ArticleInfection and immunity2002
Rickettsia-macrophage interactions: host cell responses to Rickettsia akari and Rickettsia typhi.
Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 56 citations in OpenAlex.
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- Subversion of host cell signaling: The arsenal of Rickettsial species.Frontiers in cellular and infection microbiology · 2022Review
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- Orientia tsutsugamushi selectively stimulates the C-type lectin receptor Mincle and type 1-skewed proinflammatory immune responses.PLoS pathogens · 2021Article
- Significant Growth byPathogens (Basel, Switzerland) · 2021Article
- Subversion of Host Innate Immunity byFrontiers in immunology · 2021Article
- The neglected challenge: Vaccination against rickettsiae.PLoS neglected tropical diseases · 2020Review
- Innate Immune Response to Tick-Borne Pathogens: Cellular and Molecular Mechanisms Induced in the Hosts.International journal of molecular sciences · 2020Review
- Recent research milestones in the pathogenesis of human rickettsioses and opportunities ahead.Future microbiology · 2020Review
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- Enhancer Associated Long Non-coding RNA Transcription and Gene Regulation in Experimental Models of Rickettsial Infection.Frontiers in immunology · 2018Article
- Peptidoglycan in obligate intracellular bacteria.Molecular microbiology · 2018Review
- Immune response against rickettsiae: lessons from murine infection models.Medical microbiology and immunology · 2017Review
- Cytotoxic effector functions of T cells are not required for protective immunity against fatal Rickettsia typhi infection in a murine model of infection: Role of TH1 and TH17 cytokines in protection and pathology.PLoS neglected tropical diseases · 2017Article
- Evaluation of changes to the Rickettsia rickettsii transcriptome during mammalian infection.PloS one · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The existence of intracellular rickettsiae requires entry, survival, and replication in the eukaryotic host cells and exit to initiate new infection. While endothelial cells are the preferred target cells for most pathogenic rickettsiae, infection of monocytes/macrophages may also contribute to the establishment of rickettsial infection and resulting pathogenesis. We initiated studies to characterize macrophage-Rickettsia akari and -Rickettsia typhi interactions and to determine how rickettsiae survive within phagocytic cells. Flow cytometry, microscopic analysis, and LDH release demonstrated that R. akari and R. typhi caused negligible cytotoxicity in mouse peritoneal macrophages as well as in macrophage-like cell line, P388D1. Host cells responded to rickettsial infection with increased secretion of proinflammatory cytokines such as interleukin-1beta (IL-1beta) and IL-6. Furthermore, macrophage infection with R. akari and R. typhi resulted in differential synthesis and expression of IL-beta and IL-6, which may correlate with the existence of biological differences among these two closely related bacteria. In contrast, levels of gamma interferon (IFN-gamma), IL-10, and IL-12 in supernatants of infected P388D1 cells and mouse peritoneal macrophages did not change significantly during the course of infection and remained below the enzyme-linked immunosorbent assay cytokine detection limits. In addition, differential expression of cytokines was observed between R. akari- and R. typhi-infected macrophages, which may correlate with the biological differences among these closely related bacteria.
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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.