TY - JOUR
T1 - TLR2 Regulates Mast Cell IL-6 and IL-13 Production During Listeria monocytogenes Infection
AU - Soria-Castro, Rodolfo
AU - Alfaro-Doblado, Ángel R.
AU - Rodríguez-López, Gloria
AU - Campillo-Navarro, Marcia
AU - Meneses-Preza, Yatsiri G.
AU - Galán-Salinas, Adrian
AU - Alvarez-Jimenez, Violeta
AU - Yam-Puc, Juan C.
AU - Munguía-Fuentes, Rosario
AU - Domínguez-Flores, Adriana
AU - Estrada-Parra, Sergio
AU - Pérez-Tapia, Sonia M.
AU - Chávez-Blanco, Alma D.
AU - Chacón-Salinas, Rommel
N1 - Publisher Copyright:
© Copyright © 2021 Soria-Castro, Alfaro-Doblado, Rodríguez-López, Campillo-Navarro, Meneses-Preza, Galán-Salinas, Alvarez-Jimenez, Yam-Puc, Munguía-Fuentes, Domínguez-Flores, Estrada-Parra, Pérez-Tapia, Chávez-Blanco and Chacón-Salinas.
PY - 2021/6/14
Y1 - 2021/6/14
N2 - 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.
AB - 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.
KW - IL-13
KW - IL-6
KW - LLO
KW - Listeria monocytogenes
KW - MAPK
KW - mast cell
KW - p38
KW - toll like receptor-2
UR - http://www.scopus.com/inward/record.url?scp=85109048367&partnerID=8YFLogxK
U2 - 10.3389/fimmu.2021.650779
DO - 10.3389/fimmu.2021.650779
M3 - Artículo
C2 - 34194428
AN - SCOPUS:85109048367
SN - 1664-3224
VL - 12
JO - Frontiers in Immunology
JF - Frontiers in Immunology
M1 - 650779
ER -