ArticleJournal of immunology (Baltimore, Md. : 1950)2004
Specific engagement of TLR4 or TLR3 does not lead to IFN-beta-mediated innate signal amplification and STAT1 phosphorylation in resident murine alveolar macrophages.
Article in Journal of immunology (Baltimore, Md. : 1950), 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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
16 citing papers in PubMed, 62 citations in OpenAlex.
- Compartmentalization of the inflammatory response during bacterial sepsis and severe COVID-19.Journal of intensive medicine · 2024Review
- Soybean-derived Bowman-Birk Inhibitor (BBI) Inhibits HIV Replication in Macrophages.Scientific reports · 2016Article
- A Pathophysiological Insight into Sepsis and Its Correlation with Postmortem Diagnosis.Mediators of inflammation · 2016Review
- Lung cell-specific modulation of LPS-induced TLR4 receptor and adaptor localization.Communicative & integrative biology · 2014Review
- Type I IFN triggers RIG-I/TLR3/NLRP3-dependent inflammasome activation in influenza A virus infected cells.PLoS pathogens · 2013Article
- Virulence factors identified by Cryptococcus neoformans mutant screen differentially modulate lung immune responses and brain dissemination.The American journal of pathology · 2012Article
- Host Defense and the Airway Epithelium: Frontline Responses That Protect against Bacterial Invasion and Pneumonia.Journal of pathogens · 2011Article
- Targeted injury of type II alveolar epithelial cells induces pulmonary fibrosis.American journal of respiratory and critical care medicine · 2010Article
- Staphylococcus aureus activates type I IFN signaling in mice and humans through the Xr repeated sequences of protein A.The Journal of clinical investigation · 2009Article
- The immunopathogenesis of chronic obstructive pulmonary disease: insights from recent research.Proceedings of the American Thoracic Society · 2007Review
- Differential ex vivo nitric oxide production by acutely isolated neonatal and adult microglia.Journal of neuroimmunology · 2007Article
- Article
- Differential type I interferon activation and susceptibility of dendritic cell populations to porcine arterivirus.Immunology · 2007Article
- Should we inhibit type I interferons in sepsis?Infection and immunity · 2007Review
- Conserved nontypeable Haemophilus influenzae-derived TLR2-binding lipopeptides synergize with IFN-beta to increase cytokine production by resident murine and human alveolar macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2006Article
- Cell-mediated adaptive immune defense of the lungs.Proceedings of the American Thoracic Society · 2005Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The innate immune response must be mobilized promptly yet judiciously via TLRs to protect the lungs against pathogens. Stimulation of murine peritoneal macrophage (PMphi) TLR4 or TLR3 by pathogen-associated molecular patterns (PAMPs) typically induces type I IFN-beta, leading to autocrine activation of the transcription factor STAT1. Because it is unknown whether STAT1 plays a similar role in the lungs, we studied the response of resident alveolar macrophages (AMphi) or control PMphi from normal C57BL/6 mice to stimulation by PAMPs derived from viruses (polyriboinosinic:polyribocytidylic acid, specific for TLR3) or bacteria (Pam(3)Cys, specific for TLR2, and repurified LPS, specific for TLR4). AMphi did not activate STAT1 by tyrosine phosphorylation on Y701 following stimulation of any of these three TLRs, but readily did so in response to exogenous IFN-beta. This unique AMphi response was not due to altered TLR expression, or defective immediate-early gene response, as measured by expression of TNF-alpha and three beta chemokines. Instead, AMphi differed from PMphi in not producing bioactive IFN-beta, as confirmed by ELISA and by the failure of supernatants from TLR-stimulated AMphi to induce STAT1 phosphorylation in PMphi. Consequently, AMphi did not produce the microbicidal effector molecule NO following TLR4 or TLR3 stimulation unless exogenous IFN-beta was also added. Thus, murine AMphi respond to bacterial or viral PAMPs by producing inflammatory cytokines and chemokines, but because they lack the feed-forward amplification typically mediated by autocrine IFN-beta secretion and STAT1 activation, require exogenous IFN to mount a second phase of host defense.
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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.