Serum amyloid a promotes lung neutrophilia by increasing IL-17A levels in the mucosa and γδ T cells

Abstract

Rationale: Neutrophilic inflammation is an important pathologic feature of chronic obstructive pulmonary disease (COPD) and infectious exacerbations of COPD. Serum amyloid A (SAA) promotes neutrophilic inflammation by its interaction with lung mucosal ALX/ FPR2 receptors. However, little is knownabouthowthis endogenous mediator regulates IL-17A immunity. Objectives: To determine whether SAA causes neutrophilic inflammation by IL-17A-dependent mechanisms. Methods: The relationship between SAA and neutrophils was investigated in lung sections from patients with COPD and a chronic mouse model of SAA exposure. A neutralizing antibody to IL-17A was used to block SAA responses in vivo, and a cell-..