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
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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