Antibody responses to Porphyromonas gingivalis infection in a murine abscess model - involvement of gingipains and responses to re-infection

Background:  Porphyromonas gingivalis is one of the most important periodontopathogens. It produces cysteine proteinases named gingipains. We previously examined the effect of gingipains on abscess formation in a murine model. The rgpA rgpB double and kgp mutants induced smaller abscesses than the w...

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Veröffentlicht in:Journal of periodontal research 2003-12, Vol.38 (6), p.551-556
Hauptverfasser: Yoneda, Masahiro, Hirofuji, Takao, Motooka, Noriko, Anan, Hisashi, Hamachi, Takafumi, Miura, Mayumi, Ishihara, Yoshihisa, Maeda, Katsumasa
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container_end_page 556
container_issue 6
container_start_page 551
container_title Journal of periodontal research
container_volume 38
creator Yoneda, Masahiro
Hirofuji, Takao
Motooka, Noriko
Anan, Hisashi
Hamachi, Takafumi
Miura, Mayumi
Ishihara, Yoshihisa
Maeda, Katsumasa
description Background:  Porphyromonas gingivalis is one of the most important periodontopathogens. It produces cysteine proteinases named gingipains. We previously examined the effect of gingipains on abscess formation in a murine model. The rgpA rgpB double and kgp mutants induced smaller abscesses than the wild type. Moreover, the rgpA rgpB kgp triple (gingipain‐null) mutant hardly showed lesion formation at all under the experimental conditions used, indicating that genes encoding gingipains are important for P. gingivalis virulence. Objectives:  Here, we further report the humoral immune responses induced by P. gingivalis strains. Methods:  After the lesions were apparently cured, sera were collected from the mice and immunoglobulin G (IgG) responses against the whole cell antigens of wild‐type P. gingivalis were measured. Results:  Wild‐type strain was found to induce a strong antibody reaction. On the other hand, the rgpA rgpB kgp triple and kgp mutants induced significantly lower antibody responses compared to the wild type. Western blotting analysis confirmed the differences in antibody production. Next, these mice were re‐infected with wild‐type strain. Mice that were first infected with wild‐type strain showed significantly smaller lesion formation than control mice that were first infected with medium only. On the other hand, mice that were first infected with mutant strains devoid of gingipain activities did not show resistance to re‐infection and immunoglobulins directed against gingipains may be protective. Conclusions:  These results suggest that gingipains play an important role in abscess formation in mice, and humoral immune responses seem to be partly responsible for the resistance to re‐infection by P. gingivalis.
doi_str_mv 10.1034/j.1600-0765.2003.00685.x
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It produces cysteine proteinases named gingipains. We previously examined the effect of gingipains on abscess formation in a murine model. The rgpA rgpB double and kgp mutants induced smaller abscesses than the wild type. Moreover, the rgpA rgpB kgp triple (gingipain‐null) mutant hardly showed lesion formation at all under the experimental conditions used, indicating that genes encoding gingipains are important for P. gingivalis virulence. Objectives:  Here, we further report the humoral immune responses induced by P. gingivalis strains. Methods:  After the lesions were apparently cured, sera were collected from the mice and immunoglobulin G (IgG) responses against the whole cell antigens of wild‐type P. gingivalis were measured. Results:  Wild‐type strain was found to induce a strong antibody reaction. On the other hand, the rgpA rgpB kgp triple and kgp mutants induced significantly lower antibody responses compared to the wild type. Western blotting analysis confirmed the differences in antibody production. Next, these mice were re‐infected with wild‐type strain. Mice that were first infected with wild‐type strain showed significantly smaller lesion formation than control mice that were first infected with medium only. On the other hand, mice that were first infected with mutant strains devoid of gingipain activities did not show resistance to re‐infection and immunoglobulins directed against gingipains may be protective. Conclusions:  These results suggest that gingipains play an important role in abscess formation in mice, and humoral immune responses seem to be partly responsible for the resistance to re‐infection by P. gingivalis.