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KGF pretreatment decreases B7 and granzyme B expression and hastens repair in lungs of mice after allogeneic BMT
1 Department of Pediatrics, Division of Hematology-Oncology and Bone Marrow Transplantation, and Departments of 2 Pulmonary Critical Care Medicine and 3 Physiology, University of Minnesota, Minneapolis, Minnesota 55455; and 4 Amgen, Thousand Oaks, California 91320 We investigated keratinocyte gr...
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| Published in: | American journal of physiology. Lung cellular and molecular physiology 2000-05, Vol.278 (5), p.988-L999 |
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| container_end_page | L999 |
| container_issue | 5 |
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| container_title | American journal of physiology. Lung cellular and molecular physiology |
| container_volume | 278 |
| creator | Panoskaltsis-Mortari, Angela Ingbar, David H Jung, Patricia Haddad, Imad Y Bitterman, Peter B Wangensteen, O. Douglas Farrell, Catherine L Lacey, David L Blazar, Bruce R |
| description | 1 Department of Pediatrics, Division of
Hematology-Oncology and Bone Marrow Transplantation, and Departments of
2 Pulmonary Critical Care Medicine and
3 Physiology, University of Minnesota,
Minneapolis, Minnesota 55455; and 4 Amgen,
Thousand Oaks, California 91320
We investigated keratinocyte growth factor (KGF) as a
pretreatment therapy for idiopathic pneumonia syndrome (IPS) generated as a result of lung damage and allogeneic T cell-dependent inflammatory events occurring in the early peri-bone marrow (BM) transplant (BMT)
period. B10.BR (H2 k ) recipient mice were transplanted with
C57BL/6 (H2 b ) BM with spleen cells after lethal
irradiation with and without cyclophosphamide conditioning with and
without subcutaneous KGF pretreatment. KGF-pretreated mice had fewer
injured alveolar type II (ATII) cells at the time of BMT and exhibited
ATII cell hyperplasia at day 3 post-BMT. The composition of
infiltrating cells on day 7 post-BMT was not altered by KGF
pretreatment, but the frequencies of cells expressing the T-cell
costimulatory molecules B7.1 and B7.2 and mRNA for the cytolysin
granzyme B (usually increased in IPS) were decreased by KGF. Sera from
KGF-treated mice had increases in the Th2 cytokines interleukin (IL)-4,
IL-6, and IL-13 4 days after cessation of KGF administration (i.e., at
the time of BMT). These data suggest that KGF hinders IPS by two modes: 1 ) stimulation of alveolar epithelialization and 2 )
attenuation of immune-mediated injury as a consequence of failure to
upregulate cytolytic molecules and B7 ligand expression and the
induction of anti-inflammatory Th2 cytokines in situ.
bone marrow transplant; keratinocyte growth factor; type II
pneumocytes; cytokines; macrophages; costimulatory molecules |
| doi_str_mv | 10.1152/ajplung.2000.278.5.l988 |
| format | article |
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Hematology-Oncology and Bone Marrow Transplantation, and Departments of
2 Pulmonary Critical Care Medicine and
3 Physiology, University of Minnesota,
Minneapolis, Minnesota 55455; and 4 Amgen,
Thousand Oaks, California 91320
We investigated keratinocyte growth factor (KGF) as a
pretreatment therapy for idiopathic pneumonia syndrome (IPS) generated as a result of lung damage and allogeneic T cell-dependent inflammatory events occurring in the early peri-bone marrow (BM) transplant (BMT)
period. B10.BR (H2 k ) recipient mice were transplanted with
C57BL/6 (H2 b ) BM with spleen cells after lethal
irradiation with and without cyclophosphamide conditioning with and
without subcutaneous KGF pretreatment. KGF-pretreated mice had fewer
injured alveolar type II (ATII) cells at the time of BMT and exhibited
ATII cell hyperplasia at day 3 post-BMT. The composition of
infiltrating cells on day 7 post-BMT was not altered by KGF
pretreatment, but the frequencies of cells expressing the T-cell
costimulatory molecules B7.1 and B7.2 and mRNA for the cytolysin
granzyme B (usually increased in IPS) were decreased by KGF. Sera from
KGF-treated mice had increases in the Th2 cytokines interleukin (IL)-4,
IL-6, and IL-13 4 days after cessation of KGF administration (i.e., at
the time of BMT). These data suggest that KGF hinders IPS by two modes: 1 ) stimulation of alveolar epithelialization and 2 )
attenuation of immune-mediated injury as a consequence of failure to
upregulate cytolytic molecules and B7 ligand expression and the
induction of anti-inflammatory Th2 cytokines in situ.
