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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Role of Polymorphonuclear Leukocyte-Derived Serine Proteinases in Defense against <italic>Actinobacillus actinomycetemcomitans</italic>
</title>
<author><name sortKey="De Haar, Susanne F" sort="De Haar, Susanne F" uniqKey="De Haar S" first="Susanne F." last="De Haar">Susanne F. De Haar</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Hiemstra, Pieter S" sort="Hiemstra, Pieter S" uniqKey="Hiemstra P" first="Pieter S." last="Hiemstra">Pieter S. Hiemstra</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Van Steenbergen, Martijn T J M" sort="Van Steenbergen, Martijn T J M" uniqKey="Van Steenbergen M" first="Martijn T. J. M." last="Van Steenbergen">Martijn T. J. M. Van Steenbergen</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Everts, Vincent" sort="Everts, Vincent" uniqKey="Everts V" first="Vincent" last="Everts">Vincent Everts</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Beertsen, Wouter" sort="Beertsen, Wouter" uniqKey="Beertsen W" first="Wouter" last="Beertsen">Wouter Beertsen</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">16926422</idno>
<idno type="pmc">1594863</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1594863</idno>
<idno type="RBID">PMC:1594863</idno>
<idno type="doi">10.1128/IAI.02016-05</idno>
<date when="2006">2006</date>
<idno type="wicri:Area/Pmc/Corpus">001529</idno>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Role of Polymorphonuclear Leukocyte-Derived Serine Proteinases in Defense against <italic>Actinobacillus actinomycetemcomitans</italic>
</title>
<author><name sortKey="De Haar, Susanne F" sort="De Haar, Susanne F" uniqKey="De Haar S" first="Susanne F." last="De Haar">Susanne F. De Haar</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Hiemstra, Pieter S" sort="Hiemstra, Pieter S" uniqKey="Hiemstra P" first="Pieter S." last="Hiemstra">Pieter S. Hiemstra</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Van Steenbergen, Martijn T J M" sort="Van Steenbergen, Martijn T J M" uniqKey="Van Steenbergen M" first="Martijn T. J. M." last="Van Steenbergen">Martijn T. J. M. Van Steenbergen</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Everts, Vincent" sort="Everts, Vincent" uniqKey="Everts V" first="Vincent" last="Everts">Vincent Everts</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Beertsen, Wouter" sort="Beertsen, Wouter" uniqKey="Beertsen W" first="Wouter" last="Beertsen">Wouter Beertsen</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
</analytic>
<series><title level="j">Infection and Immunity</title>
<idno type="ISSN">0019-9567</idno>
<idno type="eISSN">1098-5522</idno>
<imprint><date when="2006">2006</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>Periodontitis is a chronic destructive infection of the tooth-supportive tissues, which is caused by pathogenic bacteria such as <italic>Actinobacillus actinomycetemcomitans</italic>
. A severe form of periodontitis is found in Papillon-Lefèvre syndrome (PLS), an inheritable disease caused by loss-of-function mutations in the cathepsin C gene. Recently, we demonstrated that these patients lack the activity of the polymorphonuclear leukocyte (PMN)-derived serine proteinases elastase, cathepsin G, and proteinase 3. In the present study we identified possible pathways along which serine proteinases may be involved in the defense against <italic>A. actinomycetemcomitans</italic>
. Serine proteinases are capable to convert the PMN-derived hCAP-18 into LL-37, an antimicrobial peptide with activity against <italic>A. actinomycetemcomitans</italic>
. We found that the PMNs of PLS patients released lower levels of LL-37. Furthermore, because of their deficiency in serine proteases, the PMNs of PLS patients were incapable of neutralizing the leukotoxin produced by this pathogen, which resulted in increased cell damage. Finally, the capacity of PMNs from PLS patients to kill <italic>A. actinomycetemcomitans</italic>
in an anaerobic environment, such as that found in the periodontal pocket, seemed to be reduced. Our report demonstrates a mechanism that suggests a direct link between an inheritable defect in PMN functioning and difficulty in coping with a periodontitis-associated pathogen.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Infect Immun</journal-id>
<journal-id journal-id-type="publisher-id">iai</journal-id>
<journal-title>Infection and Immunity</journal-title>
<issn pub-type="ppub">0019-9567</issn>
<issn pub-type="epub">1098-5522</issn>
