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IL-17C contributes to NTHi-induced inflammation and lung damage in experimental COPD and is present in sputum during

Giovanna Vella1, Felix Ritzmann1, Lisa Wolf1

  • 1Department of Internal Medicine V - Pulmonology, Allergology and Respiratory Critical Care Medicine, Saarland University, Homburg, Germany.

Plos One
|January 7, 2021
PubMed

Insights

Interleukin-17C (IL-17C) drives harmful lung inflammation in chronic obstructive pulmonary disease (COPD) exacerbations triggered by bacteria. Reducing IL-17C lessened inflammation in COPD models, suggesting it

Area of Science:

  • Pulmonary Medicine
  • Immunology
  • Respiratory Research

Background:

  • Neutrophilic inflammation is a key driver of lung function loss in chronic obstructive pulmonary disease (COPD).
  • Nontypeable Haemophilus influenzae (NTHi) and cigarette smoke (CS) are major triggers of COPD exacerbations and chronic inflammation.
  • Interleukin-17C (IL-17C), a cytokine produced by airway epithelial cells, is implicated in regulating neutrophilic responses.

Purpose of the Study:

  • To investigate the role of IL-17C in NTHi- and CS-induced COPD models.
  • To determine the association of IL-17C with COPD severity in patients.

Main Methods:

  • Utilized IL-17C-deficient (Il-17c-/-) mice exposed to chronic or acute NTHi and CS.
  • Quantified pulmonary neutrophils and assessed tissue destruction in mouse lungs.
  • Analyzed IL-17C, IL-17A, and IL-17E concentrations in sputum from COPD patients across different severity stages (GOLD I-IV).

Main Results:

  • Il-17c-/- mice exhibited reduced neutrophilic inflammation and tissue damage following chronic NTHi exposure.
  • Acute NTHi and CS co-exposure led to decreased pulmonary neutrophils in Il-17c-/- mice.
  • However, Il-17c-/- mice showed no protection against CS-induced lung inflammation.
  • IL-17C levels in sputum correlated positively with COPD severity (GOLD III/IV vs. GOLD I/II), unlike IL-17A and IL-17E.

Conclusions:

  • IL-17C plays a significant role in promoting bacterial-induced pulmonary inflammation in COPD.
  • Targeting IL-17C may offer a therapeutic strategy for bacterial-triggered COPD exacerbations.
  • IL-17C is a potential biomarker for COPD disease severity.

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