ArticleInfection and immunity2016
Toll-Like Receptor 2 Recognizes Orientia tsutsugamushi and Increases Susceptibility to Murine Experimental Scrub Typhus.
Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 24 citations in OpenAlex.
- Cytokine and chemokine profiles linked to early severity of scrub typhus: multicenter validation of soluble PD-L1.Journal of clinical microbiology · 2026Article
- Article
- Stomach as the target organ of Rickettsia heilongjiangensis infection in C57BL/6 mice identified by click chemistry.Communications biology · 2024Article
- Article
- Host transcriptomic profiling of CD-1 outbred mice with severe clinical outcomes following infection with Orientia tsutsugamushi.PLoS neglected tropical diseases · 2022Article
- Review
- Orientia tsutsugamushi selectively stimulates the C-type lectin receptor Mincle and type 1-skewed proinflammatory immune responses.PLoS pathogens · 2021Article
- Cells within cells: Rickettsiales and the obligate intracellular bacterial lifestyle.Nature reviews. Microbiology · 2021Review
- Orientia tsutsugamushi modulates cellular levels of NF-κB inhibitor p105.PLoS neglected tropical diseases · 2021Article
- Pattern Recognition Receptors in Innate Immunity to Obligate Intracellular Bacteria.Zoonoses (Shannon, Ireland) · 2021Article
- Neuroinflammation associated with scrub typhus and spotted fever group rickettsioses.PLoS neglected tropical diseases · 2020Review
- Dual RNA-seq of Orientia tsutsugamushi informs on host-pathogen interactions for this neglected intracellular human pathogen.Nature communications · 2020Article
- Orientia tsutsugamushi Is Highly Susceptible to the RNA Polymerase Switch Region Inhibitor Corallopyronin AAntimicrobial agents and chemotherapy · 2018Article
- An Update on Host-Pathogen Interplay and Modulation of Immune Responses during Orientia tsutsugamushi Infection.Clinical microbiology reviews · 2018Review
- Dysregulated Th1 Immune and Vascular Responses in Scrub Typhus Pathogenesis.Journal of immunology (Baltimore, Md. : 1950) · 2018Review
- A Type I Interferon and IL-10 Induced byFrontiers in immunology · 2018Article
- Immune response against rickettsiae: lessons from murine infection models.Medical microbiology and immunology · 2017Review
- Reply to Tantibhedhyangkul et al., 'Suspected Mycoplasma Contamination in the Study "Toll-Like Receptor 2 Recognizes Orientia tsutsugamushi and Increases Susceptibility to Murine Experimental Scrub Typhus"'.Infection and immunity · 2017Article
- Suspected Mycoplasma Contamination in the Study "Toll-Like Receptor 2 Recognizes Orientia tsutsugamushi and Increases Susceptibility to Murine Experimental Scrub Typhus".Infection and immunity · 2017Article
- Type 1-skewed neuroinflammation and vascular damage associated with Orientia tsutsugamushi infection in mice.PLoS neglected tropical diseases · 2017Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Scrub typhus is a potentially lethal infection that is caused by the obligate intracellular bacterium Orientia tsutsugamushi The roles of Toll-like receptor 2 (TLR2) and TLR4 in innate recognition of O. tsutsugamushi have not been elucidated. By overexpression of TLR2 or TLR4 in HEK293 cells, we demonstrated that TLR2, but not TLR4, recognizes heat-stable compounds of O. tsutsugamushi that were sensitive to treatment with sodium hydroxide, hydrogen peroxide, and proteinase K. TLR2 was required for the secretion of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) by dendritic cells. In an intradermal mouse infection model, TLR2-deficient mice did not show impaired control of bacterial growth or reduced survival. Moreover, after intraperitoneal infection, TLR2-deficient mice were even more resistant to lethal infection than C57BL/6 wild-type mice, which showed stronger symptoms and lower survival rates during the convalescent phase. Compared to the time of reduction of bacterial loads in TLR2-deficient mice, the reduction of bacterial loads in infected organs was accelerated in wild-type mice. The higher mortality of wild-type mice was associated with increased concentrations of serum alkaline phosphatase but not aspartate aminotransferase. The transcription of mRNA for TNF-α and IL-6 decreased more rapidly in peritoneum samples from wild-type mice than in those from TLR2-deficient mice and was therefore not a correlate of increased susceptibility. Thus, although TLR2 is an important mediator of the early inflammatory response, it is dispensable for protective immunity against O. tsutsugamushi Increased susceptibility to O. tsutsugamushi infection in TLR2-competent mice rather suggests a TLR2-related immunopathologic effect.
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