ArticlePloS one2008
MyD88 dependent signaling contributes to protective host defense against Burkholderia pseudomallei.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 68 citations in OpenAlex.
- Targeting inflammasome, IL-1β, and coagulation in melioidosis.Frontiers in microbiology · 2026Review
- Regulatory effect of inflammatory mediators in spinal cord injury.Frontiers in immunology · 2025Review
- TLR9 Negatively Regulates Intracellular Bacterial Killing by Pyroptosis in Burkholderia pseudomalleiMicrobiology spectrum · 2022Article
- Hijacking of the Host's Immune Surveillance Radars byFrontiers in immunology · 2021Review
- Human Melioidosis.Clinical microbiology reviews · 2020Review
- Role of Toll-Like Receptor 5 (TLR5) in Experimental Melioidosis.Infection and immunity · 2019Article
- Rab32 GTPase, as a direct target of miR-30b/c, controls the intracellular survival of Burkholderia pseudomallei by regulating phagosome maturation.PLoS pathogens · 2019Article
- Thrombocytopenia Impairs Host Defense Against Burkholderia pseudomallei (Melioidosis).The Journal of infectious diseases · 2019Article
- Caspase-11-dependent pyroptosis of lung epithelial cells protects from melioidosis while caspase-1 mediates macrophage pyroptosis and production of IL-18.PLoS pathogens · 2018Article
- Melioidosis.Nature reviews. Disease primers · 2018Review
- TheFrontiers in microbiology · 2018Review
- Pam2CSK4 and Pam3CSK4 induce iNOS expression via TBK1 and MyD88 molecules in mouse macrophage cell line RAW264.7.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Article
- Burkholderia pseudomallei Capsule Exacerbates Respiratory Melioidosis but Does Not Afford Protection against Antimicrobial Signaling or Bacterial Killing in Human Olfactory Ensheathing Cells.Infection and immunity · 2016Article
- Receptor for Advanced Glycation End Products (RAGE) Serves a Protective Role during Klebsiella pneumoniae - Induced Pneumonia.PloS one · 2016Article
- TRIF-dependent innate immune activation is critical for survival to neonatal gram-negative sepsis.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Differential Toll-Like Receptor-Signalling of Burkholderia pseudomallei Lipopolysaccharide in Murine and Human Models.PloS one · 2015Article
- Neutrophil extracellular traps in the host defense against sepsis induced by Burkholderia pseudomallei (melioidosis).Intensive care medicine experimental · 2014Article
- Divergent functions of Toll-like receptors during bacterial lung infections.American journal of respiratory and critical care medicine · 2014Review
- Hematopoietic but not endothelial cell MyD88 contributes to host defense during gram-negative pneumonia derived sepsis.PLoS pathogens · 2014Article
- NLRC4 and TLR5 each contribute to host defense in respiratory melioidosis.PLoS neglected tropical diseases · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundToll-like receptors (TLRs) have a central role in the recognition of pathogens and the initiation of the innate immune response. Myeloid differentiation primary-response gene 88 (MyD88) and TIR-domain-containing adaptor protein inducing IFNbeta (TRIF) are regarded as the key signaling adaptor proteins for TLRs. Melioidosis, which is endemic in SE-Asia, is a severe infection caused by the gram-negative bacterium Burkholderia pseudomallei. We here aimed to characterize the role of MyD88 and TRIF in host defense against melioidosis. METHODOLOGY AND PRINCIPAL
findingsFirst, we found that MyD88, but not TRIF, deficient whole blood leukocytes released less TNFalpha upon stimulation with B. pseudomallei compared to wild-type (WT) cells. Thereafter we inoculated MyD88 knock-out (KO), TRIF mutant and WT mice intranasally with B. pseudomallei and found that MyD88 KO, but not TRIF mutant mice demonstrated a strongly accelerated lethality, which was accompanied by significantly increased bacterial loads in lungs, liver and blood, and grossly enhanced liver damage compared to WT mice. The decreased bacterial clearance capacity of MyD88 KO mice was accompanied by a markedly reduced early pulmonary neutrophil recruitment and a diminished activation of neutrophils after infection with B. pseudomallei. MyD88 KO leukocytes displayed an unaltered capacity to phagocytose and kill B. pseudomallei in vitro.
conclusionsMyD88 dependent signaling, but not TRIF dependent signaling, contributes to a protective host response against B. pseudomallei at least in part by causing early neutrophil recruitment towards the primary site of 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.