</description><identifier>ISSN: 0022-3484</identifier><identifier>EISSN: 1600-0765</identifier><identifier>DOI: 10.1034/j.1600-0765.2003.00685.x</identifier><identifier>PMID: 14632916</identifier><language>eng</language><publisher>Oxford, UK: Munksgaard International Publishers</publisher><subject>Abscess - immunology ; Adhesins, Bacterial - genetics ; Adhesins, Bacterial - immunology ; Animals ; Antibodies, Bacterial - blood ; Antibodies, Bacterial - immunology ; Antigens, Bacterial - immunology ; Bacteroidaceae Infections - immunology ; Biological and medical sciences ; Cysteine Endopeptidases - genetics ; Cysteine Endopeptidases - immunology ; Dentistry ; Disease Models, Animal ; Disease Susceptibility - immunology ; Facial bones, jaws, teeth, parodontium: diseases, semeiology ; Female ; gingipains ; Hemagglutinins - genetics ; Hemagglutinins - immunology ; Immunoglobulin G - blood ; Immunoglobulin G - immunology ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Mice, Inbred Strains ; murine abscess model ; Mutation - genetics ; Non tumoral diseases ; Otorhinolaryngology. 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It produces cysteine proteinases named gingipains. We previously examined the effect of gingipains on abscess formation in a murine model. The rgpA rgpB double and kgp mutants induced smaller abscesses than the wild type. Moreover, the rgpA rgpB kgp triple (gingipain‐null) mutant hardly showed lesion formation at all under the experimental conditions used, indicating that genes encoding gingipains are important for P. gingivalis virulence. Objectives:  Here, we further report the humoral immune responses induced by P. gingivalis strains. Methods:  After the lesions were apparently cured, sera were collected from the mice and immunoglobulin G (IgG) responses against the whole cell antigens of wild‐type P. gingivalis were measured. Results:  Wild‐type strain was found to induce a strong antibody reaction. On the other hand, the rgpA rgpB kgp triple and kgp mutants induced significantly lower antibody responses compared to the wild type. Western blotting analysis confirmed the differences in antibody production. Next, these mice were re‐infected with wild‐type strain. Mice that were first infected with wild‐type strain showed significantly smaller lesion formation than control mice that were first infected with medium only. On the other hand, mice that were first infected with mutant strains devoid of gingipain activities did not show resistance to re‐infection and immunoglobulins directed against gingipains may be protective. Conclusions:  These results suggest that gingipains play an important role in abscess formation in mice, and humoral immune responses seem to be partly responsible for the resistance to re‐infection by P. gingivalis.</description><subject>Abscess - immunology</subject><subject>Adhesins, Bacterial - genetics</subject><subject>Adhesins, Bacterial - immunology</subject><subject>Animals</subject><subject>Antibodies, Bacterial - blood</subject><subject>Antibodies, Bacterial - immunology</subject><subject>Antigens, Bacterial - immunology</subject><subject>Bacteroidaceae Infections - immunology</subject><subject>Biological and medical sciences</subject><subject>Cysteine Endopeptidases - genetics</subject><subject>Cysteine Endopeptidases - immunology</subject><subject>Dentistry</subject><subject>Disease Models, Animal</subject><subject>Disease