The role of coaggregation between Porphyromonas gingivalis and Fusobacterium nucleatum on the host response to mixed infection

Aim To evaluate the role of coaggregation between Porphyromonas gingivalis and Fusobacterium nucleatum on the virulence of the mixed infection in mice. Materials and methods Inhibition of coaggregation was carried out using lactose. In vitro, inhibition of coaggregation was verified using a coaggreg...

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Veröffentlicht in:Journal of clinical periodontology 2012-07, Vol.39 (7), p.617-625
Hauptverfasser: Polak, David, Shapira, Lior, Weiss, Ervin I., Houri-Haddad, Yael
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container_title Journal of clinical periodontology
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creator Polak, David
Shapira, Lior
Weiss, Ervin I.
Houri-Haddad, Yael
description Aim To evaluate the role of coaggregation between Porphyromonas gingivalis and Fusobacterium nucleatum on the virulence of the mixed infection in mice. Materials and methods Inhibition of coaggregation was carried out using lactose. In vitro, inhibition of coaggregation was verified using a coaggregation assay. In vivo, the virulence of the mixed infection, with and without coaggregation, was examined in a model of experimental periodontitis in mice. The local host response to the mixed infection, with or without coaggregation, was examined using the subcutaneous chamber model of infection. Results Lactose inhibited the coaggregation between P. gingivalis and F. nucleatum at all the tested concentrations (1–0.0625 M). Surprisingly, the addition of lactose to the mixed infection increased the severity of experimental periodontitis (as measured by alveolar bone loss) compared with mixed infection with coaggregating bacteria. The addition of lactose to the mixed infection resulted in mild attenuation of TNFα and IL‐1β levels. In addition, inhibition of coaggregation resulted in inhibition of the phagocytosis of F. nucleatum and augmentation of the phagocytosis of P. gingivalis. Conclusions The ability of P. gingivalis and F. nucleatum to coaggregate may limit their ability to induce experimental periodontitis in a mixed infection model. Moreover, there is a shift in the phagocytosis pattern of the bacteria with the annulment of coaggregeaiton, with a reduction in F. nucleatum phagocytosis and amplification of P. gingivalis phagocytosis. The increased virulence of the mixed infection without coaggregation may surprisingly lay in the sustention of F. nucleatum in the infected sites.
doi_str_mv 10.1111/j.1600-051X.2012.01889.x
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Materials and methods Inhibition of coaggregation was carried out using lactose. In vitro, inhibition of coaggregation was verified using a coaggregation assay. In vivo, the virulence of the mixed infection, with and without coaggregation, was examined in a model of experimental periodontitis in mice. The local host response to the mixed infection, with or without coaggregation, was examined using the subcutaneous chamber model of infection. Results Lactose inhibited the coaggregation between P. gingivalis and F. nucleatum at all the tested concentrations (1–0.0625 M). Surprisingly, the addition of lactose to the mixed infection increased the severity of experimental periodontitis (as measured by alveolar bone loss) compared with mixed infection with coaggregating bacteria. The addition of lactose to the mixed infection resulted in mild attenuation of TNFα and IL‐1β levels. In addition, inhibition of coaggregation resulted in inhibition of the phagocytosis of F. nucleatum and augmentation of the phagocytosis of P. gingivalis. Conclusions The ability of P. gingivalis and F. nucleatum to coaggregate may limit their ability to induce experimental periodontitis in a mixed infection model. Moreover, there is a shift in the phagocytosis pattern of the bacteria with the annulment of coaggregeaiton, with a reduction in F. nucleatum phagocytosis and amplification of P. gingivalis phagocytosis. The increased virulence of the mixed infection without coaggregation may surprisingly lay in the sustention of F. nucleatum in the infected sites.