Variable responses of formyl peptide receptor haplotypes toward bacterial peptides
Identifieur interne : 000906 ( Pmc/Checkpoint ); précédent : 000905; suivant : 000907Variable responses of formyl peptide receptor haplotypes toward bacterial peptides
Auteurs : Jeannie M. Gripentrog [États-Unis] ; John S. Mills [États-Unis] ; George J. Saari [États-Unis] ; Heini M. Miettinen [États-Unis]Source :
- Immunogenetics [ 0093-7711 ] ; 2008.
Abstract
The chemoattractant neutrophil formyl peptide receptor (FPR) binds bacterial and mitochondrial
Url:
DOI: 10.1007/s00251-008-0277-3
PubMed: 18253729
PubMed Central: 2435592
Affiliations:
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PMC:2435592Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Variable responses of formyl peptide receptor haplotypes toward bacterial peptides</title>
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<author><name sortKey="Mills, John S" sort="Mills, John S" uniqKey="Mills J" first="John S." last="Mills">John S. Mills</name>
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<author><name sortKey="Miettinen, Heini M" sort="Miettinen, Heini M" uniqKey="Miettinen H" first="Heini M." last="Miettinen">Heini M. Miettinen</name>
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<series><title level="j">Immunogenetics</title>
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<front><div type="abstract" xml:lang="en"><p>The chemoattractant neutrophil formyl peptide receptor (FPR) binds bacterial and mitochondrial <italic>N</italic>
-formylated peptides, which allows the neutrophils to find the bacterial source and/or site of tissue damage. Certain inflammatory disorders may be due in part to an impaired innate immune system that does not respond to acute bacterial damage in a timely fashion. Because the human FPR is encoded by a large number of different haplotypes arising from ten single-nucleotide polymorphisms, we examined the possibility that some of these haplotypes are functionally distinct. We analyzed the response of three common FPR haplotypes to peptides from <italic>Escherichia coli</italic>
, <italic>Mycobacterium avium</italic>
ssp. <italic>paratuberculosis</italic>
, and human mitochondria. All three haplotypes responded similarly to the <italic>E</italic>
. <italic>coli</italic>
and mitochondrial peptides, whereas one required a higher concentration of the <italic>M</italic>
. <italic>avium</italic>
peptide fMFEDAVAWF for receptor downregulation, receptor signaling, and chemotaxis. This raises the possibility of additional bacterial species differences in functional responses among FPR variants and establishes a precedent with potentially important implications for our innate immune response against bacterial infections. We also investigated whether certain FPR haplotypes are associated with rheumatoid arthritis (RA) by sequencing <italic>FPR1</italic>
from 148 Caucasian individuals. The results suggested that FPR haplotypes do not significantly contribute toward RA.</p>
</div>
</front>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Immunogenetics</journal-id>
<journal-id journal-id-type="iso-abbrev">Immunogenetics</journal-id>
<journal-title-group><journal-title>Immunogenetics</journal-title>
</journal-title-group>
<issn pub-type="ppub">0093-7711</issn>
<issn pub-type="epub">1432-1211</issn>
<publisher><publisher-name>Springer-Verlag</publisher-name>
<publisher-loc>Berlin/Heidelberg</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">18253729</article-id>
<article-id pub-id-type="pmc">2435592</article-id>
<article-id pub-id-type="publisher-id">277</article-id>
<article-id pub-id-type="doi">10.1007/s00251-008-0277-3</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Original Paper</subject>
</subj-group>
</article-categories>
<title-group><article-title>Variable responses of formyl peptide receptor haplotypes toward bacterial peptides</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Gripentrog</surname>
<given-names>Jeannie M.</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Mills</surname>
<given-names>John S.</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Saari</surname>
<given-names>George J.</given-names>
</name>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Miettinen</surname>