Susceptibility - immunology</subject><subject>Facial bones, jaws, teeth, parodontium: diseases, semeiology</subject><subject>Female</subject><subject>gingipains</subject><subject>Hemagglutinins - genetics</subject><subject>Hemagglutinins - immunology</subject><subject>Immunoglobulin G - blood</subject><subject>Immunoglobulin G - immunology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred Strains</subject><subject>murine abscess model</subject><subject>Mutation - genetics</subject><subject>Non tumoral diseases</subject><subject>Otorhinolaryngology. Stomatology</subject><subject>Porphyromonas gingivalis</subject><subject>Porphyromonas gingivalis - enzymology</subject><subject>Porphyromonas gingivalis - immunology</subject><subject>re-infection</subject><subject>Virulence - genetics</subject><issn>0022-3484</issn><issn>1600-0765</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUctu1DAUtRCIDgO_gLyBXYJjx3Eisamq0qGaAuIhlpbjR_GQ2KmdGWb-oR9dh4ymYsfK17rn3HvPOQDAAuUFIuW7TV5UCGWIVTTHCJEcoaqm-f4JWJwaT8ECIYwzUtblGXgR4walf8Wa5-CsKCuCm6JagPtzN9rWqwMMOg7eRR3h6OEXH4Zfh-B770SEt9bd2p3obITWGS1H612qoID9NlinoWij1DHC3ivdwSz1dr7b6V67EXoz8wdhXYTCqX83BZ2dZr4Ez4zoon51fJfgx4fL7xerbP356uPF-TqTZVPTTKXLUUEqVjcSK6wpkkoVRkmiacNUiauywS1FRtcSkUm_YYVp27ZRSKjWkCV4O88dgr_b6jjy3iYBXSec9tvIWUGaGjOagPUMlMHHGLThQ7C9CAdeID4lwTd8MpxPhvMpCf43Cb5P1NfHHdu21-qReLQ-Ad4cASJK0ZkgnLTxEUcxZTTJXIL3M-6P7fThvw_g118vU5Ho2Uy3cdT7E12E37xihFH-89MVJ99uyPVqteY35AFeyLZ5</recordid><startdate>200312</startdate><enddate>200312</enddate><creator>Yoneda, Masahiro</creator><creator>Hirofuji, Takao</creator><creator>Motooka, Noriko</creator><creator>Anan, Hisashi</creator><creator>Hamachi, Takafumi</creator><creator>Miura, Mayumi</creator><creator>Ishihara, Yoshihisa</creator><creator>Maeda, Katsumasa</creator><general>Munksgaard International Publishers</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>7X8</scope></search><sort><creationdate>200312</creationdate><title>Antibody responses to Porphyromonas gingivalis infection in a murine abscess model - involvement of gingipains and responses to re-infection</title><author>Yoneda, Masahiro ; Hirofuji, Takao ; Motooka, Noriko ; Anan, Hisashi ; Hamachi, Takafumi ; Miura, Mayumi ; Ishihara, Yoshihisa ; Maeda, Katsumasa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4985-d9160136789c2d2e50cdd1fdc3e597d426492b50fe8c033484f71fbbb9d0adbf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Abscess - immunology</topic><topic>Adhesins, Bacterial - genetics</topic><topic>Adhesins, Bacterial - immunology</topic><topic>Animals</topic><topic>Antibodies, Bacterial - blood</topic><topic>Antibodies, Bacterial - immunology</topic><topic>Antigens, Bacterial - immunology</topic><topic>Bacteroidaceae Infections - immunology</topic><topic>Biological and medical sciences</topic><topic>Cysteine Endopeptidases - genetics</topic><topic>Cysteine Endopeptidases - immunology</topic><topic>Dentistry</topic><topic>Disease Models, Animal</topic><topic>Disease Susceptibility - immunology</topic><topic>Facial bones, jaws, teeth, parodontium: diseases, semeiology</topic><topic>Female</topic><topic>gingipains</topic><topic>Hemagglutinins - genetics</topic><topic>Hemagglutinins - immunology</topic><topic>Immunoglobulin G - blood</topic><topic>Immunoglobulin G - immunology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred Strains</topic><topic>murine abscess model</topic><topic>Mutation - genetics</topic><topic>Non tumoral diseases</topic><topic>Otorhinolaryngology. Stomatology</topic><topic>Porphyromonas gingivalis</topic><topic>Porphyromonas gingivalis - enzymology</topic><topic>Porphyromonas gingivalis - immunology</topic><topic>re-infection</topic><topic>Virulence - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoneda, Masahiro</creatorcontrib><creatorcontrib>Hirofuji, Takao</creatorcontrib><creatorcontrib>Motooka, Noriko</creatorcontrib><creatorcontrib>Anan, Hisashi</creatorcontrib><creatorcontrib>Hamachi, Takafumi</creatorcontrib><creatorcontrib>Miura, Mayumi</creatorcontrib><creatorcontrib>Ishihara, Yoshihisa</creatorcontrib><creatorcontrib>Maeda, Katsumasa</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>MEDLINE - Academic</collection><jtitle>Journal of periodontal research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoneda, Masahiro</au><au>Hirofuji, Takao</au><au>Motooka, Noriko</au><au>Anan, Hisashi</au><au>Hamachi, Takafumi</au><au>Miura, Mayumi</au><au>Ishihara, Yoshihisa</au><au>Maeda, Katsumasa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antibody responses to Porphyromonas gingivalis infection in a murine abscess model - involvement of gingipains and responses to re-infection</atitle><jtitle>Journal of periodontal research</jtitle><addtitle>J Periodontal Res</addtitle><date>2003-12</date><risdate>2003</risdate><volume>38</volume><issue>6</issue><spage>551</spage><epage>556</epage><pages>551-556</pages><issn>0022-3484</issn><eissn>1600-0765</eissn><abstract>Background:  Porphyromonas gingivalis is one of the most important periodontopathogens. It produces cysteine proteinases named gingipains. We previously examined the effect of gingipains on abscess formation in a murine model. The rgpA rgpB double and kgp mutants induced smaller abscesses than the wild type. Moreover, the rgpA rgpB kgp triple (gingipain‐null) mutant hardly showed lesion formation at all under the experimental conditions used, indicating that genes encoding gingipains are important for P. gingivalis virulence. Objectives:  Here, we further report the humoral immune responses induced by P. gingivalis strains. Methods:  After the lesions were apparently cured, sera were collected from the mice and immunoglobulin G (IgG) responses against the whole cell antigens of wild‐type P. gingivalis were measured. Results:  Wild‐type strain was found to induce a strong antibody reaction. On the other hand, the rgpA rgpB kgp triple and kgp mutants induced significantly lower antibody responses compared to the wild type. Western blotting analysis confirmed the differences in antibody production. Next, these mice were re‐infected with wild‐type strain. Mice that were first infected with wild‐type strain showed significantly smaller lesion formation than control mice that were first infected with medium only. On the other hand, mice that were first infected with mutant strains devoid of gingipain activities did not show resistance to re‐infection and immunoglobulins directed against gingipains may be protective. Conclusions:  These results suggest that gingipains play an important role in abscess formation in mice, and humoral immune responses seem to be partly responsible for the resistance to re‐infection by P. gingivalis.</abstract><cop>Oxford, UK</cop><pub>Munksgaard International Publishers</pub><pmid>14632916</pmid><doi>10.1034/j.1600-0765.2003.00685.x</doi><tpages>6</tpages></addata></record>
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subjects Abscess - immunology
Adhesins, Bacterial - genetics
Adhesins, Bacterial - immunology
Animals
Antibodies, Bacterial - blood
Antibodies, Bacterial - immunology
Antigens, Bacterial - immunology
Bacteroidaceae Infections - immunology
Biological and medical sciences
Cysteine Endopeptidases - genetics
Cysteine Endopeptidases - immunology
Dentistry
Disease Models, Animal
Disease Susceptibility - immunology
Facial bones, jaws, teeth, parodontium: diseases, semeiology
Female
gingipains
Hemagglutinins - genetics
Hemagglutinins - immunology
Immunoglobulin G - blood
Immunoglobulin G - immunology
Medical sciences
Mice
Mice, Inbred BALB C
Mice, Inbred Strains
murine abscess model
Mutation - genetics
Non tumoral diseases
Otorhinolaryngology. Stomatology
Porphyromonas gingivalis
Porphyromonas gingivalis - enzymology
Porphyromonas gingivalis - immunology
re-infection
Virulence - genetics
title Antibody responses to Porphyromonas gingivalis infection in a murine abscess model - involvement of gingipains and responses to re-infection
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