Different susceptibilities of PECAM-deficient mouse strains to spontaneous idiopathic pneumonitis
Platelet Endothelial Cell Adhesion Molecule (PECAM) is an adhesion and signaling molecule used for leukocyte extravasation. We have generated two strains of PECAM-deficient mouse, one in the original C57BL/6 and a second by backcrossing nice generations into the FVB/n strain. The FVB/n strain has re...
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| Veröffentlicht in: | Experimental and molecular pathology 2006-08, Vol.81 (1), p.23-30 |
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| creator | Schenkel, Alan R. Chew, Tina W. Chlipala, Elizabeth Harbord, Marcus W.N. Muller, William A. |
| description | Platelet Endothelial Cell Adhesion Molecule (PECAM) is an adhesion and signaling molecule used for leukocyte extravasation. We have generated two strains of PECAM-deficient mouse, one in the original C57BL/6 and a second by backcrossing nice generations into the FVB/n strain. The FVB/n strain has reduced responses in models of acute inflammation. We show here that this strain is also susceptible to a chronic pneumonia which leads to pulmonary fibrosis. In contrast, PECAM-deficient C57BL/6 mice do not develop this lung disease and have normal responses in acute models of inflammation. This demonstrates that PECAM-dependent and -independent mechanisms are found in both acute and chronic inflammation. Further, the PECAM-deficient FVB/n strain has many pathologic similarities to the human disease Idiopathic Pulmonary Fibrosis, suggesting that similar molecular mechanisms may play a role in human disease. |
| doi_str_mv | 10.1016/j.yexmp.2005.11.007 |
| format | Article |
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We have generated two strains of PECAM-deficient mouse, one in the original C57BL/6 and a second by backcrossing nice generations into the FVB/n strain. The FVB/n strain has reduced responses in models of acute inflammation. We show here that this strain is also susceptible to a chronic pneumonia which leads to pulmonary fibrosis. In contrast, PECAM-deficient C57BL/6 mice do not develop this lung disease and have normal responses in acute models of inflammation. This demonstrates that PECAM-dependent and -independent mechanisms are found in both acute and chronic inflammation. 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Miscellaneous investigative techniques ; Platelet Endothelial Cell Adhesion Molecule-1 - genetics ; Platelet Endothelial Cell Adhesion Molecule-1 - metabolism ; Pneumonia - genetics ; Pneumonia - pathology</subject><ispartof>Experimental and molecular pathology, 2006-08, Vol.81 (1), p.23-30</ispartof><rights>2005 Elsevier Inc.</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c487t-29243795e266df53cb1361c1a906013399f5127f6a0699616b851dab327ada463</citedby><cites>FETCH-LOGICAL-c487t-29243795e266df53cb1361c1a906013399f5127f6a0699616b851dab327ada463</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0014480005001449$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17958683$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16457810$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schenkel, Alan R.</creatorcontrib><creatorcontrib>Chew, Tina W.</creatorcontrib><creatorcontrib>Chlipala, Elizabeth</creatorcontrib><creatorcontrib>Harbord, Marcus W.N.</creatorcontrib><creatorcontrib>Muller, William A.</creatorcontrib><title>Different susceptibilities of PECAM-deficient mouse strains to spontaneous idiopathic pneumonitis</title><title>Experimental and molecular pathology</title><addtitle>Exp Mol Pathol</addtitle><description>Platelet Endothelial Cell Adhesion Molecule (PECAM) is an adhesion and signaling molecule used for leukocyte extravasation. We have generated two strains of PECAM-deficient mouse, one in the original C57BL/6 and a second by backcrossing nice generations into the FVB/n strain. The FVB/n strain has reduced responses in models of acute inflammation. We show here that this strain is also susceptible to a chronic pneumonia which leads to pulmonary fibrosis. In contrast, PECAM-deficient C57BL/6 mice do not develop this lung disease and have normal responses in acute models of inflammation. This demonstrates that PECAM-dependent and -independent mechanisms are found in both acute and chronic inflammation. Further, the PECAM-deficient FVB/n strain has many pathologic similarities to the human disease Idiopathic Pulmonary Fibrosis, suggesting that similar molecular mechanisms may play a role in human disease.