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Gram-negative bacterial populations increase at the lower esophageal sphincter during various forms of mucosal injury or disease. Their products—especially LPS—activate host immune responses that relax smooth muscle tone at this critical junction while promoting chronic inflammation. These changes underlie much of GERD pathogenesis and its complications including Barrett's metaplasia and cancer risk. Targeted modulation of this microbial community represents an emerging therapeutic strategy for related diseases.
LPS-mediated TLR activation leading to inflammation and LES relaxation
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