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1 Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA, USA; Department of Medical Pharmacology and Physiology, University of Missour-Columbia, Columbia, MO, USA; Inflammation and Immunology, Kyoto Prefectural University of Medicine, Kyoto, Japan
2 Inflammation and Immunology, Kyoto Prefectural University of Medicine, Kyoto, Japan
3 Department of Medical Pharmacology and Physiology, University of Missour-Columbia, Columbia, MO, USA
4 Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA, USA
5 Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA, USA; Inflammation and Immunology, Kyoto Prefectural University of Medicine, Kyoto, Japan
* To whom correspondence should be addressed. E-mail: KorthuisR{at}health.missouri.edu.
The aim of this study was to determine the role of calcitonin gene-related peptide (CGRP) in the postischemic anti-inflammatory effects of antecedent ethanol ingestion. Ethanol was administered to wild-type (WT) C57/BL6 mice on Day 1 as a bolus by gavage at a dose that produces a peak plasma ethanol of 45 mg/dl 30 min after administration. Twenty-four hours later (Day 2), the superior mesenteric artery was occluded for 45 min followed by 60 min of reperfusion (I/R). Intravital fluorescence microscopy was used to quantify the numbers of rolling (LR) and adherent (LA) leukocytes labeled with carboxy-fluorescein diacetate succimidyl ester in postcapillary venules of the small intestine. I/R increased LR and LA, effects that were prevented by antecedent ethanol. The postischemic anti-inflammatory effects of ethanol consumption were abolished by administration of a specific CGRP receptor antagonist (CGRP 8-37) or following sensory nerve neurotransmitter depletion (using capsaicin administered 4 days before ethanol ingestion, which initially induces rapid release of CGRP from sensory nerves, thereby depleting stored neuropeptide). Administration of exogenous CGRP or induction of endogenous CGRP release by treatment with capsaicin 24 hrs prior to I/R mimicked the postischemic anti-inflammatory effects of antecedent ethanol ingestion. Preconditioning with capsaicin 24 hr prior to I/R was prevented by coincident treatment with CGRP 8-37 while exogenous CGRP induced an anti-inflammatory phenotype in mice depleted of CGRP by capsaicin administration 4 days earlier. Our results indicate that effect of antecedent ethanol ingestion to prevent postischemic LR and LA is initiated by a CGRP-dependent mechanism.
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