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: Ayelén Ivana Pesce Viglietti, Franco Agustín Sviercz, Cinthya Alicia Marcela López, Rosa Nicole Freiberger, Jorge Quarleri, María Victoria Delpino
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Publicado: Frontiers Media S.A. 2021
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Acceso en línea:https://doaj.org/article/397eb69daa5f4501b547431ffa93d03d
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spelling oai:doaj.org-article:397eb69daa5f4501b547431ffa93d03d2021-12-02T10:35:51ZProinflammatory Microenvironment During Kingella kingae Infection Modulates Osteoclastogenesis1664-322410.3389/fimmu.2021.757827https://doaj.org/article/397eb69daa5f4501b547431ffa93d03d2021-12-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.757827/fullhttps://doaj.org/toc/1664-3224Kingella 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.Ayelén Ivana Pesce VigliettiFranco Agustín SvierczCinthya Alicia Marcela LópezRosa Nicole FreibergerJorge QuarleriMaría Victoria DelpinoFrontiers Media S.A.articleinflammationosteoclastogenesis and bone lossKingella kingaeTNF-αIL-1βImmunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution DOAJ
collection DOAJ
language EN
topic inflammation
osteoclastogenesis and bone loss
Kingella kingae
TNF-α
IL-1β
Immunologic diseases. Allergy
RC581-607
spellingShingle inflammation
osteoclastogenesis and bone loss
Kingella kingae
TNF-α
IL-1β
Immunologic diseases. Allergy
RC581-607
Ayelén Ivana Pesce Viglietti
Franco Agustín Sviercz
Cinthya Alicia Marcela López
Rosa Nicole Freiberger
Jorge Quarleri
María Victoria Delpino
Proinflammatory Microenvironment During Kingella kingae Infection Modulates Osteoclastogenesis
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.
format article
author Ayelén Ivana Pesce Viglietti
Franco Agustín Sviercz
Cinthya Alicia Marcela López
Rosa Nicole Freiberger
Jorge Quarleri
María Victoria Delpino
author_facet Ayelén Ivana Pesce Viglietti
Franco Agustín Sviercz
Cinthya Alicia Marcela López
Rosa Nicole Freiberger
Jorge Quarleri
María Victoria Delpino
author_sort Ayelén Ivana Pesce Viglietti
title Proinflammatory Microenvironment During Kingella kingae Infection Modulates Osteoclastogenesis
title_short 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_sort proinflammatory microenvironment during kingella kingae infection modulates osteoclastogenesis
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/397eb69daa5f4501b547431ffa93d03d
work_keys_str_mv AT ayelenivanapesceviglietti proinflammatorymicroenvironmentduringkingellakingaeinfectionmodulatesosteoclastogenesis
AT francoagustinsviercz proinflammatorymicroenvironmentduringkingellakingaeinfectionmodulatesosteoclastogenesis
AT cinthyaaliciamarcelalopez proinflammatorymicroenvironmentduringkingellakingaeinfectionmodulatesosteoclastogenesis
AT rosanicolefreiberger proinflammatorymicroenvironmentduringkingellakingaeinfectionmodulatesosteoclastogenesis
AT jorgequarleri proinflammatorymicroenvironmentduringkingellakingaeinfectionmodulatesosteoclastogenesis
AT mariavictoriadelpino proinflammatorymicroenvironmentduringkingellakingaeinfectionmodulatesosteoclastogenesis
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