ArticleInfection and immunity2011
Ehrlichia chaffeensis induces monocyte inflammatory responses through MyD88, ERK, and NF-κB but not through TRIF, interleukin-1 receptor 1 (IL-1R1)/IL-18R1, or toll-like receptors.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
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- Review: Protective Immunity and Immunopathology of Ehrlichiosis.Zoonoses (Shannon, Ireland) · 2022Article
- MyD88 in Macrophages Enhances Liver Fibrosis by Activation of NLRP3 Inflammasome in HSCs.International journal of molecular sciences · 2021Article
- Comparative Analysis of Genome of Ehrlichia sp. HF, a Model Bacterium to Study Fatal Human Ehrlichiosis.BMC genomics · 2021Article
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- Pattern Recognition Receptors in Innate Immunity to Obligate Intracellular Bacteria.Zoonoses (Shannon, Ireland) · 2021Article
- PDX regulates inflammatory cell infiltration via resident macrophage in LPS-induced lung injury.Journal of cellular and molecular medicine · 2020Article
- Host membrane lipids are trafficked to membranes of intravacuolar bacteriumProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Discovery ofFrontiers in cellular and infection microbiology · 2020Article
- Amblyomma americanum ticks utilizes countervailing pro and anti-inflammatory proteins to evade host defense.PLoS pathogens · 2019Article
- Emerging Roles of Autophagy and Inflammasome in Ehrlichiosis.Frontiers in immunology · 2019Review
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- Peptide Nucleic Acid Knockdown and Intra-host Cell Complementation ofFrontiers in cellular and infection microbiology · 2017Article
- Hacker within! Ehrlichia chaffeensis Effector Driven Phagocyte Reprogramming Strategy.Frontiers in cellular and infection microbiology · 2016Review
- Synergistic Costimulatory Effect of Chlamydia pneumoniae with Carbon Nanoparticles on NLRP3 Inflammasome-Mediated Interleukin-1β Secretion in Macrophages.Infection and immunity · 2015Article
- The Anaplasma phagocytophilum effector AmpA hijacks host cell SUMOylation.Cellular microbiology · 2015Article
- Alteration of lysosome fusion and low-grade inflammation mediated by super-low-dose endotoxin.The Journal of biological chemistry · 2015Article
- Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Human monocytic ehrlichiosis, an influenza-like illness accompanied by signs of hepatitis, is caused by infection of monocytes/macrophages with a lipopolysaccharide-deficient bacterium, Ehrlichia chaffeensis. The E. chaffeensis strain Wakulla induces diffuse hepatitis with neutrophil infiltration in mice with severe combined immunodeficiency, which is accompanied by strong CXCL2 (mouse functional homolog of interleukin-8 [IL-8]) and tumor necrosis factor alpha (TNF-α) expression in the liver. In this study, we found that expression of IL-1β, CXCL2, and TNF-α was induced by strain Wakulla in mouse bone marrow-derived macrophages; this expression was dependent on MyD88, but not on TRIF, TLR2/4, IL-1R1/IL-18R1, or endosome acidification. When the human leukemia cell line THP-1 was exposed to E. chaffeensis, significant upregulation of IL-8, IL-1β, and TNF-α mRNA and extracellular regulated kinase 2 (ERK2) activation were detected. U0126 (inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1/2 [MEK1/2] upstream of ERK), manumycin A (Ras inhibitor), BAY43-9006 (Raf-1 inhibitor), and NS-50 (inhibitor of NF-κB nuclear translocation) inhibited the cytokine gene expression. A luciferase reporter assay using HEK293 cells, which lack Toll-like receptors (TLRs), showed activation of both the IL-8 promoter and NF-κB by E. chaffeensis. Activation of the IL-8 promoter in transfected HEK293 cells was inhibited by manumycin A, BAY43-9006, U0126, and transfection with a dominant-negative Ras mutant. These results indicate that the E. chaffeensis Wakulla strain can induce inflammatory responses through MyD88-dependent NF-κB and ERK pathways, without the involvement of TRIF and TLRs.
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