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 K.
AU - Walker, David H.
N1 - Publisher Copyright:
© 2019 by Annual Reviews. All rights reserved.
PY - 2019
Y1 - 2019
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
C2 - 30148688
AN - SCOPUS:85060510748
SN - 1553-4006
VL - 14
SP - 127
EP - 152
JO - Annual Review of Pathology: Mechanisms of Disease
JF - Annual Review of Pathology: Mechanisms of Disease
ER -