Proinflammatory Microenvironment During Kingella kingae Infection Modulates Osteoclastogenesis
Neisseriaceae Infections
Osteoclasts
Kingella kingae
Osteolysis
Mice
https://purl.org/becyt/ford/3.3
Osteogenesis
Diagnosis and Treatment of Spinal Infections
Internal medicine
0303 health sciences
Proinflammatory cytokine
3. Good health
Chemistry
Cellular Microenvironment
OSTEOCLASTOGENESIS AND BONE LOSS
IL-1β
osteoclastogenesis and bone loss
Medicine
Osteoclast
Receptor
Immunology
Infection Risk Factors
Microbiology
Cell Line
03 medical and health sciences
Diagnosis and Treatment of Prosthetic Joint Infections
INFLAMMATION
Rheumatology
IL-1Β
TNF-Α
Health Sciences
Animals
Humans
https://purl.org/becyt/ford/3
KINGELLA KINGAE
Biology
Autoinflammatory Bone Disorders
Inflammation
Macrophages
FOS: Clinical medicine
Arthritis
RC581-607
RAW 264.7 Cells
inflammation
TNF-α
FOS: Biological sciences
Dentistry
Septic arthritis
Surgery
Immunologic diseases. Allergy
DOI:
10.3389/fimmu.2021.757827
Publication Date:
2021-12-02T10:36:12Z
AUTHORS (6)
ABSTRACT
Kingella kingae is an emerging pathogen that causes septic arthritis, osteomyelitis, and bacteremia in children from 6 to 48 months of age. The presence of bacteria within or near the bone is associated with an inflammatory process that results in osteolysis, but the underlying pathogenic mechanisms involved are largely unknown. To determine the link between K. kingae and bone loss, we have assessed whether infection per se or through the genesis of a pro-inflammatory microenvironment can promote osteoclastogenesis. For that purpose, we examined both the direct effect of K. kingae and the immune-mediated mechanism involved in K. kingae-infected macrophage-induced osteoclastogenesis. Our results indicate that osteoclastogenesis is stimulated by K. kingae infection directly and indirectly by fueling a potent pro-inflammatory response that drives macrophages to undergo functional osteoclasts via TNF-α and IL-1β induction. Such osteoclastogenic capability of K. kingae is counteracted by their outer membrane vesicles (OMV) in a concentration-dependent manner. In conclusion, this model allowed elucidating the interplay between the K. kingae and their OMV to modulate osteoclastogenesis from exposed macrophages, thus contributing to the modulation in joint and bone damage.
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CITATIONS (6)
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