ArticlePLoS neglected tropical diseases2016
Liver Necrosis and Lethal Systemic Inflammation in a Murine Model of Rickettsia typhi Infection: Role of Neutrophils, Macrophages and NK Cells.
Article in PLoS neglected tropical diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 29 citations in OpenAlex.
- Brucella melitensis infection complicated by secondary hemophagocytic lymphohistiocytosis, meningitis, and multiorgan damage: a case report and literature review.BMC infectious diseases · 2026Review
- Innate immune responses to Rickettsia: emerging themes and contrasts between species.Current opinion in microbiology · 2026Review
- Acupuncture accelerates wound healing via CGRP-RAMP1-TSP1-mediated macrophage M2 polarization.Chinese medicine · 2025Article
- Phosphatidylserine-binding receptor, CD300f, on macrophages mediates host invasion of pathogenic and non-pathogenic rickettsiae.Infection and immunity · 2025Article
- In silico construction of a multi-epitope vaccine (RGME-VAC/ATS-1) against the Rickettsia genus using immunoinformatics.Memorias do Instituto Oswaldo Cruz · 2025Article
- Touching Base with Some Mediterranean Diseases of Interest from Paradigmatic Cases at the "Magna Graecia" University Unit of Infectious Diseases: A Didascalic Review.Diagnostics (Basel, Switzerland) · 2023Review
- Traditional Chinese medicines and natural products targeting immune cells in the treatment of metabolic-related fatty liver disease.Frontiers in pharmacology · 2023Review
- FTY720 attenuates APAP‑induced liver injury via the JAK2/STAT3 signaling pathway.International journal of molecular medicine · 2022Article
- Graphene-Based Biosensors for Molecular Chronic Inflammatory Disease Biomarker Detection.Biosensors · 2022Review
- Review
- Pathogenic, but Not Nonpathogenic,mBio · 2021Article
- Article
- 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
- Global Transcriptomic Profiling of Pulmonary Gene Expression in an Experimental Murine Model ofGenes · 2019Article
- Serum cytokine responses in Rickettsia felis infected febrile children, Ghana.Medical microbiology and immunology · 2018Article
- Extracellular Vesicles From the HelminthFrontiers in microbiology · 2018Article
- Immune response against rickettsiae: lessons from murine infection models.Medical microbiology and immunology · 2017Review
- Article
- GFPuv-Expressing Recombinant Rickettsia typhi: a Useful Tool for the Study of Pathogenesis and CD8Infection and immunity · 2017Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rickettsia (R.) typhi is the causative agent of endemic typhus, an emerging febrile disease that is associated with complications such as pneumonia, encephalitis and liver dysfunction. To elucidate how innate immune mechanisms contribute to defense and pathology we here analyzed R. typhi infection of CB17 SCID mice that are congenic to BALB/c mice but lack adaptive immunity. CB17 SCID mice succumbed to R. typhi infection within 21 days and showed high bacterial load in spleen, brain, lung, and liver. Most evident pathological changes in R. typhi-infected CB17 SCID mice were massive liver necrosis and splenomegaly due to the disproportionate accumulation of neutrophils and macrophages (MΦ). Both neutrophils and MΦ infiltrated the liver and harbored R. typhi. Both cell populations expressed iNOS and produced reactive oxygen species (ROS) and, thus, exhibited an inflammatory and bactericidal phenotype. Surprisingly, depletion of neutrophils completely prevented liver necrosis but neither altered bacterial load nor protected CB17 SCID mice from death. Furthermore, the absence of neutrophils had no impact on the overwhelming systemic inflammatory response in these mice. This response was predominantly driven by activated MΦ and NK cells both of which expressed IFNγ and is considered as the reason of death. Finally, we observed that iNOS expression by MΦ and neutrophils did not correlate with R. typhi uptake in vivo. Moreover, we demonstrate that MΦ hardly respond to R. typhi in vitro. These findings indicate that R. typhi enters MΦ and also neutrophils unrecognized and that activation of these cells is mediated by other mechanisms in the context of tissue damage in vivo.
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