Corynebacterium striatum drives neutrophilic asthma via IL-17 signaling activation.

Abstract

Corynebacterium striatum has recently been recognized as an emerging multidrug-resistant pathogen capable of causing both nosocomial and community-acquired infections, particularly in immunocompromised individuals and those with chronic conditions. However, direct evidence regarding the pathogenicity of C. striatum and its association with neutrophilic asthma remains poorly understood. In this study, a BALB/c mouse model infected with C. striatum was established at first to investigate its potential role in acute lung injury. The results demonstrated that C. striatum infection induced significant lung inflammation and pathological alterations, with more pronounced inflammatory responses observed in immunocompromised mice. Hematological analysis and fluorescence in situ hybridization (FISH) revealed a marked increase in neutrophil levels and confirmed the colonization of C. striatum in lung tissues. Furthermore, in an ovalbumin (OVA)-induced asthma model, C. striatum infection exacerbated neutrophilic inflammation and induced the significant upregulation of Interleukin (IL)-17, IL-6, and CXCL-8, alongside activation of the NF-κB signaling pathway. These findings suggest that C. striatum drives neutrophil recruitment and amplifies inflammatory responses by promoting a Th2/Th17 immune shift, highlighting the critical involvement of the IL-17 signaling pathway in C. striatum-associated asthma. This study provides novel experimental evidence supporting C. striatum as a respiratory pathogen and offers further theoretical rationale for targeting IL-17 in the treatment of C. striatum-related neutrophilic asthma.