HS1 deficiency protects against sepsis by attenuating neutrophil-inflicted lung damage.

ABSTRACT: Sepsis remains an important health problem worldwide due to inefficient treatments often resulting in multi-organ failure. Neutrophil recruitment is critical during sepsis. While neutrophils are required to combat invading bacteria, excessive neutrophil recruitment contributes to tissue damage due to their arsenal of molecular weapons that do not distinguish between host and pathogen. Thus, neutrophil recruitment needs to be fine-tuned to ensure bacterial killing, while avoiding neutrophil-inflicted tissue damage. We recently showed that the actin-binding protein HS1 promotes neutrophil extravasation; and hypothesized that HS1 is also a critical regulator of sepsis progression. We evaluated the role of HS1 in a model of lethal sepsis induced by cecal-ligation and puncture. We found that se

SUBMITTER: Guerrero-Fonseca IM 

PROVIDER: S-EPMC10170315 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature