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Simon P. Hogan, PhDAssociate Professor Department of Pediatrics; Division of Allergy and ImmunologyVisit the Hogan Lab site.
Dr. Hogan's research group is focused on understanding the effect of allergic and non-allergic inflammatory reactions on intestinal epithelial function. In particular, he studies the effects of inflammation (T-cell and innate) on gastrointestinal function in food-induced anaphylaxis and inflammatory bowel diseases. He is defining the role of mast cells, IL-9, and IL-13 on the regulation of homeostatic intestinal permeability. Dr. Hogan is also identifying CCL11, eosinophil activation, and recruitment of Paired immunoglobulin receptor-B in intestinal inflammation and colonic injury. His approach integrates basic, translational and clinical research streams with advanced molecular and cellular biological techniques and state-of-the-art mouse models of disease. He hopes that by delineating the cellular and molecular inflammatory cascades involved in food-induced anaphylaxis and IBD, he will be able to better understanding the functional consequences of intestinal inflammatory diseases. Furthermore, it is hoped that these studies will identify new therapeutics targets for the treatment and prevention of these debilitating diseases.
Dr. Hogan has used the Gene and Protein Expression and Bioinformatics Cores in collaboration with Dr. Aronow to identify the role of Relm-beta in colonic injury. He has also utilized the Integrative Morphology Core to detect chemokines in the GI tract. Additionally, Dr. Hogan collaborates with Drs. Denson, Han, Shroyer and Steinbrecher investigating the underlying molecular pathways involved in the regulation of IBD. Anticipated Core use: Integrative Morphology, Gene and Protein Expression, and Bioinformatics Core.
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Decreased claudin-3 expression in jejunal crypt epithelium of Mcpt4-/- and Wsh mice. (A) E-cadherin, claudin-1, -2, and -3 and actin were evaluated by Western blot. (B) Densitometric analysis of claudin-3 expression normalized to -actin. (C) Quantitative real-time PCR analysis of claudin-3 normalized to HPRT. (D) Claudin-3 (green) and E-cadherin (red) immunofluorescence of the villi (Top) and crypts (Bottom) of jejunum from WT (Left), Mcpt4-/- (Middle), and Wsh (Right) mice; nuclei stained by DAPI (blue). Western representative of three individual experiments. Densitometry represents mean ± SEM; n = 10 mice. PCR represents n = 6–8 mice per group. Statistical significance is: **, P < 0.01, ***, P < 0.001. Figure 3 from Proc Natl Acad Sci USA, 2009;106:22381-6.
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