ArticleBMC infectious diseases2013
Nucleotide-binding oligomerization domain containing-like receptor family, caspase recruitment domain (CARD) containing 4 (NLRC4) regulates intrapulmonary replication of aerosolized Legionella pneumophila.
Article in BMC infectious diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 10 citations in OpenAlex.
- Design of fast proteolysis-based signaling and logic circuits in mammalian cells.Nature chemical biology · 2019Article
- Lung epithelial cells: therapeutically inducible effectors of antimicrobial defense.Mucosal immunology · 2018Review
- NLRC4 and TLR5 each contribute to host defense in respiratory melioidosis.PLoS neglected tropical diseases · 2014Article
- Investigating the role of nucleotide-binding oligomerization domain-like receptors in bacterial lung infection.American journal of respiratory and critical care medicine · 2014Review
- Collaborative action of Toll-like and NOD-like receptors as modulators of the inflammatory response to pathogenic bacteria.Mediators of inflammation · 2014Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundLegionella pneumophila (Lp) flagellin activates signaling pathways in murine macrophages that control Lp replication. Nucleotide-binding oligomerization domain (NOD) containing-like receptor (NLR) family, caspase recruitment domain (CARD) containing 4 (NLRC4) and Toll-like Receptor (TLR5) both recognize Lp flagellin in vitro, but whether these two receptors play redundant or separate functional roles in vivo is unknown.
methodsThe immune response of Nlrc4-/-, Nlrc4-/-/Tlr5-/-, and wild type C57Bl/6 mice was analyzed after in vivo infection with aerosolized Lp.
resultsLp clearance from the lungs was delayed in Nlrc4-/- mice over seven days in comparison to wild type controls. Nlrc4-/-/Tlr5-/- mice had no additional defect. In contrast to TLR5, NLRC4 did not regulate recruitment of neutrophils to the lung. Although there were no differences among the mouse strains in the lung transcriptome at 4 hours, Nlrc4-/- and Nlrc4-/-Tlr5-/- mice had increased lung inflammation at 72 hours in comparison to WT. Nlrc4-/-/Tlr5-/- mice also had altered cytokine production at both 4 and 24 hours post infection when compared to wild-type (WT) and Nlrc4-/- mice. Lp replication in murine alveolar macrophages was NLRC4-dependent and TLR5-independent.
conclusionThese studies reveal that NLRC4 and TLR5 mediate different roles in the inflammatory response to Lp flagellin in an aerosolized infection model and NLRC4 regulates replication in both lungs and alveolar macrophages.
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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.