Studies on the regulatory roles for Retinoic Acid RA during host microbial interaction implications for S aureus and C albicans infections

Abstract

Chronic inflammatory disorder is one of the leading causes of morbidity and mortality newlineworldwide. It underlies the development of metabolic diseases and arises in concert to newlinegenetic polymorphism and risk factors including infectious diseases etc. Association between newlinepathogenic infection and inflammation governs tissue homeostasis, which often relies on newlineextensive crosstalk among signaling networks and host derived immune modulating factors. newlineSensing of pathogen associated molecular patterns (PAMPs) such as cell wall components newlineand cytosolic constituents relies on the expression of plethora of pattern recognition receptors(PRRs) displayed on or expressed inside immune and non-immune cells. PRRs can be classified into various families based on structural and functional divergence. These include: newlineToll like Receptors (TLRs), C-type lectins receptors (CLRs), Nucleotide binding and newlineoligomerisation domain (NOD) - like receptors (NLR) and Retinoic acid inducible gene newline(RIG) like receptors (RLRs). Interestingly, recent insight into studies on inflammatory newlinedisorders have shown that, vitamins play a central role in governing fate of diseases by newlineregulating cellular metabolism. Significantly, vitamin A deficiency is known to effectuate several aberrations in innate and adaptive immune responses. In this regard, our current study involves exploration of regulatory role of vitamin A metabolite Retinoic Acid (RA) in newlinemodulating host-microbial interaction. newline