bone marrow transplant; keratinocyte growth factor; type II
pneumocytes; cytokines; macrophages; costimulatory molecules</description><identifier>ISSN: 1040-0605</identifier><identifier>EISSN: 1522-1504</identifier><identifier>DOI: 10.1152/ajplung.2000.278.5.l988</identifier><identifier>PMID: 10781430</identifier><language>eng</language><publisher>United States</publisher><subject>AIDS/HIV ; Animals ; Antigens, CD - genetics ; B7-1 Antigen - genetics ; B7-2 Antigen ; Bone Marrow Transplantation - adverse effects ; Bone Marrow Transplantation - immunology ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factor 7 ; Fibroblast Growth Factors ; Gene Expression - immunology ; Granzymes ; Growth Substances - pharmacology ; Hypersensitivity - immunology ; In Situ Hybridization ; Interleukin-13 - blood ; Interleukin-13 - genetics ; Interleukin-13 - immunology ; Interleukin-4 - blood ; Interleukin-4 - genetics ; Interleukin-4 - immunology ; Interleukin-6 - blood ; Interleukin-6 - immunology ; Macrophages, Alveolar - immunology ; Membrane Glycoproteins - genetics ; Mice ; Mice, Inbred C57BL ; Microscopy, Electron ; Monocytes - immunology ; Pneumonia - etiology ; Pneumonia - immunology ; Pulmonary Alveoli - enzymology ; Pulmonary Alveoli - immunology ; Pulmonary Alveoli - ultrastructure ; RNA, Messenger - analysis ; Serine Endopeptidases - genetics ; Th2 Cells - immunology ; Transplantation Conditioning</subject><ispartof>American journal of physiology. Lung cellular and molecular physiology, 2000-05, Vol.278 (5), p.988-L999</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c397t-a69f7e1be0a6148b8ab010aef0971de203f510453e97b0dcd563713a23df8abc3</citedby><cites>FETCH-LOGICAL-c397t-a69f7e1be0a6148b8ab010aef0971de203f510453e97b0dcd563713a23df8abc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27911,27912</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10781430$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Panoskaltsis-Mortari, Angela</creatorcontrib><creatorcontrib>Ingbar, David H</creatorcontrib><creatorcontrib>Jung, Patricia</creatorcontrib><creatorcontrib>Haddad, Imad Y</creatorcontrib><creatorcontrib>Bitterman, Peter B</creatorcontrib><creatorcontrib>Wangensteen, O. Douglas</creatorcontrib><creatorcontrib>Farrell, Catherine L</creatorcontrib><creatorcontrib>Lacey, David L</creatorcontrib><creatorcontrib>Blazar, Bruce R</creatorcontrib><title>KGF pretreatment decreases B7 and granzyme B expression and hastens repair in lungs of mice after allogeneic BMT</title><title>American journal of physiology. Lung cellular and molecular physiology</title><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><description>1 Department of Pediatrics, Division of
Hematology-Oncology and Bone Marrow Transplantation, and Departments of
2 Pulmonary Critical Care Medicine and
3 Physiology, University of Minnesota,
Minneapolis, Minnesota 55455; and 4 Amgen,
Thousand Oaks, California 91320
We investigated keratinocyte growth factor (KGF) as a
pretreatment therapy for idiopathic pneumonia syndrome (IPS) generated as a result of lung damage and allogeneic T cell-dependent inflammatory events occurring in the early peri-bone marrow (BM) transplant (BMT)
period. B10.BR (H2 k ) recipient mice were transplanted with
C57BL/6 (H2 b ) BM with spleen cells after lethal
irradiation with and without cyclophosphamide conditioning with and
without subcutaneous KGF pretreatment. KGF-pretreated mice had fewer
