M Wang, S Liang, K B Hosur, H Domon, F Yoshimura, A Amano, G Hajishengallis
{"title":"牙龈卟啉单胞菌I型和II型菌毛基因型的不同毒力和先天免疫相互作用。","authors":"M Wang, S Liang, K B Hosur, H Domon, F Yoshimura, A Amano, G Hajishengallis","doi":"10.1111/j.1399-302X.2009.00545.x","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>The fimA-encoded fimbriae of the periodontal pathogen Porphyromonas gingivalis display genetic diversity. Type I fimbriated P. gingivalis (Pg-I) has been most widely studied at the molecular level, whereas Pg-II is the most frequent isolate from severe periodontitis.</p><p><strong>Methods: </strong>To investigate virulence differences between Types I and II fimbriae, we examined strains 33277 (Pg-I) and OMZ314 (Pg-II), reciprocal swap mutants (i.e. expressing the heterologous fimbrial type), and their respective FimA-deficient derivatives. These organisms were tested in a mouse periodontitis model and in interactions with mouse macrophages, a cell type that plays important roles in chronic infections.</p><p><strong>Results: </strong>Strain 33277 induced significantly more periodontal bone loss than OMZ314 and substitution of Type II fimbriae with Type I in OMZ314 resulted in a more virulent strain than the parent organism. However, the presence of Type II fimbriae was associated with increased proinflammatory and invasive activities in macrophages.</p><p><strong>Conclusion: </strong>The inverse relationship between proinflammatory potential and ability to cause experimental periodontitis may suggest that an aggressive phenotype could provoke a host response that would compromise the persistence of the pathogen.</p>","PeriodicalId":19630,"journal":{"name":"Oral microbiology and immunology","volume":"24 6","pages":"478-84"},"PeriodicalIF":0.0000,"publicationDate":"2009-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-302X.2009.00545.x","citationCount":"36","resultStr":"{\"title\":\"Differential virulence and innate immune interactions of Type I and II fimbrial genotypes of Porphyromonas gingivalis.\",\"authors\":\"M Wang, S Liang, K B Hosur, H Domon, F Yoshimura, A Amano, G Hajishengallis\",\"doi\":\"10.1111/j.1399-302X.2009.00545.x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>The fimA-encoded fimbriae of the periodontal pathogen Porphyromonas gingivalis display genetic diversity. Type I fimbriated P. gingivalis (Pg-I) has been most widely studied at the molecular level, whereas Pg-II is the most frequent isolate from severe periodontitis.</p><p><strong>Methods: </strong>To investigate virulence differences between Types I and II fimbriae, we examined strains 33277 (Pg-I) and OMZ314 (Pg-II), reciprocal swap mutants (i.e. expressing the heterologous fimbrial type), and their respective FimA-deficient derivatives. These organisms were tested in a mouse periodontitis model and in interactions with mouse macrophages, a cell type that plays important roles in chronic infections.</p><p><strong>Results: </strong>Strain 33277 induced significantly more periodontal bone loss than OMZ314 and substitution of Type II fimbriae with Type I in OMZ314 resulted in a more virulent strain than the parent organism. However, the presence of Type II fimbriae was associated with increased proinflammatory and invasive activities in macrophages.</p><p><strong>Conclusion: </strong>The inverse relationship between proinflammatory potential and ability to cause experimental periodontitis may suggest that an aggressive phenotype could provoke a host response that would compromise the persistence of the pathogen.</p>\",\"PeriodicalId\":19630,\"journal\":{\"name\":\"Oral microbiology and immunology\",\"volume\":\"24 6\",\"pages\":\"478-84\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2009-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1111/j.1399-302X.2009.00545.x\",\"citationCount\":\"36\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Oral microbiology and immunology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1111/j.1399-302X.2009.00545.x\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Oral microbiology and immunology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1111/j.1399-302X.2009.00545.x","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Differential virulence and innate immune interactions of Type I and II fimbrial genotypes of Porphyromonas gingivalis.
Introduction: The fimA-encoded fimbriae of the periodontal pathogen Porphyromonas gingivalis display genetic diversity. Type I fimbriated P. gingivalis (Pg-I) has been most widely studied at the molecular level, whereas Pg-II is the most frequent isolate from severe periodontitis.
Methods: To investigate virulence differences between Types I and II fimbriae, we examined strains 33277 (Pg-I) and OMZ314 (Pg-II), reciprocal swap mutants (i.e. expressing the heterologous fimbrial type), and their respective FimA-deficient derivatives. These organisms were tested in a mouse periodontitis model and in interactions with mouse macrophages, a cell type that plays important roles in chronic infections.
Results: Strain 33277 induced significantly more periodontal bone loss than OMZ314 and substitution of Type II fimbriae with Type I in OMZ314 resulted in a more virulent strain than the parent organism. However, the presence of Type II fimbriae was associated with increased proinflammatory and invasive activities in macrophages.
Conclusion: The inverse relationship between proinflammatory potential and ability to cause experimental periodontitis may suggest that an aggressive phenotype could provoke a host response that would compromise the persistence of the pathogen.