</description><identifier>ISSN: 0303-6979</identifier><identifier>EISSN: 1600-051X</identifier><identifier>DOI: 10.1111/j.1600-051X.2012.01889.x</identifier><identifier>PMID: 22607053</identifier><language>eng</language><publisher>Oxford: Blackwell Publishing Ltd</publisher><subject>Alveolar Bone Loss - microbiology ; Animal models ; Animals ; Bacterial Adhesion - drug effects ; Bacterial Adhesion - physiology ; Bacterial infections ; Bacteriological Techniques ; Bacteroidaceae Infections - microbiology ; Biological and medical sciences ; Bone (alveolar) ; coaggregation ; Coinfection - microbiology ; Dentistry ; Diffusion Chambers, Culture ; F. nucleatum ; Facial bones, jaws, teeth, parodontium: diseases, semeiology ; Female ; Fusobacterium Infections - microbiology ; Fusobacterium nucleatum ; Fusobacterium nucleatum - drug effects ; Fusobacterium nucleatum - pathogenicity ; host response ; Host-Pathogen Interactions - physiology ; Interleukin 1 ; Interleukin-1beta - analysis ; Lactose ; Lactose - pharmacology ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Mixed infection ; Non tumoral diseases ; Otorhinolaryngology. Stomatology ; P. gingivalis ; Periodontitis ; Periodontitis - microbiology ; Phagocytosis ; Phagocytosis - physiology ; Porphyromonas gingivalis ; Porphyromonas gingivalis - drug effects ; Porphyromonas gingivalis - pathogenicity ; Rodents ; Subcutaneous chambers ; Superinfection - microbiology ; Tumor necrosis factor- alpha ; Tumor Necrosis Factor-alpha - analysis ; Virulence ; X-Ray Microtomography</subject><ispartof>Journal of clinical periodontology, 2012-07, Vol.39 (7), p.617-625</ispartof><rights>2012 John Wiley &amp; Sons A/S</rights><rights>2015 INIST-CNRS</rights><rights>2012 John Wiley &amp; Sons A/S.</rights><rights>Copyright © 2012 John Wiley &amp; Sons A/S</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4999-e554b1bafe0742ac803bf771c6ac69c37aaa90e8bc970bf85bc54d8bde28a2aa3</citedby><cites>FETCH-LOGICAL-c4999-e554b1bafe0742ac803bf771c6ac69c37aaa90e8bc970bf85bc54d8bde28a2aa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1600-051X.2012.01889.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1600-051X.2012.01889.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=26020466$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22607053$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Polak, David</creatorcontrib><creatorcontrib>Shapira, Lior</creatorcontrib><creatorcontrib>Weiss, Ervin I.</creatorcontrib><creatorcontrib>Houri-Haddad, Yael</creatorcontrib><title>The role of coaggregation between Porphyromonas gingivalis and Fusobacterium nucleatum on the host response to mixed infection</title><title>Journal of clinical periodontology</title><addtitle>J Clin Periodontol</addtitle><description>Aim To evaluate the role of coaggregation between Porphyromonas gingivalis and Fusobacterium nucleatum on the virulence of the mixed infection in mice. Materials and methods Inhibition of coaggregation was carried out using lactose. In vitro, inhibition of coaggregation was verified using a coaggregation assay. In vivo, the virulence of the mixed infection, with and without coaggregation, was examined in a model of experimental periodontitis in mice. The local host response to the mixed infection, with or without coaggregation, was examined using the subcutaneous chamber model of infection. Results Lactose inhibited the coaggregation between P. gingivalis and F. nucleatum at all the tested concentrations (1–0.0625 M). Surprisingly, the addition of lactose to the mixed infection increased the severity of experimental periodontitis (as measured by alveolar bone loss) compared with mixed infection with coaggregating bacteria. The addition of lactose to the mixed infection resulted in mild attenuation of TNFα and IL‐1β levels. In addition, inhibition of coaggregation resulted in inhibition of the phagocytosis of F. nucleatum and augmentation of the phagocytosis of P. gingivalis. Conclusions The ability of P. gingivalis and F. nucleatum to coaggregate may limit their ability to induce experimental periodontitis in a mixed infection model. Moreover, there is a shift in the phagocytosis pattern of the bacteria with the annulment of coaggregeaiton, with a reduction in F. nucleatum phagocytosis and amplification of P. gingivalis phagocytosis. The increased virulence of the mixed infection without coaggregation may surprisingly lay in the sustention of F. nucleatum in the infected sites.