Mechanisms of suppression of poly I:C-induced activation of NK cells by ethanol
We have previously reported that ethanol (EtOH) decreases polyinosinic–polycytidylic acid (poly I:C) and interleukin-2 (IL-2)-induced upregulation of natural killer (NK) cell lytic activity in mice. The present study was designed to determine if decreased production of or response to interferon-α (I...
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| Veröffentlicht in: | Alcohol (Fayetteville, N.Y.) N.Y.), 2000-05, Vol.21 (1), p.87-95 |
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| creator | Collier, Stephanie D Pruett, Stephen B |
| description | We have previously reported that ethanol (EtOH) decreases polyinosinic–polycytidylic acid (poly I:C) and interleukin-2 (IL-2)-induced upregulation of natural killer (NK) cell lytic activity in mice. The present study was designed to determine if decreased production of or response to interferon-α (IFN-α) is involved and if this is associated with inhibited upregulation of perforin or granzyme B. Treatment of mice with poly I:C upregulated IFN-α and granzyme B, but not perforin, in the spleen. Administration of EtOH before poly I:C prevented the upregulation of IFN-α and granzyme B and decreased perforin levels. EtOH exposure in vivo rendered splenocytes less able to respond to IFN-α upon in vitro exposure to poly I:C. Exogenous IFN-α only partially prevented this decreased response. Thus, decreased production of and response to IFN-α as well as decreased levels of granzyme B and perforin are implicated in the diminished activation of NK cell lytic function in EtOH-treated mice. |
| doi_str_mv | 10.1016/S0741-8329(00)00087-2 |
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The present study was designed to determine if decreased production of or response to interferon-α (IFN-α) is involved and if this is associated with inhibited upregulation of perforin or granzyme B. Treatment of mice with poly I:C upregulated IFN-α and granzyme B, but not perforin, in the spleen. Administration of EtOH before poly I:C prevented the upregulation of IFN-α and granzyme B and decreased perforin levels. EtOH exposure in vivo rendered splenocytes less able to respond to IFN-α upon in vitro exposure to poly I:C. Exogenous IFN-α only partially prevented this decreased response. Thus, decreased production of and response to IFN-α as well as decreased levels of granzyme B and perforin are implicated in the diminished activation of NK cell lytic function in EtOH-treated mice.</description><identifier>ISSN: 0741-8329</identifier><identifier>EISSN: 1873-6823</identifier><identifier>DOI: 10.1016/S0741-8329(00)00087-2</identifier><identifier>PMID: 10946161</identifier><identifier>CODEN: ALCOEX</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Alcoholism and acute alcohol poisoning ; Animals ; Biological and medical sciences ; Blotting, Western ; Central Nervous System Depressants - pharmacology ; Ethanol ; Ethanol - pharmacology ; Female ; Granzyme B ; Granzymes ; Interferon Inducers - pharmacology ; Interferon-alpha - drug effects ; Interferon-alpha - metabolism ; Interferon-α ; Killer Cells, Natural - drug effects ; Killer Cells, Natural - metabolism ; Lymphocyte Activation - drug effects ; Medical sciences ; Membrane Glycoproteins - blood ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Natural killer cells ; Perforin ; Poly I-C - pharmacology ; Poly I:C ; Pore Forming Cytotoxic Proteins ; Serine Endopeptidases - blood ; Spleen - cytology ; Spleen - drug effects ; Spleen - metabolism ; Toxicology</subject><ispartof>Alcohol (Fayetteville, N.Y.), 2000-05, Vol.21 (1), p.87-95</ispartof><rights>2000 Elsevier Science Inc.