Abstract
Intestinal mononuclear phagocytes (MPs) comprise dendritic cells (DCs) and macrophages (Mφs) that play different roles in response to Salmonella infection. After phagocytosis, DCs expressing CD103 transport Salmonella from the intestinal tract to the mesenteric lymph nodes (MLN) and induce adaptive immune responses whereas resident Mφs expressing CX3CR1 capture bacteria in the lumen and reside in the lamina propria (LP) where they induce a local immune response. CX3CR1+ Mφs are generated from Ly6Chi monocytes that enter the colonic mucosa and differentiate locally. We previously demonstrated that the probiotic yeast Saccharomyces boulardii CNCM I-745 (S.b) prevents infection by Salmonella enterica serovar Typhimurium (ST), decreases ST translocation to the peripheral organs and modifies the pro-and anti-inflammatory cytokine profiles in the gut. In the present study, we investigated the effect of S.b on the migratory CD103+ DCs and the resident CX3CR1+ Mφs. MPs were isolated from the LP of streptomycin-treated mice infected by ST with or without S.b treatment before or during the infection. In S.b-pretreated mice, we observed a decrease of the CD103+ DCs in the LP that was associated with the drop of ST recovery from MLN. Interestingly, S.b induced an infiltration of LP by classical Ly6Chi monocytes, and S.b modified the monocyte-Mφ maturation process in ST-infected mice. Our results showed that S.b treatment induced the expansion of Ly6Chi monocytes in the blood as well as in the bone marrow (BM) of mice, thus contributing to the Mφ replenishment in LP from blood monocytes. In vitro experiments conducted on BM cells confirmed that S.b induced the expansion of CX3CR1+ Mφs and concomitantly ST phagocytosis. Altogether, these data demonstrate that Saccharomyces boulardii CNCM I-745 modulates the innate immune response. Although here, we cannot explicitly delineate direct effects on ST from innate immunity, S. b-amplified innate immunity correlated with partial protection from ST infection. This study shows that S.b can induce the expansion of classical monocytes that are precursors of resident Mφs in the LP.
Highlights
The intestinal innate immune system plays a crucial role in limiting microbial access to the gut tissue
As CD103+ dendritic cells (DCs) constitute the migratory cells that translocate serovar Typhimurium (ST) from the lamina propria (LP) to the mesenteric lymph nodes (MLNs) [19], this result suggests a lower traffic of these cells from the LP to the MLN of treated mice
Mice were infected intra-gastrically for 3 days and LP and MLNs were dissected for further analyzes. (A) The number of viable ST bacteria recovered from the MLNs was determined in control mice and in mice infected with ST alone or infected in the presence of S.b or pretreated with the yeast before infection
Summary
The intestinal innate immune system plays a crucial role in limiting microbial access to the gut tissue. The first MP subclass, referred to as classical dendritic cells (DCs), is exclusively capable to migrate from the intestine to the mesenteric lymph nodes (MLNs) where they initiate adaptive immune responses [reviewed in [1]] These DCs are routinely identified by their co-expression of αE integrin (CD103) and CCR7 that controls DC migration from the lamina propria (LP) to the MLNs [2,3,4]. The second MP subclass, described in the literature as “non-conventional DCs” or “resident” macrophages (Mφs), resides in the intestinal LP [5, 6] These Mφs possess a high phagocytic activity and express CX3CR1, the fractalkine receptor (CX3CR1+ Mφs)
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