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Sal4 is a monoclonal polymeric IgA antibody directed against the O antigen (O-Ag) ofSalmonella enterica serovar Typhimurium (S . Typhimurium), which is sufficient to protect mice against intestinal infections fromS . Typhimurium. We recently reported that the exposure ofS . Typhimurium to Sal4 results in the immediate loss of flagellum-based motility, in alterations to the outer membrane (OM) integrity, and in the concomitant appearance of a mucoid phenotype that is reminiscent of cells in the earliest stages of biofilm formation. We demonstrate here that prolonged (&gt;4 h) exposure ofS . Typhimurium to Sal4 at 37°C (but not at ambient temperature [25°C]) results in measurable exopolysaccharide (EPS) accumulation and biofilm formation on both borosilicate glass surfaces and polystyrene microtiter plates. The polysaccharide produced byS . Typhimurium in response to Sal4 contains cellulose, in addition to O-Ag capsule and colanic acid. EPS production was dependent on YeaJ, a proposed inner membrane-localized diguanylate cyclase (DGC) and a known regulator of cellulose biosynthesis. AnS . Typhimurium ΔyeaJ strain was unable to produce cellulose or form a biofilm in response to Sal4. Conversely, the overexpression ofyeaJ inS . Typhimurium enhanced Sal4-induced biofilm formation and resulted in increased intracellular levels of cyclic dimeric guanosine monophosphate (c-di-GMP) compared to that of a wild-type control; this strongly suggests that YeaJ is indeed a functional DGC. Based on these data, we speculate that Sal4, by virtue of its ability to associate with the O-Ag and to induce OM stress, rendersS . Typhimurium avirulent by triggering a c-di-GMP-dependent signaling pathway via YeaJ that leads to the suppression of bacterial motility while simultaneously stimulating EPS production.

infection and immunity

Exposure of Salmonella enterica Serovar Typhimurium to a Protective Monoclonal IgA Triggers Exopolysaccharide Production via a Diguanylate Cyclase-Dependent Pathway