Contribution of CARD9 signaling to wound healing in skin promoted by topical administration of heat-killed <i>Enterococcus faecalis</i> strain KH2 and the involvement of Dectin-2.

ABSTRACT:

Introduction

Lactic acid bacteria (LAB) are well known for their beneficial effects on the regulation of immune responses and host protection against microbial infections. We previously reported that heat-killed Enterococcus faecalis strain KH2 (heat-killed KH2), a species of LAB, enhances inflammatory responses at wound sites and accelerates the skin wound healing process. In this study, we aimed to clarify the pathway underlying the wound-healing effects of heat-killed KH2. We focused on CARD9, a common adaptor molecule for C-type lectin receptors and Dectin-2, the upstream receptor for this adaptor molecule.

Methods

Four full-thickness dermal wounds were created on the backs of wild-type (WT) mice, CARD9 KO mice, and Dectin-2 KO mice, and the effects of heat-killed

SUBMITTER: Kurosaka S 

PROVIDER: S-EPMC12198255 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature