Predictive value of IL-35 and IL-17 in diagnosis of childhood asthma

Amira Ibrahim Mansour1, Eman Rateb Abd Almonaem2, Ola Galal Behairy2

  • 1a Departments of Clinical and Chemical Pathology , Benha University , Benha , Egypt.

Insights

Interleukin-17 (IL-17) levels are higher and Interleukin-35 (IL-35) levels are lower in children with asthma. These cytokines show a negative correlation and may play a role in childhood asthma development.

Area of Science:

  • Immunology
  • Pediatrics
  • Respiratory Medicine

Background:

  • Childhood asthma is a prevalent chronic respiratory disease.
  • The roles of specific cytokines, such as IL-17 and IL-35, in asthma pathogenesis require further elucidation.

Purpose of the Study:

  • To investigate the correlation between serum levels of IL-17 and IL-35 and the presence and severity of childhood asthma.
  • To assess the diagnostic potential of IL-17 and IL-35 in childhood asthma.

Main Methods:

  • Serum levels of IL-17 and IL-35 were measured using ELISA in 60 asthmatic children and 30 healthy controls.
  • Participants underwent clinical evaluation, pulmonary function tests, and laboratory assessments including CBC and total IgE.
  • Asthmatic children were classified based on GINA guidelines for asthma severity.

Main Results:

  • Asthmatic children exhibited significantly higher eosinophil counts, total IgE, and IL-17 levels compared to controls (p < .001).
  • Conversely, IL-35 levels were significantly lower in asthmatic children (p < .001).
  • IL-17 showed a positive correlation with IgE and eosinophils, while IL-35 showed negative correlations. A strong negative correlation existed between IL-17 and IL-35.

Conclusions:

  • IL-17 is upregulated and IL-35 is downregulated in childhood asthma, with a significant negative correlation between them.
  • Serum IL-35 levels <189.5 pg/mL and IL-17 levels >13.1 pg/mL can predict childhood asthma.
  • Combined analysis of IL-17 and IL-35 enhances diagnostic sensitivity to 95%, suggesting their crucial roles in asthma pathogenesis.

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