Introduction Pseudomonas aeruginosa is a major cause of opportunistic infections, partly due to its ability to evade the complement system, a critical component of early innate immunity. Understanding the molecular mechanisms underlying complement evasion is essential for identifying new therapeutic targets. Methods We investigated the role of the major outer membrane porin OprG in complement resistance. Ligand blotting and whole-cell binding assays were used to evaluate binding of Factor H (FH) to bacteria. Functional assays measured C3 fragments deposition, membrane attack complex (MAC) formation, and bacterial survival in normal human serum, comparing an oprG-deficient mutant with the parental and complemented strain. The contribution of OprG to the virulence of P. aeruginosa was tested in vivo using a murine systemic infection model. Results OprG was identified as a novel ligand for FH. The oprG-deficient mutant exhibited significantly reduced FH binding, which was restored upon genetic complementation. Loss of OprG led to increased C3 fragment deposition and MAC formation, resulting in reduced bacterial survival in serum. In contrast, in the murine infection model, the oprG-deficient strain showed reduced survival and competitive fitness compared to the parental isolate, indicating attenuated virulence. Conclusions These findings establish OprG as a key mediator of complement resistance in P. aeruginosa by promoting FH recruitment. This mechanism enhances bacterial survival in serum and contributes to virulence, underscoring OprG-FH interaction as an immune evasion strategy and a potential target for therapeutic intervention.

عنوان المؤتمر

XII Jornades IdISBa (Theme: Ciències Òmiques: predir per prevenir)

دولة المؤتمر

أسبانيا

تاريخ المؤتمر

27 نوفمبر، 2025 - 28 نوفمبر، 2025

راعي المؤتمر

IdISBa (Institut d'Investigació Sanitària de les Illes Balears)

معلومات إضافية

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