Topical nicotinic receptor activation improves wound bacterial infection outcomes and TLR2-mediated inflammation in diabetic mouse wounds.

ABSTRACT: The cholinergic anti-inflammatory pathway can directly affect skin antibacterial responses via nicotinic acetylcholine receptors (nAChRs). In particular, α7 nAChR (CHRNA7) present in the epidermis modulates the host response to wounding and/or wound bacterial infection. While physiologic inflammation is required to initiate normal wound repair and can be triggered by Toll-like receptor (TLR) activation, chronic inflammation is frequently observed in diabetic wounds and can occur, in part, via excessive TLR2 activation or production. Consequently, this can delay physiologic wound healing responses and increase diabetic host susceptibility to bacterial infection. In this study, we demonstrate that topical nAChR activation diminishes bacterial survival and systemic dissemination in a mouse mo

SUBMITTER: Kishibe M 

PROVIDER: S-EPMC6295218 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature