[Expression of serum Clara cell secretory protein 10 in wheezing children under 5 years old]

Xiu-Fang Wang1, Ying-Ying Hou, Dan Bi

  • 1Department of Pediatrics, Third Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China. wxf456@126.com

Insights

Serum Clara cell secretory protein 10 (CC10) levels are lower in wheezing children, especially those with atopic risks. Lower CC10 correlates with higher IgE in atopic wheezing children.

Area of Science:

  • Pediatric Allergy and Immunology
  • Respiratory Medicine
  • Biochemistry

Context:

  • Recurrent wheezing in children under 5 is a significant clinical challenge.
  • Atopy is a known risk factor for persistent wheezing and asthma development.
  • Clara cell secretory protein 10 (CC10) is an anti-inflammatory protein produced in the airways.

Purpose:

  • To investigate the association between serum levels of Clara cell secretory protein 10 (CC10) and total IgE in young children experiencing recurrent wheezing.
  • To compare CC10 and IgE levels between wheezing children with and without high atopic risk, and a healthy control group.

Summary:

  • Serum CC10 levels were significantly lower in both wheezing groups compared to controls.
  • Wheezing children with high atopic risks exhibited lower CC10 levels than those without atopic risks.
  • Serum IgE levels were elevated in the atopic wheezing group compared to the non-atopic wheezing and control groups.
  • A strong negative correlation was observed between serum CC10 and IgE levels in wheezing children with atopic high risks.

Impact:

  • Findings suggest CC10 may play a protective role in pediatric wheezing, with diminished levels indicating increased susceptibility, particularly in atopic individuals.
  • The inverse relationship between CC10 and IgE in atopic wheezing children highlights potential biomarkers for disease severity and risk stratification.
  • This research contributes to understanding the pathophysiology of childhood wheezing and may inform future therapeutic strategies targeting CC10 or IgE pathways.
Abstract

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