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The “Bacterial Contamination Theory” proposes that such dysbiosis introduces lipopolysaccharides (LPS) into the uterine environment, which activate pattern recognition receptors through binding to the TLR4/MD2 complex, triggering MyD88-dependent signaling that phosphorylates IκB and liberates NF-κB for nuclear translocation, ultimately inducing chronic inflammatory cascades and further exacerbating endometriotic pathology