ArticleInfection and immunity2004
Toll-like receptor 4-dependent early elicited tumor necrosis factor alpha expression is critical for innate host defense against Bordetella bronchiseptica.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 54 citations in OpenAlex.
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- Simultaneous CRISPR screening and spatial transcriptomics reveals intracellular, intercellular, and functional transcriptional circuits.bioRxiv : the preprint server for biology · 2023Article
- Pathogenicity of Bordetella bronchiseptica isolated from apparently healthy rabbits in guinea pig, rat, and mouse.The Journal of veterinary medical science · 2022Article
- Enhancement of immune response against Bordetella spp. by disrupting immunomodulation.Scientific reports · 2019Article
- Immunomodulation as a Novel Strategy for Prevention and Treatment ofFrontiers in immunology · 2019Review
- Cross-Foster Rederivation Compared with Antibiotic Administration in the Drinking Water to EradicateJournal of the American Association for Laboratory Animal Science : JAALAS · 2017Article
- Nilotinib reduces muscle fibrosis in chronic muscle injury by promoting TNF-mediated apoptosis of fibro/adipogenic progenitors.Nature medicine · 2015Article
- Bordetella pertussis pathogenesis: current and future challenges.Nature reviews. Microbiology · 2014Review
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- Interaction of Bordetella bronchiseptica and Its Lipopolysaccharide with In Vitro Culture of Respiratory Nasal Epithelium.Veterinary medicine international · 2013Article
- sigE facilitates the adaptation of Bordetella bronchiseptica to stress conditions and lethal infection in immunocompromised mice.BMC microbiology · 2012Article
- Contribution of Bordetella filamentous hemagglutinin and adenylate cyclase toxin to suppression and evasion of interleukin-17-mediated inflammation.Infection and immunity · 2012Article
- Effects of Differences in Lipid A Structure on TLR4 Pro-Inflammatory Signaling and Inflammasome Activation.Frontiers in immunology · 2012Article
- A Type VI secretion system encoding locus is required for Bordetella bronchiseptica immunomodulation and persistence in vivo.PloS one · 2012Article
- Role of pagL and lpxO in Bordetella bronchiseptica lipid A biosynthesis.Journal of bacteriology · 2011Article
- Interleukin-1 receptor signaling is required to overcome the effects of pertussis toxin and for efficient infection- or vaccination-induced immunity against Bordetella pertussis.Infection and immunity · 2011Article
- PAD4 is essential for antibacterial innate immunity mediated by neutrophil extracellular traps.The Journal of experimental medicine · 2010Article
- Role of the type III secretion system in a hypervirulent lineage of Bordetella bronchiseptica.Infection and immunity · 2009Article
- Constraint-based network model of pathogen-immune system interactions.Journal of the Royal Society, Interface · 2009Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Toll-like receptor 4 (TLR4) mediates the response to lipopolysaccharide, and its activation induces the expression of a large number of inflammatory genes, many of which are also induced by other pathogen-associated molecular patterns. Interestingly, the subset of genes that are dependent on TLR4 for optimal expression during gram-negative bacterial infection has not been determined. We have previously shown that TLR4-deficient mice rapidly develop acute pneumonia after inoculation with Bordetella bronchiseptica, suggesting that TLR4 is required for expression of early elicited gene products in this model. Microarray analysis with macrophages derived from wild-type and TLR4-deficient mice was used to identify genes whose expression, within 1 h of bacterial exposure, is dependent on TLR4. The results of this investigation suggest that TLR4 is not required for the majority of the transcriptional response to B. bronchiseptica. However, early tumor necrosis factor alpha (TNF-alpha) mRNA expression is primarily dependent on TLR4 and in vitro and in vivo protein levels substantiate this finding. TLR4-deficient mice and TNF-alpha-/- mice are similarly susceptible to infection with relatively low doses of B. bronchiseptica and in vivo neutralization studies indicate that it is the TLR4-dependent early elicited TNF-alpha response that is critical for preventing severe pneumonia and limiting bacterial growth. These results suggest that one critical role for TLR4 is the generation of a robust but transient TNF-alpha response that is critical to innate host defense during acute gram-negative respiratory infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.