injured alveolar type II (ATII) cells at the time of BMT and exhibited
ATII cell hyperplasia at day 3 post-BMT. The composition of
infiltrating cells on day 7 post-BMT was not altered by KGF
pretreatment, but the frequencies of cells expressing the T-cell
costimulatory molecules B7.1 and B7.2 and mRNA for the cytolysin
granzyme B (usually increased in IPS) were decreased by KGF. Sera from
KGF-treated mice had increases in the Th2 cytokines interleukin (IL)-4,
IL-6, and IL-13 4 days after cessation of KGF administration (i.e., at
the time of BMT). These data suggest that KGF hinders IPS by two modes: 1 ) stimulation of alveolar epithelialization and 2 )
attenuation of immune-mediated injury as a consequence of failure to
upregulate cytolytic molecules and B7 ligand expression and the
induction of anti-inflammatory Th2 cytokines in situ.
bone marrow transplant; keratinocyte growth factor; type II
pneumocytes; cytokines; macrophages; costimulatory molecules</description><subject>AIDS/HIV</subject><subject>Animals</subject><subject>Antigens, CD - genetics</subject><subject>B7-1 Antigen - genetics</subject><subject>B7-2 Antigen</subject><subject>Bone Marrow Transplantation - adverse effects</subject><subject>Bone Marrow Transplantation - immunology</subject><subject>Fibroblast Growth Factor 10</subject><subject>Fibroblast Growth Factor 7</subject><subject>Fibroblast Growth Factors</subject><subject>Gene Expression - immunology</subject><subject>Granzymes</subject><subject>Growth Substances - pharmacology</subject><subject>Hypersensitivity - immunology</subject><subject>In Situ Hybridization</subject><subject>Interleukin-13 - blood</subject><subject>Interleukin-13 - genetics</subject><subject>Interleukin-13 - immunology</subject><subject>Interleukin-4 - blood</subject><subject>Interleukin-4 - genetics</subject><subject>Interleukin-4 - immunology</subject><subject>Interleukin-6 - blood</subject><subject>Interleukin-6 - immunology</subject><subject>Macrophages, Alveolar - immunology</subject><subject>Membrane Glycoproteins - genetics</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microscopy, Electron</subject><subject>Monocytes - immunology</subject><subject>Pneumonia - etiology</subject><subject>Pneumonia - immunology</subject><subject>Pulmonary Alveoli - enzymology</subject><subject>Pulmonary Alveoli - immunology</subject><subject>Pulmonary Alveoli - ultrastructure</subject><subject>RNA, Messenger - analysis</subject><subject>Serine Endopeptidases - genetics</subject><subject>Th2 Cells - immunology</subject><subject>Transplantation Conditioning</subject><issn>1040-0605</issn><issn>1522-1504</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNp1kMFO3DAQhq2qqFDgFVqfeksYJ3GcHFnUpRWLuCxny0nGu0aOE-xEZfv09Xa3hQsnjzTfP575CPnKIGWMZ1fqabSz26QZAKSZqFKe2rqqPpCz2M0SxqH4GGsoIIES-Cn5HMJTZDlA-YmcMhAVK3I4I-Pd7ZKOHiePaurRTbTDNtYBA10IqlxHN16537se6YLiS0RDMIP729mqMKEL1OOojKfG0f1SgQ6a9qZFqvSEniprhw06NC1d3K8vyIlWNuDl8T0nj8vv65sfyerh9ufN9Spp81pMiSprLZA1CKpkRdVUqgEGCjXUgnWYQa55PI_nWIsGurbjZS5YrrK805Ft83Py7TB39MPzjGGSvQktWqscDnOQgkFZRB0RFAew9UMIHrUcvemV30kGci9bHmXLvWwZZUsuV1F2TH45fjE3PXZvcge7EagPwNZstr-MRzlud9Fe9LGTy9naNb5M_8a_DpZjp2M2eT_7f6PXZf4A1tyjkQ</recordid><startdate>20000501</startdate><enddate>20000501</enddate><creator>Panoskaltsis-Mortari, Angela</creator><creator>Ingbar, David H</creator><creator>Jung, Patricia</creator><creator>Haddad, Imad Y</creator><creator>Bitterman, Peter