</description><subject>Alveolar Bone Loss - microbiology</subject><subject>Animal models</subject><subject>Animals</subject><subject>Bacterial Adhesion - drug effects</subject><subject>Bacterial Adhesion - physiology</subject><subject>Bacterial infections</subject><subject>Bacteriological Techniques</subject><subject>Bacteroidaceae Infections - microbiology</subject><subject>Biological and medical sciences</subject><subject>Bone (alveolar)</subject><subject>coaggregation</subject><subject>Coinfection - microbiology</subject><subject>Dentistry</subject><subject>Diffusion Chambers, Culture</subject><subject>F. nucleatum</subject><subject>Facial bones, jaws, teeth, parodontium: diseases, semeiology</subject><subject>Female</subject><subject>Fusobacterium Infections - microbiology</subject><subject>Fusobacterium nucleatum</subject><subject>Fusobacterium nucleatum - drug effects</subject><subject>Fusobacterium nucleatum - pathogenicity</subject><subject>host response</subject><subject>Host-Pathogen Interactions - physiology</subject><subject>Interleukin 1</subject><subject>Interleukin-1beta - analysis</subject><subject>Lactose</subject><subject>Lactose - pharmacology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mixed infection</subject><subject>Non tumoral diseases</subject><subject>Otorhinolaryngology. Stomatology</subject><subject>P. gingivalis</subject><subject>Periodontitis</subject><subject>Periodontitis - microbiology</subject><subject>Phagocytosis</subject><subject>Phagocytosis - physiology</subject><subject>Porphyromonas gingivalis</subject><subject>Porphyromonas gingivalis - drug effects</subject><subject>Porphyromonas gingivalis - pathogenicity</subject><subject>Rodents</subject><subject>Subcutaneous chambers</subject><subject>Superinfection - microbiology</subject><subject>Tumor necrosis factor- alpha</subject><subject>Tumor Necrosis Factor-alpha - analysis</subject><subject>Virulence</subject><subject>X-Ray Microtomography</subject><issn>0303-6979</issn><issn>1600-051X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU9v1DAQxSMEokvhKyBLCIlLgh0nsXNBQqu2QKtSpPLnZk28k10vib3YCd298Nlx2GWRONUXj-TfezPjlySE0YzF83qdsYrSlJbsW5ZTlmeUSVln2wfJ7PjwMJlRTnla1aI-SZ6EsKaUCc754-QkzysqaMlnya_bFRLvOiSuJdrBculxCYNxljQ43CFacuP8ZrXzrncWAlkauzQ_oTOBgF2Q8zG4BvSA3ow9saPuEIZYRf0QnVcuDMRj2DgbkAyO9GaLC2Jsi3pq8jR51EIX8NnhPk0-n5_dzt-lVx8v3s_fXqW6qOs6xbIsGtZAi1QUOWhJedMKwXQFuqo1FwBQU5SNrgVtWlk2uiwWsllgLiEH4KfJq73vxrsfI4ZB9SZo7Dqw6MagGOWyonlV1PdA8_i9NBc0oi_-Q9du9DYuoljBuRR5wWSk5J7S3oXgsVUbb3rwu2ilpjjVWk2pqSk1NcWp_sSptlH6_NBgbHpcHIV_84vAywMAQUPXerDahH9c3IkWVRW5N3vuznS4u_cA6sP85mwqo0G6NzBhwO3RAPx3VQkuSvX1-kJdykt2_emLVAX_DTKzzMg</recordid><startdate>201207</startdate><enddate>201207</enddate><creator>Polak, David</creator><creator>Shapira, Lior</creator><creator>Weiss, Ervin I.</creator><creator>Houri-Haddad, Yael</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>K9.</scope><scope>7X8</scope><scope>7QL</scope><scope>C1K</scope></search><sort><creationdate>201207</creationdate><title>The role of coaggregation between Porphyromonas gingivalis and Fusobacterium nucleatum on the host response to mixed infection</title><author>Polak, David ; Shapira, Lior ; Weiss, Ervin I. ; Houri-Haddad, Yael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4999-e554b1bafe0742ac803bf771c6ac69c37aaa90e8bc970bf85bc54d8bde28a2aa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Alveolar Bone Loss - microbiology</topic><topic>Animal models</topic><topic>Animals</topic><topic>Bacterial Adhesion - drug effects</topic><topic>Bacterial Adhesion - physiology</topic><topic>Bacterial infections</topic><topic>Bacteriological Techniques</topic><topic>Bacteroidaceae Infections - microbiology</topic><topic>Biological and medical sciences</topic><topic>Bone (alveolar)</topic><topic>coaggregation</topic><topic>Coinfection - microbiology</topic><topic>Dentistry</topic><topic>Diffusion Chambers, Culture</topic><topic>F. nucleatum</topic><topic>Facial bones, jaws, teeth, parodontium: diseases, semeiology</topic><topic>Female</topic><topic>Fusobacterium Infections - microbiology</topic><topic>Fusobacterium nucleatum</topic><topic>Fusobacterium nucleatum - drug effects</topic><topic>Fusobacterium nucleatum - pathogenicity</topic><topic>host response</topic><topic>Host-Pathogen Interactions - physiology</topic><topic>Interleukin 1</topic><topic>Interleukin-1beta - analysis</topic><topic>Lactose</topic><topic>Lactose - pharmacology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mixed infection</topic><topic>Non tumoral diseases</topic><topic>Otorhinolaryngology. Stomatology</topic><topic>P. gingivalis</topic><topic>Periodontitis</topic><topic>Periodontitis - microbiology</topic><topic>Phagocytosis</topic><topic>Phagocytosis - physiology</topic><topic>Porphyromonas gingivalis</topic><topic>Porphyromonas gingivalis - drug effects</topic><topic>Porphyromonas gingivalis - pathogenicity</topic><topic>Rodents</topic><topic>Subcutaneous chambers</topic><topic>Superinfection - microbiology</topic><topic>Tumor necrosis factor- alpha</topic><topic>Tumor Necrosis Factor-alpha - analysis</topic><topic>Virulence</topic><topic>X-Ray Microtomography</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Polak, David</creatorcontrib><creatorcontrib>Shapira, Lior</creatorcontrib><creatorcontrib>Weiss, Ervin I.</creatorcontrib><creatorcontrib>Houri-Haddad, Yael</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Journal of clinical periodontology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Polak, David</au><au>Shapira, Lior</au><au>Weiss, Ervin I.</au><au>Houri-Haddad, Yael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of coaggregation between Porphyromonas gingivalis and Fusobacterium nucleatum on the host response to mixed infection</atitle><jtitle>Journal of clinical periodontology</jtitle><addtitle>J Clin Periodontol</addtitle><date>2012-07</date><risdate>2012</risdate><volume>39</volume><issue>7</issue><spage>617</spage><epage>625</epage><pages>617-625</pages><issn>0303-6979</issn><eissn>1600-051X</eissn><abstract>Aim To evaluate the role of coaggregation between Porphyromonas gingivalis and Fusobacterium nucleatum on the virulence of the mixed infection in mice. Materials and methods Inhibition of coaggregation was carried out using lactose. In vitro, inhibition of coaggregation was verified using a coaggregation assay. In vivo, the virulence of the mixed infection, with and without coaggregation, was examined in a model of experimental periodontitis in mice. The local host response to the mixed infection, with or without coaggregation, was examined using the subcutaneous chamber model of infection. Results Lactose inhibited the coaggregation between P. gingivalis and F. nucleatum at all the tested concentrations (1–0.0625 M). Surprisingly, the addition of lactose to the mixed infection increased the severity of experimental periodontitis (as measured by alveolar bone loss) compared with mixed infection with coaggregating bacteria. The addition of lactose to the mixed infection resulted in mild attenuation of TNFα and IL‐1β levels. In addition, inhibition of coaggregation resulted in inhibition of the phagocytosis of F. nucleatum and augmentation of the phagocytosis of P. gingivalis. Conclusions The ability of P. gingivalis and F. nucleatum to coaggregate may limit their ability to induce experimental periodontitis in a mixed infection model. Moreover, there is a shift in the phagocytosis pattern of the bacteria with the annulment of coaggregeaiton, with a reduction in F. nucleatum phagocytosis and amplification of P. gingivalis phagocytosis. The increased virulence of the mixed infection without coaggregation may surprisingly lay in the sustention of F. nucleatum in the infected sites.</abstract><cop>Oxford</cop><pub>Blackwell Publishing Ltd</pub><pmid>22607053</pmid><doi>10.1111/j.1600-051X.2012.01889.x</doi><tpages>9</tpages></addata></record>
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subjects Alveolar Bone Loss - microbiology
Animal models
Animals
Bacterial Adhesion - drug effects
Bacterial Adhesion - physiology
Bacterial infections
Bacteriological Techniques
Bacteroidaceae Infections - microbiology
Biological and medical sciences
Bone (alveolar)
coaggregation
Coinfection - microbiology
Dentistry
Diffusion Chambers, Culture
F. nucleatum
Facial bones, jaws, teeth, parodontium: diseases, semeiology
Female
Fusobacterium Infections - microbiology
Fusobacterium nucleatum
Fusobacterium nucleatum - drug effects
Fusobacterium nucleatum - pathogenicity
host response
Host-Pathogen Interactions - physiology
Interleukin 1
Interleukin-1beta - analysis
Lactose
Lactose - pharmacology
Medical sciences
Mice
Mice, Inbred BALB C
Mixed infection
Non tumoral diseases
Otorhinolaryngology. Stomatology
P. gingivalis
Periodontitis
Periodontitis - microbiology
Phagocytosis
Phagocytosis - physiology
Porphyromonas gingivalis
Porphyromonas gingivalis - drug effects
Porphyromonas gingivalis - pathogenicity
Rodents
Subcutaneous chambers
Superinfection - microbiology
Tumor necrosis factor- alpha
Tumor Necrosis Factor-alpha - analysis
Virulence
X-Ray Microtomography
title The role of coaggregation between Porphyromonas gingivalis and Fusobacterium nucleatum on the host response to mixed infection
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