Entry Route of Salmonella typhimurium Directs the Type of Induced Immune Response

Abstract

Secretory immunoglobulin A (SIgA) represents a first line of defense against mucosal pathogens by limiting their entrance. By using different strains of Salmonella typhimurium that target the two mechanisms of bacterial entry (microfold cell [M cell]- or dendritic cell-mediated), we demonstrated here that the distribution of bacteria after oral infection directed the type of induced immune response. M cell-penetrating invasive, but not noninvasive, S. typhimurium was found in large numbers in Peyer's patches (PPs), leading to the activation of immune cells and the release of fecal IgA. In contrast, both strains of bacteria were equally capable of reaching the mesenteric lymph node and the spleen and inducing IgG responses. These data suggest that PPs are absolutely required for the initiation of an IgA response to Salmonella, whereas they are dispensable for a systemic response. This compartmentalization could allow the fast generation of both mucosal and systemic acquired immunity to pathogens.

Chemokine Receptor CXCR5 Supports Solitary Intestinal Lymphoid Tissue Formation, B Cell Homing, and Induction of Intestinal IgA Responses

“…Therefore, the exclusive role of PP for the induction of IgA has been a matter of debate for a long time. Recent observations indicate that PP appear to be essential for intestinal immune responses to Salmonella (45)(46)(47), even though conflicting results have been obtained regarding the role of SILT in anti-Salmonella responses (48).…”

Delivery strategies to enhance oral vaccination against enteric infections

“…As in the case of PPs, a follicle associated epithelium with M cells is present on the lumen facing side of ILFs. Uptake of pathogens including S. typhimurium, leads to the formation of germinal centers (GCs) in mature ILFs [64][65][66]. Interestingly, it was found that the presence or absence of GCs in ILFs did not influence the active class switching of naïve B cells to active IgA secreting B cells [67].…”

Different Bacterial Pathogens, Different Strategies, Yet the Aim Is the Same: Evasion of Intestinal Dendritic Cell Recognition

“…This in turn promotes bacterial escape into the subepithelial compartment (36) and dissemination of the bacteria both locally and systemically. Surprisingly, the SPI-1-dependent pathway of invasion appears to be less important, because SPI-1-deficient Salmonellae still infect mice and cause colitis (34), although mucosal IgA responses are reduced (37). This observation raises the question as to what the biological relevance of the SPI-1-dependent invasion pathway might be.…”