B</creator><creator>Wangensteen, O. Douglas</creator><creator>Farrell, Catherine L</creator><creator>Lacey, David L</creator><creator>Blazar, Bruce R</creator><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>20000501</creationdate><title>KGF pretreatment decreases B7 and granzyme B expression and hastens repair in lungs of mice after allogeneic BMT</title><author>Panoskaltsis-Mortari, Angela ; Ingbar, David H ; Jung, Patricia ; Haddad, Imad Y ; Bitterman, Peter B ; Wangensteen, O. Douglas ; Farrell, Catherine L ; Lacey, David L ; Blazar, Bruce R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c397t-a69f7e1be0a6148b8ab010aef0971de203f510453e97b0dcd563713a23df8abc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>AIDS/HIV</topic><topic>Animals</topic><topic>Antigens, CD - genetics</topic><topic>B7-1 Antigen - genetics</topic><topic>B7-2 Antigen</topic><topic>Bone Marrow Transplantation - adverse effects</topic><topic>Bone Marrow Transplantation - immunology</topic><topic>Fibroblast Growth Factor 10</topic><topic>Fibroblast Growth Factor 7</topic><topic>Fibroblast Growth Factors</topic><topic>Gene Expression - immunology</topic><topic>Granzymes</topic><topic>Growth Substances - pharmacology</topic><topic>Hypersensitivity - immunology</topic><topic>In Situ Hybridization</topic><topic>Interleukin-13 - blood</topic><topic>Interleukin-13 - genetics</topic><topic>Interleukin-13 - immunology</topic><topic>Interleukin-4 - blood</topic><topic>Interleukin-4 - genetics</topic><topic>Interleukin-4 - immunology</topic><topic>Interleukin-6 - blood</topic><topic>Interleukin-6 - immunology</topic><topic>Macrophages, Alveolar - immunology</topic><topic>Membrane Glycoproteins - genetics</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microscopy, Electron</topic><topic>Monocytes - immunology</topic><topic>Pneumonia - etiology</topic><topic>Pneumonia - immunology</topic><topic>Pulmonary Alveoli - enzymology</topic><topic>Pulmonary Alveoli - immunology</topic><topic>Pulmonary Alveoli - ultrastructure</topic><topic>RNA, Messenger - analysis</topic><topic>Serine Endopeptidases - genetics</topic><topic>Th2 Cells - immunology</topic><topic>Transplantation Conditioning</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Panoskaltsis-Mortari, Angela</creatorcontrib><creatorcontrib>Ingbar, David H</creatorcontrib><creatorcontrib>Jung, Patricia</creatorcontrib><creatorcontrib>Haddad, Imad Y</creatorcontrib><creatorcontrib>Bitterman, Peter B</creatorcontrib><creatorcontrib>Wangensteen, O. Douglas</creatorcontrib><creatorcontrib>Farrell, Catherine L</creatorcontrib><creatorcontrib>Lacey, David L</creatorcontrib><creatorcontrib>Blazar, Bruce R</creatorcontrib><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>American journal of physiology. Lung cellular and molecular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Panoskaltsis-Mortari, Angela</au><au>Ingbar, David H</au><au>Jung, Patricia</au><au>Haddad, Imad Y</au><au>Bitterman, Peter B</au><au>Wangensteen, O. Douglas</au><au>Farrell, Catherine L</au><au>Lacey, David L</au><au>Blazar, Bruce R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>KGF pretreatment decreases B7 and granzyme B expression and hastens repair in lungs of mice after allogeneic BMT</atitle><jtitle>American journal of physiology. Lung cellular and molecular physiology</jtitle><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><date>2000-05-01</date><risdate>2000</risdate><volume>278</volume><issue>5</issue><spage>988</spage><epage>L999</epage><pages>988-L999</pages><issn>1040-0605</issn><eissn>1522-1504</eissn><abstract>1 Department of Pediatrics, Division of
