Defective phagocyte association during infection of <i>Galleria mellonella</i> with <i>Yersinia pseudotuberculosis</i> is detrimental to both insect host and microbe

Adhesins facilitate bacterial colonization and invasion of host tissues are considered virulence factors, but their impact on immune-mediated damage as a driver pathogenesis remains unclear. Yersinia pseudotuberculosis encodes for multivalent adhesion molecule (MAM), mammalian cell entry (MCE) family protein adhesin. MAMs widespread in Gram-negative bacteria enable enteric to colonize epithelial tissues. Their role interactions with the innate immune system contribution pathogenicity Here, we investigated howY. MAM contributes during infection Galleria mellonella insect model. We show that Y. is required efficient binding uptake by hemocytes, phagocytes. phagocytes determined factors. Loss MAM, deficient microbe–phagocyte interaction, increased G. mellonella. Diminished phagocyte association also led clearance. Furthermore, failed engage hyperactivated humoral responses, most notably melanin production. Despite clearing pathogen, excessive melanization death mortality. Our findings provide basis further studies investigating how microbe- host-factors integrate drive tractable experimental system.