</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-9e15464565aa3c6397ee6049bfe9c3c6b4c51a5a448da72e05e9d9433a41190a3</citedby><cites>FETCH-LOGICAL-c421t-9e15464565aa3c6397ee6049bfe9c3c6b4c51a5a448da72e05e9d9433a41190a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0741832900000872$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1466629$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10946161$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Collier, Stephanie D</creatorcontrib><creatorcontrib>Pruett, Stephen B</creatorcontrib><title>Mechanisms of suppression of poly I:C-induced activation of NK cells by ethanol</title><title>Alcohol (Fayetteville, N.Y.)</title><addtitle>Alcohol</addtitle><description>We have previously reported that ethanol (EtOH) decreases polyinosinic–polycytidylic acid (poly I:C) and interleukin-2 (IL-2)-induced upregulation of natural killer (NK) cell lytic activity in mice. The present study was designed to determine if decreased production of or response to interferon-α (IFN-α) is involved and if this is associated with inhibited upregulation of perforin or granzyme B. Treatment of mice with poly I:C upregulated IFN-α and granzyme B, but not perforin, in the spleen. Administration of EtOH before poly I:C prevented the upregulation of IFN-α and granzyme B and decreased perforin levels. EtOH exposure in vivo rendered splenocytes less able to respond to IFN-α upon in vitro exposure to poly I:C. Exogenous IFN-α only partially prevented this decreased response. Thus, decreased production of and response to IFN-α as well as decreased levels of granzyme B and perforin are implicated in the diminished activation of NK cell lytic function in EtOH-treated mice.</description><subject>Alcoholism and acute alcohol poisoning</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Central Nervous System Depressants - pharmacology</subject><subject>Ethanol</subject><subject>Ethanol - pharmacology</subject><subject>Female</subject><subject>Granzyme B</subject><subject>Granzymes</subject><subject>Interferon Inducers - pharmacology</subject><subject>Interferon-alpha - drug effects</subject><subject>Interferon-alpha - metabolism</subject><subject>Interferon-α</subject><subject>Killer Cells, Natural - drug effects</subject><subject>Killer Cells, Natural - metabolism</subject><subject>Lymphocyte Activation - drug effects</subject><subject>Medical sciences</subject><subject>Membrane Glycoproteins - blood</subject><subject>Mice</subject><subject>Mice, Inbred C3H</subject><subject>Mice, Inbred C57BL</subject><subject>Natural killer cells</subject><subject>Perforin</subject><subject>Poly I-C - pharmacology</subject><subject>Poly I:C</subject><subject>Pore Forming Cytotoxic Proteins</subject><subject>Serine Endopeptidases - blood</subject><subject>Spleen - cytology</subject><subject>Spleen - drug effects</subject><subject>Spleen - metabolism</subject><subject>Toxicology</subject><issn>0741-8329</issn><issn>1873-6823</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEuP0zAQgC0Eot3CTwDlgNByCPjtmAtC1QIVhR6As-U6E2GUJllPslL__TptBdz2NJqZbx76CHnB6FtGmX73gxrJykpwe03pG0ppZUr-iCxZZUSpKy4ek-VfZEGuEP9kyBhjn5IFo1ZqptmS7L5B-O27iAcs-qbAaRgSIMa-m9Ohb4_F5v26jF09BagLH8Z458dL-_vXIkDbYrE_FjDmNX37jDxpfIvw_BJX5Nenm5_rL-V293mz_rgtg-RsLC0wJbVUWnkvghbWAGgq7b4BG3JhL4NiXnkpq9obDlSBra0UwkvGLPViRV6f9w6pv50AR3eIOD_jO-gndIYZZbkWD4KZ01xVNoPqDIbUIyZo3JDiwaejY9TNyt1JuZt9OkrdSbnjee7l5cC0P0D939TZcQZeXQCPwbdN8l2I-I-TWms-3_9wxiBru4uQHIYIXbYeE4TR1X184JN7X0mbyA</recordid><startdate>20000501</startdate><enddate>20000501</enddate><creator>Collier, Stephanie D</creator><creator>Pruett, Stephen B</creator><general>Elsevier Inc</general><general>Elsevier Science</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>7U7</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>20000501</creationdate><title>Mechanisms of suppression of poly I:C-induced activation of NK cells by ethanol</title><author>Collier, Stephanie D ; Pruett, Stephen B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-9e15464565aa3c6397ee6049bfe9c3c6b4c51a5a448da72e05e9d9433a41190a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Alcoholism