From gut entry to hepatic defense: spatial and temporal coordination of host immunity to Listeria infection
- 1aboratory of Microbiology and Immunology, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka, Japan
Abstract
Listeria monocytogenes, a facultative intracellular bacterium that causes listeriosis, infects the host primarily through contaminated food. After translocating across the intestinal epithelium, L. monocytogenes multiplies and spreads to secondary organs, such as the liver and spleen. While L. monocytogenes employs multiple mechanisms to invade host tissues, survive within host cells, and modulate immune responses, the host mounts coordinated innate and adaptive immune responses to restrict bacterial dissemination and establish protective immunity. In Peyer’s patches (PPs), a subset of mononuclear phagocytes termed LysoDCs captures bacteria translocated through M cells and contributes to the induction of Listeria-specific T-cell responses. Adaptive immune responses in PPs and mesenteric lymph nodes (MLNs), particularly CTL and Th1 responses, contribute to the establishment of long-term protection. Inflammatory monocytes are recruited to infected tissues, including the intestine and liver, where they contribute to bacterial control through antimicrobial effector mechanisms, including the production of inducible nitric oxide synthase (iNOS) and tumor necrosis factor-alpha (TNF-α). In this review, we summarize the mechanisms underlying intestinal invasion by L. monocytogenes, bacterial strategies that interfere with host defense, and the immune responses that control infection from the intestinal mucosa to systemic organs, particularly the liver. We focus on immune responses in PPs and MLNs and the mechanisms regulating inflammatory monocyte trafficking and function during L. monocytogenes infection. We also discuss recent findings showing that the pyruvate–GPR31 axis promotes dendrite extension by LysoDCs into M-cell pockets and facilitates bacterial sampling, whereas GPR35 promotes recruitment of inflammatory monocytes from the circulation into infected tissues. Together, these findings highlight immune-cell positioning and trafficking as important components of the spatial and temporal coordination of host defense against L. monocytogenes.
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BibTeX
@article{okamura2026from,
title = {{From gut entry to hepatic defense: spatial and temporal coordination of host immunity to Listeria infection}},
author = {Yo Okamura and Katsuhiro Nakanishi and Eiji Umemoto},
journal = {Frontiers in Immunology},
year = {2026},
month = nov,
doi = {10.3389/fimmu.2026.2000061},
url = {https://doi.org/10.3389/fimmu.2026.2000061},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - From gut entry to hepatic defense: spatial and temporal coordination of host immunity to Listeria infection
AU - Yo Okamura
AU - Katsuhiro Nakanishi
AU - Eiji Umemoto
PY - 2026
DA - 2026/11/06
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.2000061
UR - https://doi.org/10.3389/fimmu.2026.2000061
AB - Listeria monocytogenes, a facultative intracellular bacterium that causes listeriosis, infects the host primarily through contaminated food. After translocating across the intestinal epithelium, L. monocytogenes multiplies and spreads to secondary organs, such as the liver and spleen. While L. monocytogenes employs multiple mechanisms to invade host tissues, survive within host cells, and modulate immune responses, the host mounts coordinated innate and adaptive immune responses to restrict bacterial dissemination and establish protective immunity. In Peyer’s patches (PPs), a subset of mononuclear phagocytes termed LysoDCs captures bacteria translocated through M cells and contributes to the induction of Listeria-specific T-cell responses. Adaptive immune responses in PPs and mesenteric lymph nodes (MLNs), particularly CTL and Th1 responses, contribute to the establishment of long-term protection. Inflammatory monocytes are recruited to infected tissues, including the intestine and liver, where they contribute to bacterial control through antimicrobial effector mechanisms, including the production of inducible nitric oxide synthase (iNOS) and tumor necrosis factor-alpha (TNF-α). In this review, we summarize the mechanisms underlying intestinal invasion by L. monocytogenes, bacterial strategies that interfere with host defense, and the immune responses that control infection from the intestinal mucosa to systemic organs, particularly the liver. We focus on immune responses in PPs and MLNs and the mechanisms regulating inflammatory monocyte trafficking and function during L. monocytogenes infection. We also discuss recent findings showing that the pyruvate–GPR31 axis promotes dendrite extension by LysoDCs into M-cell pockets and facilitates bacterial sampling, whereas GPR35 promotes recruitment of inflammatory monocytes from the circulation into infected tissues. Together, these findings highlight immune-cell positioning and trafficking as important components of the spatial and temporal coordination of host defense against L. monocytogenes.
SN - 1664-3224
ER -