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Thus, enriched G- in patients with GER symptoms may induce esophageal barrier dysfunction via the LPS-TLR2-IL-6-claudin-1-DIS pathway ( TLR4 expression is increased in patients with GERD, triggering an inflammatory response involved in the further development of GERD.TLR4 expression in normal squamous epithelial samples is mainly confined to the basal layer of the squamous epithelium, which routinely may not come into contact with PAMPs expressed by the esophageal microbiota, and reflux increases TLR4 expression ( 4.2 Dysbiotic microbiome stimulates cyclooxygenase-2 expression, affects gastric emptying, and induces GERD Cyclooxygenase-2 (COX-2) is the rate-limiting enzyme that catalyzes the initiating step in the metabolism of arachidonic acid to prostaglandin H2 and is a precursor to prostaglandins such as prostaglandins, thromboxanes, and prostacyclins, which act as autocrine and paracrine lipid mediators in the maintenance of local homeostasis by mediating vascular function, wound healing, and inflammation ( 4.3 Dysbiosis leads to overexpression of inducible nitric oxide synthase affecting LES function and inducing GERD Inducible Nitric Oxide Synthase (iNOS) is an enzyme that produces nitric oxide (NO) by oxidizing L -arginine

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TB-500 has a distinct amino acid segment [(17)LKKTETQ(23)] which is hypothesized to be responsible for actin binding and potentially enhancing cellular motility

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