed in SIT prescription following molecular etiological diagnosis by means of a multi-parameter microarray.

Conclusions: Molecular diagnosis by means of multi-parameter tests increases the accuracy of etiological diagnosis and helps to define an accurate composition of SIT.

Background: Chronic obstructive pulmonary disease (COPD) is a familiar disease, and owns high morbidity and mortality, which critically damages the health of patients. Ubiquitin-specific peptidase 8 (USP8) is a pivotal protein to join in the regulation of some diseases. In a previous report, it was determined that USP8 expression is down-regulated in LPS-treated BEAS-2B cells, and USP8 restrains inflammatory response and accelerates cell viability. However, the regulatory roles of USP8 on ferroptosis in COPD are rarely reported, and the associated molecular mechanisms keep vague.

Objective: To investigate the regulatory functions of USP8 in COPD progression.

Material and methods: The lung functions were measured through the Buxco Fine Pointe Series Whole Body Plethysmography (WBP). The Fe level was tested through the Fe assay kit. The protein expressions were assessed through western blot. The levels of tumor necrosis -factor-α, interleukin 6, and interleukin 8 were evaluated through enzyme-linked immunosorbent serologic assay. Cell viability was tested through CCK-8 assay.

Results: In this work, it was discovered that overexpression of USP8 improved lung function in COPD mice. In addition, overexpression of USP8 repressed ferroptosis by regulating glutathione peroxidase 4 and acyl-CoA synthetase long-chain family 4 expressions in COPD mice. Overexpression of USP8 suppressed inflammation in COPD mice. Furthermore, overexpression of USP8 suppressed ferroptosis in COPD cell model. At last, it was verified that overexpression of USP8 accelerated ubiquitin aldehyde-binding protein 1 (OTUB1)/solute carrier family 7 member 11 (SLC7A11) pathway.

Conclusion: This study manifested that overexpression of USP8 restrained inflammation and ferroptosis in COPD by regulating the OTUB1/SLC7A11 signaling pathway. This discovery hinted that USP8 could be a potential target for COPD treatment.

Asthma is a common chronic lung disease, and COVID-19 pandemic as a respiratory viral disease led to lung infection and resulted in millions of deaths. So, the impact of COVID-19 on asthma outcomes and the risk of being infected or hospitalized should be clarified. Systematic review and meta-analysis on the outcomes and risk of asthma for people with COVID-19 was done by searching electronic databases between 1 December 2019 and 31 July 2023. A total of 48 studies from 27 countries spread across all continents were included in the review. The prevalence of asthma among COVID-19 patients was 7.9%, and the analysis demonstrated a 16.5% reduction in the risk ratio for acquiring COVID-19 among subjects with asthma compared to those without asthma. There was no statistically significant difference in hospitalization risk, ICU admission risk, and death risk for COVID-19 patients with no asthma compared to those with asthma. The risk of death from COVID-19 was similar between nonasthmatics and asthmatics. The findings indicated that subjects with asthma may be at a lower risk of having infection with COVID-19 compared to those without asthma, but they have a similar risk of hospitalization and mortality.

Background: Pulmonary fibrosis is a pathological hallmark of lung injury. It is an aggressive disease that replaces normal lung parenchyma by fibrotic tissue. The transforming growth factor-beta-mothers against decapentaplegic homolog 3 (TGF-β1-Smad3) signaling pathway plays a key role in regulating lung fibrosis. Decorin (DCN), a small leucine-rich proteoglycan, has a modulatory effect on the immune system by reversibly binding with TGF-β and reducing its bioavailability. Mesenchymal stem cell (MSC) therapy is a new strategy that has an immune-modulatory capacity.

Objective: The aim of this study was to introduce a new therapeutic approach to harness remodeling in injured lung.

Material and methods: Bone marrow MSCs were isolated and transduced by decorin gene. Lung injury was induced by bleomycin and mice were treated with MSCs, MSCs-decorin, and decorin. Then, oxidative stress biomarkers, remodeling biomarkers, bronchoalveolar lavage cells, and histopathology study were conducted.

Results: Reduced catalase and superoxide dismutase increased due to treatments. Elevated malondialdehyde, hydroxyproline, TGF-β levels, and polymorphonuclear cells count decreased in the treated groups. Additionally, the histopathology of lung tissues showed controlled inflammation and fibrosis.

Conclusion: Transfected decorin gene to MSCs and used cell therapy could control remodeling and bleomycin-induced lung injury.

Background: Allergy to lipid transfer proteins (LPT) is common in Mediterranean Europe, and it causes severe reactions in patients and affects multiple foods, impairing the quality of life.

Objective: This study aimed to describe the clinical and sensitization profile of patients with LTP syndrome and to determine a clinical pattern of severity. Molecular diagnosis is shown in a broad population through microarrays.

