The osteoclast, a target cell for microorganisms.
Bacteria
Bone defects
Innate immunity
Osteoclasts
Viruses
Journal
Bone
ISSN: 1873-2763
Titre abrégé: Bone
Pays: United States
ID NLM: 8504048
Informations de publication
Date de publication:
10 2019
10 2019
Historique:
received:
15
03
2019
revised:
11
06
2019
accepted:
21
06
2019
pubmed:
25
6
2019
medline:
5
9
2020
entrez:
25
6
2019
Statut:
ppublish
Résumé
Bone is a highly adaptive tissue with regenerative properties that is subject to numerous diseases. Infection is one of the causes of altered bone homeostasis. Bone infection happens subsequently to bone surgery or to systemic spreading of microorganisms. In addition to osteoblasts, osteoclasts (OCs) also constitute cell targets for pathogens. OCs are multinucleated cells that have the exclusive ability to resorb bone mineral tissue. However, the OC is much more than a bone eater. Beyond its role in the control of bone turnover, the OC is an immune cell that produces and senses inflammatory cytokines, ingests microorganisms and presents antigens. Today, increasing evidence shows that several pathogens use OC as a host cell to grow, generating debilitating bone defects. In this review, we exhaustively inventory the bacteria and viruses that infect OC and report the present knowledge in this topic. We point out that most of the microorganisms enhance the bone resorption activity of OC. We notice that pathogen interactions with the OC require further investigation, in particular to validate the OC as a host cell in vivo and to identify the cellular mechanisms involved in altered bone resorption. Thus, we conclude that the OC is a new cell target for pathogens; this new research area paves the way for new therapeutic strategies in the infections causing bone defects.
Identifiants
pubmed: 31233933
pii: S8756-3282(19)30255-8
doi: 10.1016/j.bone.2019.06.023
pii:
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
315-323Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.