Hematology-Oncology and Bone Marrow Transplantation, and Departments of
2 Pulmonary Critical Care Medicine and
3 Physiology, University of Minnesota,
Minneapolis, Minnesota 55455; and 4 Amgen,
Thousand Oaks, California 91320
We investigated keratinocyte growth factor (KGF) as a
pretreatment therapy for idiopathic pneumonia syndrome (IPS) generated as a result of lung damage and allogeneic T cell-dependent inflammatory events occurring in the early peri-bone marrow (BM) transplant (BMT)
period. B10.BR (H2 k ) recipient mice were transplanted with
C57BL/6 (H2 b ) BM with spleen cells after lethal
irradiation with and without cyclophosphamide conditioning with and
without subcutaneous KGF pretreatment. KGF-pretreated mice had fewer
injured alveolar type II (ATII) cells at the time of BMT and exhibited
ATII cell hyperplasia at day 3 post-BMT. The composition of
infiltrating cells on day 7 post-BMT was not altered by KGF
pretreatment, but the frequencies of cells expressing the T-cell
costimulatory molecules B7.1 and B7.2 and mRNA for the cytolysin
granzyme B (usually increased in IPS) were decreased by KGF. Sera from
KGF-treated mice had increases in the Th2 cytokines interleukin (IL)-4,
IL-6, and IL-13 4 days after cessation of KGF administration (i.e., at
the time of BMT). These data suggest that KGF hinders IPS by two modes: 1 ) stimulation of alveolar epithelialization and 2 )
attenuation of immune-mediated injury as a consequence of failure to
upregulate cytolytic molecules and B7 ligand expression and the
induction of anti-inflammatory Th2 cytokines in situ.
bone marrow transplant; keratinocyte growth factor; type II
pneumocytes; cytokines; macrophages; costimulatory molecules</abstract><cop>United States</cop><pmid>10781430</pmid><doi>10.1152/ajplung.2000.278.5.l988</doi></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1040-0605 |
| ispartof | American journal of physiology. Lung cellular and molecular physiology, 2000-05, Vol.278 (5), p.988-L999 |
| issn | 1040-0605 1522-1504 |
| language | eng |
| recordid | cdi_pubmed_primary_10781430 |
| source | American Physiological Society Journals |
| subjects | AIDS/HIV Animals Antigens, CD - genetics B7-1 Antigen - genetics B7-2 Antigen Bone Marrow Transplantation - adverse effects Bone Marrow Transplantation - immunology Fibroblast Growth Factor 10 Fibroblast Growth Factor 7 Fibroblast Growth Factors Gene Expression - immunology Granzymes Growth Substances - pharmacology Hypersensitivity - immunology In Situ Hybridization Interleukin-13 - blood Interleukin-13 - genetics Interleukin-13 - immunology Interleukin-4 - blood Interleukin-4 - genetics Interleukin-4 - immunology Interleukin-6 - blood Interleukin-6 - immunology Macrophages, Alveolar - immunology Membrane Glycoproteins - genetics Mice Mice, Inbred C57BL Microscopy, Electron Monocytes - immunology Pneumonia - etiology Pneumonia - immunology Pulmonary Alveoli - enzymology Pulmonary Alveoli - immunology Pulmonary Alveoli - ultrastructure RNA, Messenger - analysis Serine Endopeptidases - genetics Th2 Cells - immunology Transplantation Conditioning |
| title | KGF pretreatment decreases B7 and granzyme B expression and hastens repair in lungs of mice after allogeneic BMT |
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