Review: Protective Immunity and Immunopathology of Ehrlichiosis.
Ehrlichia
Ehrlichiosis
Obligate intracellular bacteria
autophagy
immunity
inflammasomes
macrophage polarization
pattern recognition receptors
type I interferon
Journal
Zoonoses (Burlington, Mass.)
ISSN: 2737-7474
Titre abrégé: Zoonoses (Burlingt)
Pays: United States
ID NLM: 9918300982006676
Informations de publication
Date de publication:
06 Jan 2022
06 Jan 2022
Historique:
entrez:
25
7
2022
pubmed:
26
7
2022
medline:
26
7
2022
Statut:
ppublish
Résumé
Human monocytic ehrlichiosis, a tick transmitted infection, ranges in severity from apparently subclinical to a fatal toxic shock-like fatal disease. Models in immunocompetent mice range from an abortive infection to uniformly lethal depending on the infecting Ehrlichia species, dose of inoculum, and route of inoculation. Effective immunity is mediated by CD4+ T lymphocytes and gamma interferon. Lethal infection occurs with early overproduction of proinflammatory cytokines and overproduction of TNF alpha and IL-10 by CD8+ T lymphocytes. Furthermore, fatal ehrlichiosis is associated with signaling via TLR 9/MyD88 with upregulation of several inflammasome complexes and secretion of IL-1 beta, IL-1 alpha, and IL-18 by hepatic mononuclear cells, suggesting activation of canonical and noncanonical inflammasome pathways, a deleterious role for IL-18, and the protective role for caspase 1. Autophagy promotes ehrlichial infection, and MyD88 signaling hinders ehrlichial infection by inhibiting autophagy induction and flux. Activation of caspase 11 during infection of hepatocytes by the lethal ehrlichial species after interferon alpha receptor signaling results in the production of inflammasome-dependent IL-1 beta, extracellular secretion of HMGB1, and pyroptosis. The high level of HMGB1 in lethal ehrlichiosis suggests a role in toxic shock. Studies of primary bone marrow-derived macrophages infected by highly avirulent or mildly avirulent ehrlichiae reveal divergent M1 and M2 macrophage polarization that links with generation of pathogenic CD8 T cells, neutrophils, and excessive inflammation or with strong expansion of protective Th1 and NKT cells, resolution of inflammation and clearance of infection, respectively.
Identifiants
pubmed: 35876763
doi: 10.15212/zoonoses-2022-0009
pmc: PMC9300479
mid: NIHMS1824000
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : NIAID NIH HHS
ID : R01 AI132674
Pays : United States
Organisme : NIGMS NIH HHS
ID : SC3 GM089641
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI156536
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI021242
Pays : United States
Organisme : NIAID NIH HHS
ID : R56 AI097679
Pays : United States
Déclaration de conflit d'intérêts
Conflict of Interest: The authors have declared that no competing interests exist.
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