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Proinflammatory Microenvironment During Kingella kingae Infection Modulates Osteoclastogenesis

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...

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Autores principales: Pesce Viglietti, Ayelén Ivana, Sviercz, Franco Agustín, López, Cinthya Alicia Marcela, Freiberger, Rosa Nicole, Quarleri, Jorge, Delpino, María Victoria
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8674944/
https://www.ncbi.nlm.nih.gov/pubmed/34925328
http://dx.doi.org/10.3389/fimmu.2021.757827
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author Pesce Viglietti, Ayelén Ivana
Sviercz, Franco Agustín
López, Cinthya Alicia Marcela
Freiberger, Rosa Nicole
Quarleri, Jorge
Delpino, María Victoria
author_facet Pesce Viglietti, Ayelén Ivana
Sviercz, Franco Agustín
López, Cinthya Alicia Marcela
Freiberger, Rosa Nicole
Quarleri, Jorge
Delpino, María Victoria
author_sort Pesce Viglietti, Ayelén Ivana
collection PubMed
description 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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spelling pubmed-86749442021-12-17 Proinflammatory Microenvironment During Kingella kingae Infection Modulates Osteoclastogenesis Pesce Viglietti, Ayelén Ivana Sviercz, Franco Agustín López, Cinthya Alicia Marcela Freiberger, Rosa Nicole Quarleri, Jorge Delpino, María Victoria Front Immunol Immunology 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. Frontiers Media S.A. 2021-12-02 /pmc/articles/PMC8674944/ /pubmed/34925328 http://dx.doi.org/10.3389/fimmu.2021.757827 Text en Copyright © 2021 Pesce Viglietti, Sviercz, López, Freiberger, Quarleri and Delpino https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the oriwginal publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Pesce Viglietti, Ayelén Ivana
Sviercz, Franco Agustín
López, Cinthya Alicia Marcela
Freiberger, Rosa Nicole
Quarleri, Jorge
Delpino, María Victoria
Proinflammatory Microenvironment During Kingella kingae Infection Modulates Osteoclastogenesis
title Proinflammatory Microenvironment During Kingella kingae Infection Modulates Osteoclastogenesis
title_full Proinflammatory Microenvironment During Kingella kingae Infection Modulates Osteoclastogenesis
title_fullStr Proinflammatory Microenvironment During Kingella kingae Infection Modulates Osteoclastogenesis
title_full_unstemmed Proinflammatory Microenvironment During Kingella kingae Infection Modulates Osteoclastogenesis
title_short Proinflammatory Microenvironment During Kingella kingae Infection Modulates Osteoclastogenesis
title_sort proinflammatory microenvironment during kingella kingae infection modulates osteoclastogenesis
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8674944/
https://www.ncbi.nlm.nih.gov/pubmed/34925328
http://dx.doi.org/10.3389/fimmu.2021.757827
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