and acute alcohol poisoning</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Central Nervous System Depressants - pharmacology</topic><topic>Ethanol</topic><topic>Ethanol - pharmacology</topic><topic>Female</topic><topic>Granzyme B</topic><topic>Granzymes</topic><topic>Interferon Inducers - pharmacology</topic><topic>Interferon-alpha - drug effects</topic><topic>Interferon-alpha - metabolism</topic><topic>Interferon-α</topic><topic>Killer Cells, Natural - drug effects</topic><topic>Killer Cells, Natural - metabolism</topic><topic>Lymphocyte Activation - drug effects</topic><topic>Medical sciences</topic><topic>Membrane Glycoproteins - blood</topic><topic>Mice</topic><topic>Mice, Inbred C3H</topic><topic>Mice, Inbred C57BL</topic><topic>Natural killer cells</topic><topic>Perforin</topic><topic>Poly I-C - pharmacology</topic><topic>Poly I:C</topic><topic>Pore Forming Cytotoxic Proteins</topic><topic>Serine Endopeptidases - blood</topic><topic>Spleen - cytology</topic><topic>Spleen - drug effects</topic><topic>Spleen - metabolism</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Collier, Stephanie D</creatorcontrib><creatorcontrib>Pruett, Stephen B</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>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>Alcohol (Fayetteville, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Collier, Stephanie D</au><au>Pruett, Stephen B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms of suppression of poly I:C-induced activation of NK cells by ethanol</atitle><jtitle>Alcohol (Fayetteville, N.Y.)</jtitle><addtitle>Alcohol</addtitle><date>2000-05-01</date><risdate>2000</risdate><volume>21</volume><issue>1</issue><spage>87</spage><epage>95</epage><pages>87-95</pages><issn>0741-8329</issn><eissn>1873-6823</eissn><coden>ALCOEX</coden><abstract>We have previously reported that ethanol (EtOH) decreases polyinosinic–polycytidylic acid (poly I:C) and interleukin-2 (IL-2)-induced upregulation of natural killer (NK) cell lytic activity in mice. The present study was designed to determine if decreased production of or response to interferon-α (IFN-α) is involved and if this is associated with inhibited upregulation of perforin or granzyme B. Treatment of mice with poly I:C upregulated IFN-α and granzyme B, but not perforin, in the spleen. Administration of EtOH before poly I:C prevented the upregulation of IFN-α and granzyme B and decreased perforin levels. EtOH exposure in vivo rendered splenocytes less able to respond to IFN-α upon in vitro exposure to poly I:C. Exogenous IFN-α only partially prevented this decreased response. Thus, decreased production of and response to IFN-α as well as decreased levels of granzyme B and perforin are implicated in the diminished activation of NK cell lytic function in EtOH-treated mice.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10946161</pmid><doi>10.1016/S0741-8329(00)00087-2</doi><tpages>9</tpages></addata></record> |
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| subjects | Alcoholism and acute alcohol poisoning Animals Biological and medical sciences Blotting, Western Central Nervous System Depressants - pharmacology Ethanol Ethanol - pharmacology Female Granzyme B Granzymes Interferon Inducers - pharmacology Interferon-alpha - drug effects Interferon-alpha - metabolism Interferon-α Killer Cells, Natural - drug effects Killer Cells, Natural - metabolism Lymphocyte Activation - drug effects Medical sciences Membrane Glycoproteins - blood Mice Mice, Inbred C3H Mice, Inbred C57BL Natural killer cells Perforin Poly I-C - pharmacology Poly I:C Pore Forming Cytotoxic Proteins Serine Endopeptidases - blood Spleen - cytology Spleen - drug effects Spleen - metabolism Toxicology |
| title | Mechanisms of suppression of poly I:C-induced activation of NK cells by ethanol |
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