[Effect of interleukin-17 on neutrophil apoptosis in patients with tuberculosis]

Lina Jiang1, Chunyan Yao2, Qili Jin2

  • 1Department of Pathophysiology, Anhui Key Laboratory of Infection and Immunity; Bengbu 233030, China.

Abstract

Insights

Neutrophil apoptosis increases with culture time, and is higher in tuberculosis patients. Interleukin-17 (IL-17) at low doses delays neutrophil apoptosis, while high doses accelerate it, potentially via the ERK pathway.

Area of Science:

  • Immunology
  • Cell Biology

Context:

  • Pulmonary tuberculosis (TB) is a significant global health challenge.
  • Neutrophils play a critical role in the immune response to TB.
  • Dysregulation of neutrophil apoptosis may contribute to TB pathogenesis.

Purpose:

  • To investigate the effect of interleukin-17 (IL-17) on neutrophil apoptosis in TB patients.
  • To explore the signaling pathway involved in IL-17-mediated neutrophil apoptosis.

Summary:

  • Neutrophil apoptosis rates increased with culture time and were higher in TB patients compared to healthy adults.
  • Low concentrations of IL-17 delayed neutrophil apoptosis, while high concentrations accelerated it in both groups.
  • The anti-apoptotic effect of IL-17 was partially inhibited by a MAPK pathway inhibitor (U0126), suggesting involvement of the ERK pathway.

Impact:

  • This study elucidates the complex role of IL-17 in neutrophil apoptosis during TB.
  • Findings may offer insights into novel therapeutic strategies targeting neutrophil apoptosis in TB management.
  • Understanding IL-17's influence on neutrophils could improve TB treatment outcomes.