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Article: Metronidazole-Treated Porphyromonas gingivalis Persisters Invade Human Gingival Epithelial Cells and Perturb Innate Responses

TitleMetronidazole-Treated Porphyromonas gingivalis Persisters Invade Human Gingival Epithelial Cells and Perturb Innate Responses
Authors
Keywordsmetronidazole
Porphyromonas gingivalis
persisters
human gingival epithelial cell
innate response
Issue Date2020
PublisherAmerican Society for Microbiology. The Journal's web site is located at http://aac.asm.org/
Citation
Antimicrobial Agents and Chemotherapy, 2020, v. 64 n. 6, p. article no. e02529-19 How to Cite?
AbstractPeriodontitis as a biofilm-associated inflammatory disease is highly prevalent worldwide. It severely affects oral health and yet closely links to systemic diseases like diabetes and cardiovascular disease. Porphyromonas gingivalis as a “keystone” periodontopathogen drives the shift of microbe-host symbiosis to dysbiosis and critically contributes to the pathogenesis of periodontitis. Persisters represent a tiny subset of biofilm-associated microbes highly tolerant to lethal treatment of antimicrobials, and, notably, metronidazole-tolerant P. gingivalis persisters have recently been identified by our group. This study further explored the interactive profiles of metronidazole-treated P. gingivalis persisters (M-PgPs) with human gingival epithelial cells (HGECs). P. gingivalis cells (ATCC 33277) at stationary phase were treated with a lethal dosage of metronidazole (100 μg/ml, 6 h) for generating M-PgPs. The interaction of M-PgPs with HGECs was assessed by microscopy, flow cytometry, cytokine profiling, and quantitative PCR (qPCR). We demonstrated that the overall morphology and ultracellular structure of M-PgPs remained unchanged. Importantly, M-PgPs maintained the capabilities to adhere to and invade HGECs. Moreover, M-PgPs significantly suppressed proinflammatory cytokine expression in HGECs at a level comparable to that seen with the untreated P. gingivalis cells, through the thermosensitive components. The present report reveals that P. gingivalis persisters induced by lethal treatment of antibiotics were able to maintain their capabilities to adhere to and invade human gingival epithelial cells and to perturb the innate host responses. Novel strategies and approaches need to be developed for tackling P. gingivalis and favorably modulating the dysregulated immunoinflammatory responses for oral/periodontal health and general well-being.
Persistent Identifierhttp://hdl.handle.net/10722/282871
ISSN
2020 Impact Factor: 5.191
2015 SCImago Journal Rankings: 2.322
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWANG, C-
dc.contributor.authorCheng, T-
dc.contributor.authorLi, X-
dc.contributor.authorJin, L-
dc.date.accessioned2020-06-05T06:22:31Z-
dc.date.available2020-06-05T06:22:31Z-
dc.date.issued2020-
dc.identifier.citationAntimicrobial Agents and Chemotherapy, 2020, v. 64 n. 6, p. article no. e02529-19-
dc.identifier.issn0066-4804-
dc.identifier.urihttp://hdl.handle.net/10722/282871-
dc.description.abstractPeriodontitis as a biofilm-associated inflammatory disease is highly prevalent worldwide. It severely affects oral health and yet closely links to systemic diseases like diabetes and cardiovascular disease. Porphyromonas gingivalis as a “keystone” periodontopathogen drives the shift of microbe-host symbiosis to dysbiosis and critically contributes to the pathogenesis of periodontitis. Persisters represent a tiny subset of biofilm-associated microbes highly tolerant to lethal treatment of antimicrobials, and, notably, metronidazole-tolerant P. gingivalis persisters have recently been identified by our group. This study further explored the interactive profiles of metronidazole-treated P. gingivalis persisters (M-PgPs) with human gingival epithelial cells (HGECs). P. gingivalis cells (ATCC 33277) at stationary phase were treated with a lethal dosage of metronidazole (100 μg/ml, 6 h) for generating M-PgPs. The interaction of M-PgPs with HGECs was assessed by microscopy, flow cytometry, cytokine profiling, and quantitative PCR (qPCR). We demonstrated that the overall morphology and ultracellular structure of M-PgPs remained unchanged. Importantly, M-PgPs maintained the capabilities to adhere to and invade HGECs. Moreover, M-PgPs significantly suppressed proinflammatory cytokine expression in HGECs at a level comparable to that seen with the untreated P. gingivalis cells, through the thermosensitive components. The present report reveals that P. gingivalis persisters induced by lethal treatment of antibiotics were able to maintain their capabilities to adhere to and invade human gingival epithelial cells and to perturb the innate host responses. Novel strategies and approaches need to be developed for tackling P. gingivalis and favorably modulating the dysregulated immunoinflammatory responses for oral/periodontal health and general well-being.-
dc.languageeng-
dc.publisherAmerican Society for Microbiology. The Journal's web site is located at http://aac.asm.org/-
dc.relation.ispartofAntimicrobial Agents and Chemotherapy-
dc.rightsAntimicrobial Agents and Chemotherapy. Copyright © American Society for Microbiology.-
dc.subjectmetronidazole-
dc.subjectPorphyromonas gingivalis-
dc.subjectpersisters-
dc.subjecthuman gingival epithelial cell-
dc.subjectinnate response-
dc.titleMetronidazole-Treated Porphyromonas gingivalis Persisters Invade Human Gingival Epithelial Cells and Perturb Innate Responses-
dc.typeArticle-
dc.identifier.emailCheng, T: chengtfc@hku.hk-
dc.identifier.emailLi, X: llx815@hku.hk-
dc.identifier.emailJin, L: ljjin@hkucc.hku.hk-
dc.identifier.authorityLi, X=rp02494-
dc.identifier.authorityJin, L=rp00028-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1128/AAC.02529-19-
dc.identifier.pmid32205352-
dc.identifier.scopuseid_2-s2.0-85085266172-
dc.identifier.hkuros310125-
dc.identifier.volume64-
dc.identifier.issue6-
dc.identifier.spagearticle no. e02529-
dc.identifier.epage19-
dc.identifier.isiWOS:000535946300053-
dc.publisher.placeUnited States-
dc.identifier.issnl0066-4804-

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