학술논문

Lack of Platelet-Activating Factor Receptor Attenuates Experimental Food Allergy but Not Its Metabolic Alterations regarding Adipokine Levels.
Document Type
Article
Source
BioMed Research International. 5/25/2016, Vol. 2016, p1-10. 10p.
Subject
*ADIPOSE tissues
*ANIMAL experimentation
*BLOOD platelets
*BLOOD platelet activation
*BODY weight
*CELL receptors
*CELLULAR signal transduction
*ENZYME-linked immunosorbent assay
*FOOD allergy
*IMMUNOGLOBULINS
*INFLAMMATION
*SMALL intestine
*LEUCOCYTES
*RESEARCH methodology
*MICE
*MICROSCOPY
*PEPTIDE hormones
*PHOTOGRAPHY
*PROBABILITY theory
*RESEARCH funding
*STATISTICS
*TISSUE culture
*DATA analysis
*ALBUMINS
*PRE-tests & post-tests
*REPEATED measures design
*DATA analysis software
*DESCRIPTIVE statistics
*ONE-way analysis of variance
Language
ISSN
2314-6133
Abstract
Platelet-activating factor (PAF) is known to be an important mediator of anaphylaxis. However, there is a lack of information in the literature about the role of PAF in food allergy. The aim of this work was to elucidate the participation of PAF during food allergy development and the consequent adipose tissue inflammation along with its alterations. Our data demonstrated that, both before oral challenge and after 7 days receiving ovalbumin (OVA) diet, OVA-sensitized mice lacking the PAF receptor (PAFR) showed a decreased level of anti-OVA IgE associated with attenuated allergic markers in comparison to wild type (WT) mice. Moreover, there was less body weight and adipose tissue loss in PAFR-deficient mice. However, some features of inflamed adipose tissue presented by sensitized PAFR-deficient and WT mice after oral challenge were similar, such as a higher rate of rolling leukocytes in this tissue and lower circulating levels of adipokines (resistin and adiponectin) in comparison to nonsensitized mice. Therefore, PAF signaling through PAFR is important for the allergic response to OVA but not for the adipokine alterations caused by this inflammatory process. Our work clarifies some effects of PAF during food allergy along with its role on the metabolic consequences of this inflammatory process. [ABSTRACT FROM AUTHOR]