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Cell Physiol Biochem. 2013;32(6):1878-90. doi: 10.1159/000356644. Epub 2013 Dec 20.

CCK1-receptor stimulation protects against gut mediator-induced lung damage during endotoxemia.

Author information

1
Department of General, Visceral and Transplant Surgery, University Hospital of Tuebingen, Tuebingen, Germany.

Abstract

BACKGROUND/AIMS:

Cholecystokinin 1-receptor (CCK1-R) activation by long chain fatty acid (LCFA) absorption stimulates vago-vagal reflex pathways in the brain stem. The present study determines whether this reflex also activates the cholinergic anti-inflammatory pathway, a pathway known to modulate cytokine release during endotoxemia.

METHODS:

Mesenteric lymph was obtained from wild type (WT) and CCK1-R knockout (CCK1-R(-/-)) mice intraperitoneally challenged with Lipopolysaccharid (LPS) (endotoxemic lymph, EL) and intestinally infused with vehicle or LCFA-enriched solution. The lymph was analyzed for TNFα, IL-6 and IL-10 concentration and administered to healthy recipient mice via jugular infusion. Alveolar wall thickness, myeloperoxidase (MPO) and TUNEL positive cells were determined in lung tissue of recipient mice.

RESULTS:

LCFA infusion in WT mice reduced TNFα concentration in EL by 49% compared to vehicle infusion, but had no effect in CCK1-R(-/-) mice. EL significantly increased the alveolar wall thickness, the number of MPO-positive and TUNEL-positive cells compared to control lymph administration. LCFA infusion in WT, but not in CCK1R(-/-) mice, significantly reduced these pathological effects of EL.

CONCLUSION:

During endotoxemia enteral LCFA absorption reduces TNFα release into mesenteric lymph and attenuates histomorphologic parameters of lung dysfunction. Failure to elicit this effect in CCK1R(-/-) mice demonstrates that anti-inflammatory properties of LCFAs are mediated through CCK1-Rs.

PMID:
24356325
PMCID:
PMC3959982
DOI:
10.1159/000356644
[Indexed for MEDLINE]
Free PMC Article

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