ArticleInfection and immunity2009
Role of p38 and early growth response factor 1 in the macrophage response to group B streptococcus.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 23 citations in OpenAlex.
- PGFEMBO molecular medicine · 2023Article
- Distinct Group BInfection and immunity · 2021Article
- Modulation of Death and Inflammatory Signaling in Decidual Stromal Cells following Exposure to Group BInfection and immunity · 2019Article
- Sustained Egr-1 Response via p38 MAP Kinase Signaling Modulates Early Immune Responses of Dendritic Cells Parasitized byFrontiers in cellular and infection microbiology · 2019Article
- Codevelopment of Microbiota and Innate Immunity and the Risk for Group B Streptococcal Disease.Frontiers in immunology · 2017Review
- Implication of TLR- but not of NOD2-signaling pathways in dendritic cell activation by group B Streptococcus serotypes III and V.PloS one · 2014Article
- Neonatal immune adaptation of the gut and its role during infections.Clinical & developmental immunology · 2013Review
- Insulin modulates the inflammatory granulocyte response to streptococci via phosphatidylinositol 3-kinase.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Genome-wide mapping of cystitis due to Streptococcus agalactiae and Escherichia coli in mice identifies a unique bladder transcriptome that signifies pathogen-specific antimicrobial defense against urinary tract infection.Infection and immunity · 2012Article
- Up-regulation of the neuronal nicotinic receptor α7 by HIV glycoprotein 120: potential implications for HIV-associated neurocognitive disorder.The Journal of biological chemistry · 2012Article
- NO is a macrophage autonomous modifier of the cytokine response to streptococcal single-stranded RNA.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Macrophages recognize streptococci through bacterial single-stranded RNA.EMBO reports · 2011Article
- Coxiella burnetii, the agent of Q fever, replicates within trophoblasts and induces a unique transcriptional response.PloS one · 2010Article
- Macrophage migration inhibitory factor regulates interleukin-6 production by facilitating nuclear factor-kappa B activation during Vibrio vulnificus infection.BMC immunology · 2010Article
- Mal connects TLR2 to PI3Kinase activation and phagocyte polarization.The EMBO journal · 2009Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Group B streptococcus (GBS), the most frequent single isolate in neonatal sepsis and meningitis, potently activates inflammatory macrophage genes via myeloid differentiation antigen 88 (MyD88). However, events parallel to and downstream of MyD88 that instruct the macrophage response are incompletely understood. In this study, we found that only MyD88, not the Toll-like receptor (TLR) adapter proteins MAL/TIRAP, TRIF, and TRAM, essentially mediates the cytokine (tumor necrosis factor [TNF] and interleukin-6) and chemokine (RANTES) responses to whole GBS organisms, although MAL, TRIF, and TRAM have been shown to mediate the responses to substructures in other gram-positive and gram-negative bacteria. GBS-induced, MyD88-dependent phosphorylation of the mitogen-activated protein kinase p38 activated the transcription factor AP-1 and early growth response factor 1 (Egr-1) but not NF-kappaB. Furthermore, phosphorylation of Ets-like molecule 1 (Elk-1) was mediated by p38. However, in contrast to Egr-1 and AP-1, Elk-1 was dispensable for transcriptional activation of TNF by GBS organisms. Studies of macrophages from Elk-1-deficient mice revealed that Elk-1 was furthermore nonessential for the TNF responses to purified TLR2 and TLR4 agonists, which was in notable contrast to what was revealed in studies employing in vitro expression systems. In conclusion, MyD88, p38, and Egr-1, but not Elk-1, essentially mediate the inflammatory cytokine response to GBS organisms.
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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.