Abstract
Listeria monocytogenes (L.m) is efficiently controlled by several cells of the innate immunity, including the Mast Cell (MC). MC is activated by L.m inducing its degranulation, cytokine production and microbicidal mechanisms. TLR2 is required for the optimal control of L.m infection by different cells of the immune system. However, little is known about the MC receptors involved in recognizing this bacterium and whether these interactions mediate MC activation. In this study, we analyzed whether TLR2 is involved in mediating different MC activation responses during L.m infection. We found that despite MC were infected with L.m, they were able to clear the bacterial load. In addition, MC degranulated and produced ROS, TNF-α, IL-1β, IL-6, IL-13 and MCP-1 in response to bacterial infection. Interestingly, L.m induced the activation of signaling proteins: ERK, p38 and NF-κB. When TLR2 was blocked, L.m endocytosis, bactericidal activity, ROS production and mast cell degranulation were not affected. Interestingly, only IL-6 and IL-13 production were affected when TLR2 was inhibited in response to L.m infection. Furthermore, p38 activation depended on TLR2, but not ERK or NF-κB activation. These results indicate that TLR2 mediates only some MC activation pathways during L.m infection, mainly those related to IL-6 and IL-13 production.
Highlights
Mast cells (MC) are associated with type I hypersensitivity reactions [1]
We detected viable bacteria within bone-marrow-derived MCs (BMMC) at 0-hour post-infection with the different MOI of L.m tested; we recovered small amounts of this bacterium at 24h, corresponding to a reduction of more than 3 logarithms for any MOI tested (Figure 1D). These results indicate that BMMC degranulate and produce reactive oxygen species (ROS) with high amounts of L.m and that BMMC are capable of internalizing and controlling L.m infection
We observed that blocking this receptor significantly reduced the levels of IL-6 (Figure 5C) and IL-13 (Figure 5D) in both Peritoneum-derived mast cells (PMC) and BMMC. These results show that Mast Cell (MC) TLR2 does not participate in the production of TNF-a, IL-1b; and MCP-1; but regulates IL-6 and IL-13 production during L.m infection
Summary
Mast cells (MC) are associated with type I hypersensitivity reactions [1]. Growing evidence has placed them as initiators of the inflammatory process against several infectious agents, including bacteria [2] Due to their strategic location in mucosal epithelia, skin, and connective tissue, they can respond immediately to the signals derived from mutualistic and pathogenic bacteria, adapting their response to maintain host homeostasis [3]. In this way, MC are provided with at least one member of each of the Pattern Recognition Receptor (PRR) families. Several studies have shown that MC are involved in the immune response to pathogenic bacteria, including: Pseudomonas aeruginosa [6], Klebsiella pneumoniae [7], Staphylococcus aureus [8], Mycobacterium tuberculosis [9] and Listeria monocytogenes (L.m) [10], to mention only a few
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