Toll-Like Receptor 2 Is Required for Optimal Control of Listeria monocytogenes Infection
Open accessAbstract
The control of Listeria monocytogenes infection depends on the rapid activation of the innate immune system, likely through Toll-like receptors (TLR), since mice deficient for the common adapter protein of TLR signaling, myeloid differentiation factor 88 (MyD88), succumb to Listeria infection. In order to test whether TLR2 is involved in the control of infections, we compared the host response in TLR2-deficient mice with that in wild-type mice. Here we show that TLR2-deficient mice are more susceptible to systemic infection by Listeria than are wild-type mice, with a reduced survival rate, increased bacterial burden in the liver, and abundant and larger hepatic microabscesses containing increased numbers of neutrophils. The production of tumor necrosis factor, interleukin-12, and nitric oxide and the expression of the costimulatory molecules CD40 and CD86, which are necessary for the control of infection, were reduced in TLR2-deficient macrophages and dendritic cells stimulated by Listeria and were almost abolished in the absence of MyD88, coincident with the high susceptibility of MyD88-deficient mice to in vivo infection. Therefore, the present data demonstrate a role for TLR2 in the control of Listeria infection, but other MyD88-dependent signals may contribute to host resistance.
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Elevated levels of •NO cause bacterial lysis through nitrosation of thiol groups of proteins responsible for formation of pores in the cell membrane, preventing bacteria from leaving the infected cell and preventing spread of infection.
“Elevated levels of •NO cause bacterial lysis through nitrosation of the thiol groups of proteins responsible for the formation of pores in the cell membrane, thus preventing the bacteria from leaving the infected cell and preventing the spread of infection to other cells [132].”
From The Role of Reactive Species on Innate Immunity (2022) · cites this paper as [132]
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References 35 · Cited by 191
- Authors
- Torres, D., Barrier, M., Bihl, F., Quesniaux, V. J. F., Maillet, I., Akira, S., Ryffel, B., & Erard, F.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- CNRS, Laboratoire de Génétique expérimentale et moléculaire (GEM2358), F-45071 Orléans Cedex 2, France
- Research Institute for Microbial Diseases, The University of Osaka (JP)
- Corresponding author
- Ryffel, Bernhard
- Venue
- Infection and Immunity
- Publisher
- American Society for Microbiology
- Published
- 2004-04
- Volume
- 72
- Issue
- 4
- Pages
- 2131-2139
- ISSN
- 0019-9567 (ISSN-L)
- 1098-5522
- PMC
- PMC375211
- OpenAlex
- W2167121999
- Cited by
- 191
- References
- 35
- Citations by year
- 2026: 1 · 2025: 8 · 2024: 2 · 2023: 6 · 2022: 7 · 2021: 8 · 2020: 3 · 2019: 9 · 2018: 5 · 2017: 4 · 2016: 4 · 2015: 6 · 2014: 7 · 2013: 9 · 2012: 14
- FWCI
- 5.51
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Infection and Immunity (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- TLR2, Listeria monocytogenes, MyD88, innate immunity, host resistance to infection, TLR2-deficient mice, neutrophils, TNF-α, IL-12, nitric oxide, CD40, CD86, macrophages, dendritic cells, systemic infection
- MeSH terms
- Animals, Antigens, Differentiation, Cells, Cultured, Dendritic Cells, Listeriosis, Listeria monocytogenes, Liver, Liver Abscess, Macrophages, Membrane Glycoproteins, Mice, Inbred C57BL, Receptors, Cell Surface, Receptors, Immunologic, Adaptor Proteins, Signal Transducing, Toll-Like Receptors, Toll-Like Receptor 2, Mice, Myeloid Differentiation Factor 88
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