ArticlePLoS pathogens2006
Macrophage pro-inflammatory response to Francisella novicida infection is regulated by SHIP.
Article in PLoS pathogens, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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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Who cites it
41 citing papers in PubMed, 74 citations in OpenAlex.
- AKT Isoforms in Macrophage Activation, Polarization, and Survival.Current topics in microbiology and immunology · 2022Article
- Innate Immune Recognition: An Issue More Complex Than Expected.Frontiers in cellular and infection microbiology · 2019Review
- Purified Streptococcus pneumoniae Endopeptidase O (PepO) Enhances Particle Uptake by Macrophages in a Toll-Like Receptor 2- and miR-155-Dependent Manner.Infection and immunity · 2017Article
- Cardiac Electrical and Structural Changes During Bacterial Infection: An Instructive Model to Study Cardiac Dysfunction in Sepsis.Journal of the American Heart Association · 2016Article
- Keyhole limpet hemocyanin induces innate immunity via Syk and Erk phosphorylation.EXCLI journal · 2016Article
- Using host-pathogen protein interactions to identify and characterize Francisella tularensis virulence factors.BMC genomics · 2015Article
- Prior infection with Type A Francisella tularensis antagonizes the pulmonary transcriptional response to an aerosolized Toll-like receptor 4 agonist.BMC genomics · 2015Article
- Article
- Virulent Francisella tularensis destabilize host mRNA to rapidly suppress inflammation.Journal of innate immunity · 2014Article
- Monocyte/macrophage inflammatory response pathways to combat Francisella infection: possible therapeutic targets?Frontiers in cellular and infection microbiology · 2014Review
- Lipids derived from virulent Francisella tularensis broadly inhibit pulmonary inflammation via toll-like receptor 2 and peroxisome proliferator-activated receptor α.Clinical and vaccine immunology : CVI · 2013Article
- Francisella tularensis SchuS4 and SchuS4 lipids inhibit IL-12p40 in primary human dendritic cells by inhibition of IRF1 and IRF8.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Temporal transcriptional response during infection of type II alveolar epithelial cells with Francisella tularensis live vaccine strain (LVS) supports a general host suppression and bacterial uptake by macropinocytosis.The Journal of biological chemistry · 2013Article
- B1a cells enhance susceptibility to infection with virulent Francisella tularensis via modulation of NK/NKT cell responses.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Article
- Fine tuning inflammation at the front door: macrophage complement receptor 3-mediates phagocytosis and immune suppression for Francisella tularensis.PLoS pathogens · 2013Article
- Subversion of host recognition and defense systems by Francisella spp.Microbiology and molecular biology reviews : MMBR · 2012Review
- MiR-155 induction by microbes/microbial ligands requires NF-κB-dependent de novo protein synthesis.Frontiers in cellular and infection microbiology · 2012Article
- Article
- IFN-β mediates suppression of IL-12p40 in human dendritic cells following infection with virulent Francisella tularensis.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Francisella tularensis, a Gram-negative facultative intracellular pathogen infecting principally macrophages and monocytes, is the etiological agent of tularemia. Macrophage responses to F. tularensis infection include the production of pro-inflammatory cytokines such as interleukin (IL)-12, which is critical for immunity against infection. Molecular mechanisms regulating production of these inflammatory mediators are poorly understood. Herein we report that the SH2 domain-containing inositol phosphatase (SHIP) is phosphorylated upon infection of primary murine macrophages with the genetically related F. novicida, and negatively regulates F. novicida-induced cytokine production. Analyses of the molecular details revealed that in addition to activating the MAP kinases, F. novicida infection also activated the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in these cells. Interestingly, SHIP-deficient macrophages displayed enhanced Akt activation upon F. novicida infection, suggesting elevated PI3K-dependent activation pathways in absence of SHIP. Inhibition of PI3K/Akt resulted in suppression of F. novicida-induced cytokine production through the inhibition of NFkappaB. Consistently, macrophages lacking SHIP displayed enhanced NFkappaB-driven gene transcription, whereas overexpression of SHIP led to decreased NFkappaB activation. Thus, we propose that SHIP negatively regulates F. novicida-induced inflammatory cytokine response by antagonizing the PI3K/Akt pathway and suppressing NFkappaB-mediated gene transcription. A detailed analysis of phosphoinositide signaling may provide valuable clues for better understanding the pathogenesis of tularemia.
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Registered trials
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