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Int. J. Mol. Sci. 2017, 18(8), 1720; doi:10.3390/ijms18081720

The Role of Sphingolipids on Innate Immunity to Intestinal Salmonella Infection

Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan
Received: 30 June 2017 / Revised: 25 July 2017 / Accepted: 27 July 2017 / Published: 7 August 2017
(This article belongs to the Special Issue Sphingolipids: Signals and Disease)
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Salmonella spp. remains a major public health problem for the whole world. To reduce the use of antimicrobial agents and drug-resistant Salmonella, a better strategy is to explore alternative therapy rather than to discover another antibiotic. Sphingolipid- and cholesterol-enriched lipid microdomains attract signaling proteins and orchestrate them toward cell signaling and membrane trafficking pathways. Recent studies have highlighted the crucial role of sphingolipids in the innate immunity against infecting pathogens. It is therefore mandatory to exploit the role of the membrane sphingolipids in the innate immunity of intestinal epithelia infected by this pathogen. In the present review, we focus on the role of sphingolipids in the innate immunity of intestinal epithelia against Salmonella infection, including adhesion, autophagy, bactericidal effect, barrier function, membrane trafficking, cytokine and antimicrobial peptide expression. The intervention of sphingolipid-enhanced foods to make our life healthy or pharmacological agents regulating sphingolipids is provided at the end. View Full-Text
Keywords: sphingolipids; Salmonella; intestine epithelia; innate immunity sphingolipids; Salmonella; intestine epithelia; innate immunity

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Huang, F.-C. The Role of Sphingolipids on Innate Immunity to Intestinal Salmonella Infection. Int. J. Mol. Sci. 2017, 18, 1720.

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