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Such expansion is clinically relevant because excess microbially generated HS and related sulfur metabolites can erode the mucus layer and perturb tight-junction architecture, thereby increasing intestinal permeability and facilitating translocation of pro-inflammatory microbial products

alpha-Lipoic acid inhibits Helicobacter pylori-induced oncogene expression and hyperproliferation by suppressing the activation of NADPH oxidase in gastric epithelial cells

Norepinephrine dysregulates the immune response and compromises host defense during sepsis

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