Pathogenesis of Rickettsial Diseases

Pathogenic and Immune Mechanisms of an Endotheliotropic Infection

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Obligately intracytosolic rickettsiae that cycle between arthropod and vertebrate hosts cause human diseases with a spectrum of severity, primarily by targeting microvascular endothelial cells, resulting in endothelial dysfunction. Endothelial cells and mononuclear phagocytes have important roles in the intracellular killing of rickettsiae upon activation by the effector molecules of innate and adaptive immunity. In overwhelming infection, immunosuppressive effects contribute to the severity of illness. Rickettsia-host cell interactions involve host cell receptors for rickettsial ligands that mediate cell adhesion and, in some instances, trigger induced phagocytosis. Rickettsiae interact with host cell actin to effect both cellular entry and intracellular actin-based mobility. The interaction of rickettsiae with the host cell also involves rickettsial evasion of host defense mechanisms and exploitation of the intracellular environment. Signal transduction events exemplify these effects. An intriguing frontier is the array of rickettsial noncoding RNA molecules and their potential effects on the pathogenesis and transmission of rickettsial diseases.

Original languageEnglish (US)
Pages (from-to)127-152
Number of pages26
JournalAnnual Review of Pathology: Mechanisms of Disease
Volume14
DOIs
StatePublished - Jan 1 2019

Fingerprint

Rickettsia
Immune System Diseases
Infection
Actins
Endothelial Cells
Untranslated RNA
Arthropods
Adaptive Immunity
Immunosuppressive Agents
Phagocytes
Phagocytosis
Innate Immunity
Cell Adhesion
Cell Communication
Vertebrates
Signal Transduction
Ligands

Keywords

  • Rickettsia -host cell interactions, endothelium, vascular permeability, innate immune signaling, immunosuppression, noncoding RNA

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

@article{9c50ca87becb44b5822a49df700b3f77,
title = "Pathogenesis of Rickettsial Diseases: Pathogenic and Immune Mechanisms of an Endotheliotropic Infection",
abstract = "Obligately intracytosolic rickettsiae that cycle between arthropod and vertebrate hosts cause human diseases with a spectrum of severity, primarily by targeting microvascular endothelial cells, resulting in endothelial dysfunction. Endothelial cells and mononuclear phagocytes have important roles in the intracellular killing of rickettsiae upon activation by the effector molecules of innate and adaptive immunity. In overwhelming infection, immunosuppressive effects contribute to the severity of illness. Rickettsia-host cell interactions involve host cell receptors for rickettsial ligands that mediate cell adhesion and, in some instances, trigger induced phagocytosis. Rickettsiae interact with host cell actin to effect both cellular entry and intracellular actin-based mobility. The interaction of rickettsiae with the host cell also involves rickettsial evasion of host defense mechanisms and exploitation of the intracellular environment. Signal transduction events exemplify these effects. An intriguing frontier is the array of rickettsial noncoding RNA molecules and their potential effects on the pathogenesis and transmission of rickettsial diseases.",
keywords = "Rickettsia -host cell interactions, endothelium, vascular permeability, innate immune signaling, immunosuppression, noncoding RNA",
author = "Abha Sahni and Rong Fang and Sanjeev Sahni and David Walker",
year = "2019",
month = "1",
day = "1",
doi = "10.1146/annurev-pathmechdis-012418-012800",
language = "English (US)",
volume = "14",
pages = "127--152",
journal = "Annual Review of Phytopathology",
issn = "1553-4006",
publisher = "Annual Reviews Inc.",

}

TY - JOUR

T1 - Pathogenesis of Rickettsial Diseases

T2 - Pathogenic and Immune Mechanisms of an Endotheliotropic Infection

AU - Sahni, Abha

AU - Fang, Rong

AU - Sahni, Sanjeev

AU - Walker, David

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Obligately intracytosolic rickettsiae that cycle between arthropod and vertebrate hosts cause human diseases with a spectrum of severity, primarily by targeting microvascular endothelial cells, resulting in endothelial dysfunction. Endothelial cells and mononuclear phagocytes have important roles in the intracellular killing of rickettsiae upon activation by the effector molecules of innate and adaptive immunity. In overwhelming infection, immunosuppressive effects contribute to the severity of illness. Rickettsia-host cell interactions involve host cell receptors for rickettsial ligands that mediate cell adhesion and, in some instances, trigger induced phagocytosis. Rickettsiae interact with host cell actin to effect both cellular entry and intracellular actin-based mobility. The interaction of rickettsiae with the host cell also involves rickettsial evasion of host defense mechanisms and exploitation of the intracellular environment. Signal transduction events exemplify these effects. An intriguing frontier is the array of rickettsial noncoding RNA molecules and their potential effects on the pathogenesis and transmission of rickettsial diseases.

AB - Obligately intracytosolic rickettsiae that cycle between arthropod and vertebrate hosts cause human diseases with a spectrum of severity, primarily by targeting microvascular endothelial cells, resulting in endothelial dysfunction. Endothelial cells and mononuclear phagocytes have important roles in the intracellular killing of rickettsiae upon activation by the effector molecules of innate and adaptive immunity. In overwhelming infection, immunosuppressive effects contribute to the severity of illness. Rickettsia-host cell interactions involve host cell receptors for rickettsial ligands that mediate cell adhesion and, in some instances, trigger induced phagocytosis. Rickettsiae interact with host cell actin to effect both cellular entry and intracellular actin-based mobility. The interaction of rickettsiae with the host cell also involves rickettsial evasion of host defense mechanisms and exploitation of the intracellular environment. Signal transduction events exemplify these effects. An intriguing frontier is the array of rickettsial noncoding RNA molecules and their potential effects on the pathogenesis and transmission of rickettsial diseases.

KW - Rickettsia -host cell interactions, endothelium, vascular permeability, innate immune signaling, immunosuppression, noncoding RNA

UR - http://www.scopus.com/inward/record.url?scp=85060510748&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85060510748&partnerID=8YFLogxK

U2 - 10.1146/annurev-pathmechdis-012418-012800

DO - 10.1146/annurev-pathmechdis-012418-012800

M3 - Article

VL - 14

SP - 127

EP - 152

JO - Annual Review of Phytopathology

JF - Annual Review of Phytopathology

SN - 1553-4006

ER -