<given-names>Heini M.</given-names>
</name>
<address><phone>+1-406-9944014</phone>
<fax>+1-406-9944926</fax>
<email>heini@montana.edu</email>
</address>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<aff id="Aff1"><label>1</label>
<institution-wrap><institution-id institution-id-type="GRID">grid.41891.35</institution-id>
<institution-id institution-id-type="ISNI">0000000121566108</institution-id>
<institution>Department of Microbiology,</institution>
<institution>Montana State University,</institution>
</institution-wrap>
109 Lewis Hall, Bozeman, MT 59717 USA</aff>
<aff id="Aff2"><label>2</label>
<institution-wrap><institution-id institution-id-type="GRID">grid.41891.35</institution-id>
<institution-id institution-id-type="ISNI">0000000121566108</institution-id>
<institution>Bozeman Deaconess Health Group and WWAMI Medical Education Program,</institution>
<institution>Montana State University,</institution>
</institution-wrap>
Bozeman, MT 59717 USA</aff>
</contrib-group>
<pub-date pub-type="epub"><day>6</day>
<month>2</month>
<year>2008</year>
</pub-date>
<pub-date pub-type="ppub"><year>2008</year>
</pub-date>
<volume>60</volume>
<issue>2</issue>
<elocation-id>83</elocation-id>
<history><date date-type="received"><day>1</day>
<month>11</month>
<year>2007</year>
</date>
<date date-type="accepted"><day>14</day>
<month>1</month>
<year>2008</year>
</date>
</history>
<permissions><copyright-statement>© Springer-Verlag 2008</copyright-statement>
<license><license-p>This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.</license-p>
</license>
</permissions>
<abstract id="Abs1"><p>The chemoattractant neutrophil formyl peptide receptor (FPR) binds bacterial and mitochondrial <italic>N</italic>
-formylated peptides, which allows the neutrophils to find the bacterial source and/or site of tissue damage. Certain inflammatory disorders may be due in part to an impaired innate immune system that does not respond to acute bacterial damage in a timely fashion. Because the human FPR is encoded by a large number of different haplotypes arising from ten single-nucleotide polymorphisms, we examined the possibility that some of these haplotypes are functionally distinct. We analyzed the response of three common FPR haplotypes to peptides from <italic>Escherichia coli</italic>
, <italic>Mycobacterium avium</italic>
ssp. <italic>paratuberculosis</italic>
, and human mitochondria. All three haplotypes responded similarly to the <italic>E</italic>
. <italic>coli</italic>
and mitochondrial peptides, whereas one required a higher concentration of the <italic>M</italic>
. <italic>avium</italic>
peptide fMFEDAVAWF for receptor downregulation, receptor signaling, and chemotaxis. This raises the possibility of additional bacterial species differences in functional responses among FPR variants and establishes a precedent with potentially important implications for our innate immune response against bacterial infections. We also investigated whether certain FPR haplotypes are associated with rheumatoid arthritis (RA) by sequencing <italic>FPR1</italic>
from 148 Caucasian individuals. The results suggested that FPR haplotypes do not significantly contribute toward RA.</p>
</abstract>
<kwd-group xml:lang="en"><title>Keywords</title>
<kwd>Chemoattractant receptor</kwd>
<kwd>Inflammation</kwd>
<kwd>Chemotaxis</kwd>
<kwd>Cell signaling</kwd>
<kwd>Haplotype</kwd>
</kwd-group>
<custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name>
<meta-value>© Springer-Verlag 2008</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Montana</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Montana"><name sortKey="Gripentrog, Jeannie M" sort="Gripentrog, Jeannie M" uniqKey="Gripentrog J" first="Jeannie M." last="Gripentrog">Jeannie M. Gripentrog</name>
</region>
<name sortKey="Miettinen, Heini M" sort="Miettinen, Heini M" uniqKey="Miettinen H" first="Heini M." last="Miettinen">Heini M. Miettinen</name>
<name sortKey="Mills, John S" sort="Mills, John S" uniqKey="Mills J" first="John S." last="Mills">John S. Mills</name>
<name sortKey="Saari, George J" sort="Saari, George J" uniqKey="Saari G" first="George J." last="Saari">George J. Saari</name>
</country>
</tree>
</affiliations>
</record>
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