Sphingolipids as Mediators in the Crosstalk between Microbiota and Intestinal Cells: Implications for Inflammatory Bowel Disease

被引:35
|
作者
Bryan, Phillips-Farfan [1 ]
Karla, Carvajal [1 ]
Edgar Alejandro, Medina-Torres [2 ]
Sara Elva, Espinosa-Padilla [2 ]
Gemma, Fabrias [3 ]
Luz, Camacho [1 ]
机构
[1] Inst Nacl Pediat, Lab Nutr Expt, Ciudad De Mexico 04530, Mexico
[2] Inst Nacl Pediat, Unidad Invest Inmunodeficiencias, Ciudad De Mexico 04530, Mexico
[3] Inst Adv Chem Catalonia IQAC CSIC, Dept Biomed Chem, Res Unit Bioact Mol, Barcelona 08034, Spain
关键词
PLATELET-ACTIVATING-FACTOR; GENE-DEFICIENT MICE; EPITHELIAL BARRIER FUNCTION; SODIUM-INDUCED COLITIS; KILLER T-CELLS; ALKALINE SPHINGOMYELINASE; INCREASES INFLAMMATION; CERAMIDE ACCUMULATION; SIGNAL-TRANSDUCTION; SPHINGOSINE KINASE;
D O I
10.1155/2016/9890141
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Inflammatory bowel disease (IBD) describes different illnesses characterized by chronic inflammation of the gastrointestinal tract. Although the pathogenic mechanisms leading to IBD are poorly understood, immune system disturbances likely underlie its development. Sphingolipids (SLs) have been identified as important players and promising therapeutic targets to control inflammation in IBD. Interestingly, it seems that microorganisms of the normal gut microbiota and probiotics are involved in sphingolipid function. However, there is a great need to investigate the role of SLs as intermediates in the crosstalk between intestinal immunity and microorganisms. This review focuses on recent investigations that describe some mechanisms involved in the regulation of cytokine profiles by SLs. We also describe the importance of gut microbiota in providing signaling molecules that favor the communication between resident bacteria and intestinal cells. This, in turn, modulates the immune response in the bowel and likely in other peripheral organs. The potential of SLs and gut microbiota as targets or therapeutic agents for IBD is also discussed.
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页数:11
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