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Toll-Like Receptor 4 Dependence of Innate and Adaptive Immunity to Salmonella : Importance of the Kupffer Cell Network
Open accessAbstract
Mammalian cells recognize LPS from Gram-negative bacteria via the Toll-like receptor 4 (TLR4) complex. During experimental Salmonella infection, C3H/HeJ mice carrying a dominant-negative mutation in TLR4 exhibited delayed chemokine production, impaired NO generation, and attenuated cellular immune responses. However, dramatically enhanced bacterial growth within the Kupffer cell network before the recruitment of inflammatory cells appeared to be primarily responsible for the early demise of Salmonella-infected TLR4-deficient mice. LPS-TLR4 signaling plays an essential role in the generation of both innate and adaptive immune responses throughout the course of infection with Gram-negative bacteria. Alternative pattern-recognition receptors cannot completely compensate for the loss of TLR4, and compensation occurs at the expense of an increased microbial burden.
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“Of interest, recent evidence obtained in models of S. typhiumrium infection indicate specific compartmentalization of nitrosative and oxidative stress in macrophages and thus divergent effects on the fate and propagation of bacteria, extending previous work on cycle specific susceptibility of these bacteria to either of these stress responses (61, 68, 69).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [68]
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“This Gram-negative bacterium persists within MPS cells, including spleen and liver macrophages, it causes systemic disease in mice (Vazquez-Torres et al., 1999, 2004), and its dependence on iron is well established (Nairz et al., 2007).”
From Iron Regulatory Proteins Mediate Host Resistance to Salmonella Infection (2015) · cites this paper as Vazquez-Torres et al., 2004
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Metadata
- Authors
- Vazquez-Torres, A., Vallance, B. A., Bergman, M. A., Finlay, B. B., Cookson, B. T., Jones-Carson, J., & Fang, F. C.
- Affiliations
- Department of Microbiology, University of Colorado Health Sciences Center , Denver, CO 80262
- University of British Columbia (CA)
- University of Washington (US)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2004-05
- Volume
- 172
- Issue
- 10
- Pages
- 6202-6208
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2138298422
- Cited by
- 173
- References
- 39
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 3 · 2022: 1 · 2021: 5 · 2020: 6 · 2019: 4 · 2018: 2 · 2017: 8 · 2016: 6 · 2015: 11 · 2014: 7 · 2013: 7 · 2012: 17
- FWCI
- 6.14
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (AI54959, AI39557)
- National Institute of Allergy and Infectious Diseases (AI47242, AI 54959, AI 39557, R01AI047242, AI-10181)
- National Center for Research Resources (K01RR016082, RR16082)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- TLR4, salmonellosis, Kupffer cells, lipopolysaccharide signaling, innate immunity, adaptive immunity, chemokine production, nitric oxide, TLR4-deficient mice, bacterial clearance, Gram-negative bacteria
- MeSH terms
- Animals, Bacterial Proteins, Cytotoxicity, Immunologic, Immunity, Innate, Kupffer Cells, Liver, Membrane Glycoproteins, Mice, Inbred C3H, Phagocytosis, Receptors, Cell Surface, Salmonella Infections, Animal, Signal Transduction, Macrophages, Peritoneal, Mice, Knockout, Chemokines, CXC, Salmonella enterica, Genetic Predisposition to Disease, Mice, Congenic, Neutrophil Infiltration, Toll-Like Receptors, Toll-Like Receptor 4, Mice
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