<publisher><publisher-name>American Society for Microbiology</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">16926422</article-id>
<article-id pub-id-type="pmc">1594863</article-id>
<article-id pub-id-type="publisher-id">2016-05</article-id>
<article-id pub-id-type="doi">10.1128/IAI.02016-05</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Host Response and Inflammation</subject>
</subj-group>
</article-categories>
<title-group><article-title>Role of Polymorphonuclear Leukocyte-Derived Serine Proteinases in Defense against <italic>Actinobacillus actinomycetemcomitans</italic>
</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>de Haar</surname>
<given-names>Susanne F.</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Hiemstra</surname>
<given-names>Pieter S.</given-names>
</name>
<xref ref-type="aff" rid="aff1">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>van Steenbergen</surname>
<given-names>Martijn T. J. M.</given-names>
</name>
<xref ref-type="aff" rid="aff1">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Everts</surname>
<given-names>Vincent</given-names>
</name>
<xref ref-type="aff" rid="aff1">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Beertsen</surname>
<given-names>Wouter</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
</contrib>
</contrib-group>
<aff id="aff1">Department of Periodontology, Academic Centre for Dentistry Amsterdam, Universiteit van Amsterdam and Vrije Universiteit, Amsterdam, The Netherlands,<label>1</label>
Department of Pulmonology, Leiden University Medical Centre, Leiden, The Netherlands,<label>2</label>
Department of Oral and Maxillofacial Surgery/Oral Pathology, Academic Centre for Dentistry Amsterdam, and VU University Medical Center, Amsterdam, The Netherlands,<label>3</label>
Department of Oral Cell Biology, Academic Centre for Dentistry Amsterdam, Universiteit van Amsterdam and Vrije Universiteit, Amsterdam, The Netherlands<label>4</label>
</aff>
<author-notes><fn id="cor1"><label>*</label>
<p>Corresponding author. Mailing address: Department of Periodontology, Academic Centre for Dentistry Amsterdam (ACTA), Louwesweg 1, 1066 EA Amsterdam, The Netherlands. Phone: 31-20-5188300. Fax: 31-20-5188547. E-mail: <email>w.beertsen@acta.nl</email>
.</p>
</fn>
</author-notes>
<pub-date pub-type="ppub"><month>9</month>
<year>2006</year>
</pub-date>
<volume>74</volume>
<issue>9</issue>
<fpage>5284</fpage>
<lpage>5291</lpage>
<history><date date-type="received"><day>15</day>
<month>12</month>
<year>2005</year>
</date>
<date date-type="rev-recd"><day>29</day>
<month>1</month>
<year>2006</year>
</date>
<date date-type="accepted"><day>22</day>
<month>6</month>
<year>2006</year>
</date>
</history>
<copyright-statement>Copyright © 2006, American Society for Microbiology</copyright-statement>
<copyright-year>2006</copyright-year>
<self-uri xlink:title="pdf" xlink:href="zii00906005284.pdf"></self-uri>
<abstract><p>Periodontitis is a chronic destructive infection of the tooth-supportive tissues, which is caused by pathogenic bacteria such as <italic>Actinobacillus actinomycetemcomitans</italic>
. A severe form of periodontitis is found in Papillon-Lefèvre syndrome (PLS), an inheritable disease caused by loss-of-function mutations in the cathepsin C gene. Recently, we demonstrated that these patients lack the activity of the polymorphonuclear leukocyte (PMN)-derived serine proteinases elastase, cathepsin G, and proteinase 3. In the present study we identified possible pathways along which serine proteinases may be involved in the defense against <italic>A. actinomycetemcomitans</italic>
. Serine proteinases are capable to convert the PMN-derived hCAP-18 into LL-37, an antimicrobial peptide with activity against <italic>A. actinomycetemcomitans</italic>
. We found that the PMNs of PLS patients released lower levels of LL-37. Furthermore, because of their deficiency in serine proteases, the PMNs of PLS patients were incapable of neutralizing the leukotoxin produced by this pathogen, which resulted in increased cell damage. Finally, the capacity of PMNs from PLS patients to kill <italic>A. actinomycetemcomitans</italic>
in an anaerobic environment, such as that found in the periodontal pocket, seemed to be reduced. Our report demonstrates a mechanism that suggests a direct link between an inheritable defect in PMN functioning and difficulty in coping with a periodontitis-associated pathogen.</p>
</abstract>
</article-meta>
<notes><fn-group><fn><p><italic>Editor:</italic>
J. B. Bliska</p>
</fn>
</fn-group>
</notes>
</front>
</pmc>
</record>
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