Material and methods: This study was performed at the LTP Allergy Consultation of the Reina Sofia Hospital in Murcia, Spain. We analyzed the patients' characteristics, reactions, cofactors, food implicated, quality of life, skin prick test to food and aeroallergens, and serologic parameters, such as total immunoglobulin E, peach LTP (Pru p 3 IgE) and immunoglobulin G4, and microarray Immuno Solid-phase Allergen Chip (ISAC). We related the severity of the reactions with other variables.

Results: We presented a series of 236 patients diagnosed with LTP allergy, 54.66% suffering from anaphylaxis, 36.02% from urticaria angioedema, and 9.32% from oral allergy syndrome. The most frequently implicated food was peach, producing symptoms in 70% of patients, followed by walnut in 55%, peanut in 45%, hazelnut in 44%, and apple in 38% patients. Regarding the food that provoked anaphylaxis, walnut was the most frequent instigator, along with peach, peanut, hazelnut, almond, sunflower seed, and apple. According to the severity of LPT reaction, we did not discover significant differences in gender, age, food group involved, and serologic parameters. We found differences in the presence of cofactors, with 48.84% of cofactors in patients with anaphylaxis, compared to 27.1% in patients without anaphylaxis and in family allergy background (P < 0.0001).

Conclusion: In our series of patients, 54% presented anaphylaxis, and the foods that most frequently produced symptoms were peaches, apples, and nuts. Cofactors and family allergy backgrounds were associated with the severity of LPT reaction.

Background: Chronic idiopathic thrombocytopenic purpura (ITP) is an autoimmune disease characterized by a breakdown of immune tolerance; in ITP, the body's immune system mistakenly attacks and destroys platelets. This study aims to investigate the role and underlying mechanisms of FOXP3 in chronic ITP.

Methods: Flow cytometry was used to detect the proportion of CD4⁺CD25⁺FOXP³⁺ regulatory T cells (Tregs) in CD4⁺CD25⁺ T lymphocytes from 20 patients with chronic ITP (CITP), 20 acute ITP (AITP) controls, and 20 healthy individuals.CD4⁺CD25⁺ Treg cells were isolated from peripheral blood of patients with CITP using magnetic beads and then treated with phosphate-buffered saline solution or decitabine (a methylation inhibitor) for 48 h. The levels of interleukin-2 (IL-2), IL-10, and transforming growth factor-beta1 (TGF-β1) in the plasma and CD4⁺CD25⁺ Treg cells were assessed by Enzyme-linked-immunosorbent serologic assay and quantitative real-time polymerase chain reaction (qRT-PCR). FOXP3 level was measured by qRT-PCR and Western blot analysis. Methylation-specific PCR (MS-PCR) was adopted to detect the status of FOXP3 methylation.

Results: The number of Treg cells and the contents of IL-2, IL-10, and TGF-β1 decreased in patients with CITP, compared to the AITP control group and normal group. FOXP3 expression was reduced and FOXP3 methylation increased in patients with CITP, compared to the AITP control group and normal group. Hypermethylation of FOXP3 promoter led to decrease in FOXP3 level in Treg cells. Inhibition of FOXP3 promoter hypermethylation promoted the secretion of IL-2, IL-10, and TGF-β1 in Treg cells.

Conclusion: The number of Treg cells in CITP patients decreased, and the hypermethylation of FOXP3 promoter led to reduction of its expression in Treg cells, thus affecting the immune functioning of Treg cells.

Background: Pulmonary fibrosis (PF) is a chronic, progressive, and irreversible heterogeneous disease of lung interstitial tissue. To combat progression of PF, new drugs are required to be developed. Rhizoma coptidis (COP), one of the main alkaloids of Coptis chinensis, is a traditional herbal medicine used to treat various inflammatory diseases.

Objective: To investigate the possible effects of Coptisine (Cop) on the growth, inflammation, as well as FMT of TNF-β1-induced HFL1 cells and uncover the mechanism.

Material and methods: Human fetal lung fibroblast 1 (HFL1) was induced using 6ng/mL TGF-β1 as a model of pulmonary fibrosis. CCK-8, Brdu, and transwell assays indicated the effects on cell growth as well as motility. qPCR and the corresponding kits indicted the effects on cell inflammation. Immunoblot showed the effects on FMT and further confirmed the mechanism.

Results: Coptisine inhibits excessive growth as well as motility of TNF-β1-induced HFL1 cells. It further inhibits inflammation and ROS levels in TNF-β1-induced HFL1 cells. Coptisine inhibits the FMT process of TNF-β1-induced HFL1 cells. Mechanically, coptisine promotes the Nrf2/HO-1 pathway.

Conclusion: Coptisine can inhibit the excessive growth, inflammation as well as FMT of lung fibroblasts into myofibroblasts. It could serve as a promising drug of PF.

Purpose: To investigate the effect of metformin on gut microbiota imbalance in patients with type 2 diabetes mellitus (T2DM), and the value of probiotic supplementation.

Methods: A total of 84 newly diagnosed T2DM patients were randomly divided into probiotics group, metformin group, and control group, with 28 patients in each group. The blood glucose control, islet function, gut microbiota, and inflammatory factors were compared between three groups.

