Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-4-23
pubmed:abstractText
Stress mobilizes elements from the neuroendocrine system to modulate immune responses. Cholinergic stimulation via nicotinic receptor (nAchR) is a major neuroendocrine signaling axis associated with the stress response whose specific effects on the immune system are unknown. Here, we show that nAchR activation by topical agonist application or deletion of the nAChR antagonist catestatin (Chga(-/-)) reduced antimicrobial peptide (AMP) activity in skin extracts and increased susceptibility to methicillin-resistant Staphylococcus aureus and Group A Streptococcus infections. The adverse effects on AMP expression and infection were rescued by topical application of a nAChR antagonist. Stress-induced nAChR activation increased infection in wild-type, but not Chga(-/-) or cathelicidin-deficient, mice. These data identify a mechanism for the negative regulation of host-innate AMP response to infection through cholinergic activation and indicate nAChR-mediated cathelicidin dysregulation as a potential mechanism for increased susceptibility to infection following prolonged stress or nicotine use.
pubmed:grant
pubmed:commentsCorrections
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pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1934-6069
pubmed:author
pubmed:copyrightInfo
Copyright 2010 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
22
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
277-89
pubmed:dateRevised
2011-7-27
pubmed:meshHeading
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