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Updated: Oct 31, 2025
Measuring Bacterial Load and Immune Responses in Mice Infected with Listeria monocytogenes
Published on: August 9, 2011
TLR2 Regulates Mast Cell IL-6 and IL-13 Production During Listeria monocytogenes Infection
Rodolfo Soria-Castro1, Ángel R Alfaro-Doblado1, Gloria Rodríguez-López1
1Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional (ENCB-IPN), Mexico City, Mexico.
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.
Insights
Mast cells (MC) control Listeria monocytogenes (L.m) infection. Toll-like receptor 2 (TLR2) partially mediates MC activation, influencing IL-6 and IL-13 production but not bacterial clearance or degranulation.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Mast cells (MC) are key innate immune cells controlling Listeria monocytogenes (L.m) infection through degranulation and cytokine release.
- Toll-like receptor 2 (TLR2) is crucial for immune control of L.m, but its role in MC activation during infection is unclear.
Purpose of the Study:
- To investigate the role of TLR2 in mediating mast cell activation in response to L.m infection.
- To determine if TLR2 signaling influences bacterial clearance, degranulation, cytokine production, and intracellular signaling pathways in MCs.
Main Methods:
- Mast cells were infected with L.m, with and without TLR2 inhibition.
- Assessed bacterial load, degranulation, reactive oxygen species (ROS) production, and cytokine secretion (TNF-α, IL-1β, IL-6, IL-13, MCP-1).
- Analyzed activation of signaling proteins ERK, p38, and NF-κB.
Main Results:
- MCs cleared L.m, degranulated, and produced ROS and various cytokines (TNF-α, IL-1β, IL-6, IL-13, MCP-1).
- L.m infection activated ERK, p38, and NF-κB signaling pathways.
- TLR2 inhibition did not affect L.m endocytosis, bacterial clearance, ROS production, or MC degranulation.
- IL-6 and IL-13 production were significantly reduced upon TLR2 inhibition.
- p38 activation was TLR2-dependent, while ERK and NF-κB were not.
Conclusions:
- TLR2 plays a partial role in MC activation during L.m infection.
- TLR2 specifically mediates IL-6 and IL-13 production and p38 activation, but not bacterial clearance or degranulation.
- These findings elucidate specific pathways of MC response to L.m mediated by TLR2.