Results: After 3 months of treatment, fasting plasma glucose (FPG), 2-h postprandial plasma glucose (2-h PG), and glycosylated hemoglobin A1c (HbA1c) were evidently decreased in both probiotics and metformin groups (P < 0.05) and were lower than that in the control group prior to treatment. Besides, FPG, 2-h PG, and HbA1c were lower in the metformin group than that in the control group. FPG, 2-h PG, and HbA1c were further lower in the probiotic group than in the metformin group (P < 0.05). Fasting insulin (FINS) and islet β cell (HOMA-β) -function were dramatically increased in the same group (P < 0.05), while insulin-resistant islet β cells (HOMA-IR) were significantly lower in the same group (P < 0.05); FINS and HOMA-β were significantly higher, while HOMA-IR was significantly lower (P < 0.05) in both groups than in the control group prior to treatment. HOMA-IR was also lower in the probiotic group than in the metformin group after treatment (P < 0.05); the number of lactobacilli and bifidobacteria increased (P < 0.05) in both probiotic and metformin groups than in the control group prior to treatment, and the number of Enterobacteriaceae and Enterococcus was lower in the control group prior to treatment (P < 0.05). In addition, the number of lactobacilli and bifidobacteria was higher and the number of enterobacteria and enterococci was lower in the probiotic group than that in the metformin group after treatment, and the differences were statistically significant (P < 0.05). Lipopolysaccharide (LPS), interleukin 6 (IL-6), and C-reactive protein (CRP) levels were lower in both probiotic and metformin groups (P < 0.05). The serum LPS, IL-6, and CRP levels were lower in both probiotic and metformin groups, compared to the control group prior to the treatment (P < 0.05).

Conclusion: Metformin while treating T2DM assists in improving the imbalance of gut microbiota.

Background: Dermatophagoides pteronyssinus and Dermatophagoides farinae belong to the family Pyroglyphidae (subfamily: "Dermatophagoidinae") and have the respective allergenic proteins of Der p1, Der p2, and Der p23 and Der f1 and Der f2. Euroglyphus maynei, belongs to the family Pyroglyphidae (subfamily: "Pyroglyphinae") and its main allergenic protein is Eur m1, a source of sensitization. Sensitization to D. pteronyssinus and D. farinae is assessed through skin tests, while sensitization to E. maynei is assessed less frequently.

Objective: This experimental work aims to analyze the prevalence of sensitization to E. maynei in patients with respiratory allergies treated at M. Albanesi Allergy and Immunology Unit in Bari, Italy, and the sequence homology of major allergenic proteins of E. maynei with D. farinae and D. pteronyssinus was analyzed.

Methods: In this real-life study, 65 patients were enrolled. In particular, patients with respiratory allergy were subjected to skin prick tests for common respiratory allergens, including Euroglyphus maynei. The sequence homology analysis was performed between the major allergenic proteins of E. maynei and those of D. pteronyssinus and D. farinae.

Results: Sensitization to E. maynei accounts for 41.5% of patients. All patients with E. maynei sensitization had concomitant sensitization to D. farinae and D. pteronyssinus. The analysis of sequence homology of Der p1 and Der f1 proteins with the sequence of Eur m1 protein demonstrated an identity of 84.4% and 86%, respectively.

Conclusions: Nearly 50% of house dust mites-sensitized patients have a concomitant sensitization to E. maynei. The cross-sensitization could be due to Der f1, Der p1, and Eur m1 similarity.

Introduction: Severe cutaneous adverse reactions (SCARs) arising from drug interactions can carry life-threatening implications and result in lasting effects. SCARs can be triggered by various factors, with trimethoprim/sulfamethoxazole identified as a primary culprit. Anticonvulsants and antineoplastic agents have been noted as secondary triggers. Notably, antineoplastics linked to SCARs include immunomodulatory agents. The higher mortality rates among cancer patients with SCARs underscore the significance of comprehending cancer--specific risk factors. Our objective is to present the case of a boy with acute lymphocytic leukemia (ALL) who developed Stevens-Johnson syndrome (SJS) following MTX treatment.

Case report: We present the case of a three-year-old male patient diagnosed with ALL who developed Stevens-Johnson syndrome (SJS) subsequent to the administration of MTX, following the "BFM 2009" protocol. He had undergone intrathecal MTX administration on six previous occasions. Our patient received IVIG at a dose of 2g/kg along with steroids, resulting in partial clinical improvement after 21 days. An innovative protocol was developed, involving IVIG before MTX infusion and dexamethasone before MTXi, with folinic acid rescue. Intravenous immunoglobulin (IVIG) mitigates SJS/TEN via type IV hypersensitivity down-regulation and apoptosis curbing.

Conclusion: As far as we know, the prophylactic use of IVIG to counteract SCARs in a pediatric leukemia patient represents uncharted territory. Moreover, research into the immune system dynamics within these patients and the preservation of indispensable treatments should involve allergist-immunologists as part of the multidisciplinary team attending to neoplastic conditions.