</description><subject>Animals</subject><subject>beta-N-Acetylhexosaminidases - analysis</subject><subject>Biological and medical sciences</subject><subject>Chronic Disease</subject><subject>Disease Models, Animal</subject><subject>Disease Susceptibility - metabolism</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Lectins - analysis</subject><subject>Lung - pathology</subject><subject>Medical sciences</subject><subject>Mice - genetics</subject><subject>Mice, Knockout</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>Platelet Endothelial Cell Adhesion Molecule-1 - genetics</subject><subject>Platelet Endothelial Cell Adhesion Molecule-1 - metabolism</subject><subject>Pneumonia - genetics</subject><subject>Pneumonia - pathology</subject><issn>0014-4800</issn><issn>1096-0945</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUtv1DAUhS0EokPhFyChbOgu4d48nHgBUjWUh9SqLGBtOY5N7yiJg-1U7b_Hw4wo3bCyZH_3-NxzGHuNUCAgf7cr7s3dtBQlQFMgFgDtE7ZBEDwHUTdP2QYA67zuAE7YixB2ACAAy-fsBHndtB3ChqmPZK3xZo5ZWIM2S6SeRopkQuZs9u1ie36VD8aSpj0zuTWYLESvaA5ZdFlY3BzVbNJ9RgO5RcUb0tkym3Vyc9IJL9kzq8ZgXh3PU_bj08X37Zf88vrz1-35Za7rro15Kcq6akVjSs4H21S6x4qjRiWAA1aVELbBsrVcAReCI--7BgfVV2WrBlXz6pR9OOguaz-ZQSe7Xo1y8TQpfy-dIvn4ZaYb-dPdSqw73naQBM6OAt79Wk2IcqKUyDge1pO841C2WCewOoDauxC8sX8_QZD7auRO_qlG7quRiDJVk6be_OvvYebYRQLeHgEVtBqtV7Om8MClcDreVYl7f-BMSvOWjJdhX442A3mjoxwc_dfIbxFZr90</recordid><startdate>20060801</startdate><enddate>20060801</enddate><creator>Schenkel, Alan R.</creator><creator>Chew, Tina W.</creator><creator>Chlipala, Elizabeth</creator><creator>Harbord, Marcus W.N.</creator><creator>Muller, William A.</creator><general>Elsevier Inc</general><general>Elsevier</general><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><scope>5PM</scope></search><sort><creationdate>20060801</creationdate><title>Different susceptibilities of PECAM-deficient mouse strains to spontaneous idiopathic pneumonitis</title><author>Schenkel, Alan R. ; Chew, Tina W. ; Chlipala, Elizabeth ; Harbord, Marcus W.N. ; Muller, William A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c487t-29243795e266df53cb1361c1a906013399f5127f6a0699616b851dab327ada463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>beta-N-Acetylhexosaminidases - analysis</topic><topic>Biological and medical sciences</topic><topic>Chronic Disease</topic><topic>Disease Models, Animal</topic><topic>Disease Susceptibility - metabolism</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Lectins - analysis</topic><topic>Lung - pathology</topic><topic>Medical sciences</topic><topic>Mice - genetics</topic><topic>Mice, Knockout</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>Platelet Endothelial Cell Adhesion Molecule-1 - genetics</topic><topic>Platelet Endothelial Cell Adhesion Molecule-1 - metabolism</topic><topic>Pneumonia - genetics</topic><topic>Pneumonia - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schenkel, Alan R.</creatorcontrib><creatorcontrib>Chew, Tina W.</creatorcontrib><creatorcontrib>Chlipala, Elizabeth</creatorcontrib><creatorcontrib>Harbord, Marcus W.N.</creatorcontrib><creatorcontrib>Muller, William A.</creatorcontrib><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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Experimental and molecular pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schenkel, Alan R.</au><au>Chew, Tina W.</au><au>Chlipala, Elizabeth</au><au>Harbord, Marcus W.N.</au><au>Muller, William A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Different susceptibilities of PECAM-deficient mouse strains to spontaneous idiopathic pneumonitis</atitle><jtitle>Experimental and molecular pathology</jtitle><addtitle>Exp Mol Pathol</addtitle><date>2006-08-01</date><risdate>2006</risdate><volume>81</volume><issue>1</issue><spage>23</spage><epage>30</epage><pages>23-30</pages><issn>0014-4800</issn><eissn>1096-0945</eissn><coden>EXMPA6</coden><abstract>Platelet Endothelial Cell Adhesion Molecule (PECAM) is an adhesion and signaling molecule used for leukocyte extravasation. We have generated two strains of PECAM-deficient mouse, one in the original C57BL/6 and a second by backcrossing nice generations into the FVB/n strain. The FVB/n strain has reduced responses in models of acute inflammation. We show here that this strain is also susceptible to a chronic pneumonia which leads to pulmonary fibrosis. In contrast, PECAM-deficient C57BL/6 mice do not develop this lung disease and have normal responses in acute models of inflammation. This demonstrates that PECAM-dependent and -independent mechanisms are found in both acute and chronic inflammation. Further, the PECAM-deficient FVB/n strain has many pathologic similarities to the human disease Idiopathic Pulmonary Fibrosis, suggesting that similar molecular mechanisms may play a role in human disease.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>16457810</pmid><doi>10.1016/j.yexmp.2005.11.007</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals beta-N-Acetylhexosaminidases - analysis Biological and medical sciences Chronic Disease Disease Models, Animal Disease Susceptibility - metabolism Investigative techniques, diagnostic techniques (general aspects) Lectins - analysis Lung - pathology Medical sciences Mice - genetics Mice, Knockout Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Platelet Endothelial Cell Adhesion Molecule-1 - genetics Platelet Endothelial Cell Adhesion Molecule-1 - metabolism Pneumonia - genetics Pneumonia - pathology |
| title | Different susceptibilities of PECAM-deficient mouse strains to spontaneous idiopathic pneumonitis |
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