Background: Systemic low-grade inflammation has been demonstrated in a range of the frequent noncommunicable diseases (NCDs) proposing a shared mechanism, but is largely unexplored in relation to allergic sensitization. We therefore aimed to investigate the possible association with childhood allergic sensitization.
Methods: High-sensitivity C-reactive protein (hs-CRP), interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), and chemokine (C-X-C motif) ligand 8 (CXCL8) were measured in plasma at age 6 months (N = 214) and 7 years (N = 277) in children from the Copenhagen Prospective Studies on Asthma in Childhood (COPSAC ) birth cohort. Allergic sensitization against common inhalant and food allergens was determined longitudinally at ages ½, 1½, 4 and 6 years by specific IgE assessments and skin prick tests. Associations between inflammatory biomarkers and sensitization phenotypes were tested with logistic regression and principal component analyses (PCAs).
Results: Adjusted for gender, recent infections, and a CRP genetic risk score, hs-CRP at 7 years was associated with concurrent elevated specific IgE against any allergen [adjusted OR (aOR) = 1.40; 95% CI, 1.14-1.72; P = 0.001], aeroallergens (aOR, 1.43; 1.15-1.77; P = 0.001), food allergens (aOR, 1.31; 95% CI, 1.02-1.67; P = 0.04), sensitization without any clinical allergy symptoms (aOR = 1.40; 1.06-1.85; P = 0.02), and with similar findings for skin prick tests. The other inflammatory markers were not univariately associated with sensitization, but multiparametric PCA suggested a specific inflammatory response among sensitized children. Inflammatory markers at age 6 months were not associated with subsequent development of sensitization phenotypes.
Conclusions: Elevated hs-CRP is associated with allergic sensitization in school-aged children suggesting systemic low-grade inflammation as a phenotypic characteristic of this early-onset NCD.
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http://dx.doi.org/10.1111/all.13108 | DOI Listing |
Curr Opin Allergy Clin Immunol
January 2025
Department of Pulmonology, Allergy and Thoracic Oncology, University Hospital of Montpellier, Montpellier, France.
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Queensland Alliance for Environmental Health Sciences (QAEHS), The University of Queensland, Brisbane, Queensland 4102, Australia.
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Institute of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria; Laboratory of Immunopathology, Department of Clinical Immunology and Allergy, Sechenov First Moscow State Medical University, Moscow, Russia; Karl Landsteiner University, Krems an der Donau, Austria; National Research Center, National Research Center Institute of Immunology (NRCI) Institute of Immunology, Federal Medical-Biological Agency of Russia (FMBA), Moscow, Russia.
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Increasing epidemiological evidence has proved that early-life exposure to inorganic arsenic (As) elevates the risks of childhood asthma. The present research aimed to explore susceptibility of respiratory As exposure to allergic asthma in a mouse model. BALB/c mice on postnatal day (PND) 28 were exposed to ddHO or NaAsO aerosol for 4 hours daily over 5 consecutive weeks via respiratory tract.
View Article and Find Full Text PDFIntroduction: Allergic rhinitis (AR) is a common respiratory disorder influenced by various factors in its pathogenesis. Recent studies have begun to emphasize the significant role of gut microbiota in immune modulation and its potential association with the development of AR. This research aims to characterize the gut microbiota of patients with AR who are sensitized via inhalation, utilizing 16S rRNA sequencing to shed light on the pathogenesis of AR and identify potential therapeutic targets.
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