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Modulation of endotoxin-induced NF-kappa B activation in lung and liver through TNF type 1 and IL-1 receptors
Departments of 1 Medicine and 2 Surgery, Vanderbilt University School of Medicine, Nashville 37232-2650; and 3 Department of Veterans Affairs Medical Center, Nashville, Tennessee 37203 We investigated the requirement for tumor necrosis factor- (TNF- ) and interleukin (IL)-1 receptors in the patho...
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| Published in: | American journal of physiology. Lung cellular and molecular physiology 2002-12, Vol.283 (6), p.1247-L1254 |
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| Language: | English |
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| container_end_page | L1254 |
| container_issue | 6 |
| container_start_page | 1247 |
| container_title | American journal of physiology. Lung cellular and molecular physiology |
| container_volume | 283 |
| creator | Koay, M. Audrey Christman, John W Wudel, L. James Allos, Tara Cheng, Dong-Sheng Chapman, William C Blackwell, Timothy S |
| description | Departments of 1 Medicine and
2 Surgery, Vanderbilt University School of Medicine,
Nashville 37232-2650; and 3 Department of Veterans
Affairs Medical Center, Nashville, Tennessee 37203
We investigated the requirement
for tumor necrosis factor- (TNF- ) and interleukin (IL)-1
receptors in the pathogenesis of the pulmonary and hepatic responses to
Escherichia coli lipopolysaccharide (LPS) by studying
wild-type mice and mice deficient in TNF type 1 receptor [TNFR1
knockout (KO)] or both TNF type 1 and IL-1 receptors (TNFR1/IL-1R KO).
In lung tissue, NF- B activation was similar among the groups after
exposure to aerosolized LPS. After intraperitoneal injection of LPS,
NF- B activation in liver was attenuated in TNFR1 KO mice and further
diminished in TNFR1/IL-1R KO mice; however, in lung tissue, no
impairment in NF- B activation was found in TNFR1 KO mice and only a
modest decrease was found in TNFR1/IL-1R KO mice. Lung concentrations
of KC and macrophage-inflammatory peptide 2 were lower in TNFR1 KO and
TNFR1/IL-1R KO mice after aerosolized and intraperitoneal LPS. We
conclude that LPS-induced NF- B activation in liver is mediated
through TNF- - and IL-1 receptor-dependent pathways, but, in the
lung, LPS-induced NF- B activation is largely independent of these receptors.
sepsis; macrophage; neutrophil; cytokines; chemokines |
| doi_str_mv | 10.1152/ajplung.00036.2002 |
| format | article |
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2 Surgery, Vanderbilt University School of Medicine,
Nashville 37232-2650; and 3 Department of Veterans
Affairs Medical Center, Nashville, Tennessee 37203
We investigated the requirement
for tumor necrosis factor- (TNF- ) and interleukin (IL)-1
receptors in the pathogenesis of the pulmonary and hepatic responses to
Escherichia coli lipopolysaccharide (LPS) by studying
wild-type mice and mice deficient in TNF type 1 receptor [TNFR1
knockout (KO)] or both TNF type 1 and IL-1 receptors (TNFR1/IL-1R KO).
In lung tissue, NF- B activation was similar among the groups after
exposure to aerosolized LPS. After intraperitoneal injection of LPS,
NF- B activation in liver was attenuated in TNFR1 KO mice and further
diminished in TNFR1/IL-1R KO mice; however, in lung tissue, no
impairment in NF- B activation was found in TNFR1 KO mice and only a
modest decrease was found in TNFR1/IL-1R KO mice. Lung concentrations
of KC and macrophage-inflammatory peptide 2 were lower in TNFR1 KO and
TNFR1/IL-1R KO mice after aerosolized and intraperitoneal LPS. We
conclude that LPS-induced NF- B activation in liver is mediated
through TNF- - and IL-1 receptor-dependent pathways, but, in the
lung, LPS-induced NF- B activation is largely independent of these receptors.
sepsis; macrophage; neutrophil; cytokines; chemokines</description><identifier>ISSN: 1040-0605</identifier><identifier>EISSN: 1522-1504</identifier><identifier>DOI: 10.1152/ajplung.00036.2002</identifier><identifier>PMID: 12388356</identifier><language>eng</language><publisher>United States</publisher><subject>Aerosols ; Animals ; Antigens, CD - physiology ; Endotoxins - pharmacology ; Injections, Intraperitoneal ; Lipopolysaccharides - administration & dosage ; Liver - metabolism ; Lung - metabolism ; Mice ; Mice, Knockout - genetics ; NF-kappa B - physiology ; Pneumonia - chemically induced ; Receptors, Interleukin-1 - physiology ; Receptors, Tumor Necrosis Factor - physiology ; Receptors, Tumor Necrosis Factor, Type I</subject><ispartof>American journal of physiology. Lung cellular and molecular physiology, 2002-12, Vol.283 (6), p.1247-L1254</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c389t-155d2903c3a13a9344bf0958d02d5177ac7045d52eb15e49a2dd29d0aeed83913</citedby><cites>FETCH-LOGICAL-c389t-155d2903c3a13a9344bf0958d02d5177ac7045d52eb15e49a2dd29d0aeed83913</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12388356$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Koay, M. Audrey</creatorcontrib><creatorcontrib>Christman, John W</creatorcontrib><creatorcontrib>Wudel, L. James</creatorcontrib><creatorcontrib>Allos, Tara</creatorcontrib><creatorcontrib>Cheng, Dong-Sheng</creatorcontrib><creatorcontrib>Chapman, William C</creatorcontrib><creatorcontrib>Blackwell, Timothy S</creatorcontrib><title>Modulation of endotoxin-induced NF-kappa B activation in lung and liver through TNF type 1 and IL-1 receptors</title><title>American journal of physiology. Lung cellular and molecular physiology</title><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><description>Departments of 1 Medicine and
2 Surgery, Vanderbilt University School of Medicine,
Nashville 37232-2650; and 3 Department of Veterans
Affairs Medical Center, Nashville, Tennessee 37203
We investigated the requirement
for tumor necrosis factor- (TNF- ) and interleukin (IL)-1
receptors in the pathogenesis of the pulmonary and hepatic responses to
Escherichia coli lipopolysaccharide (LPS) by studying
wild-type mice and mice deficient in TNF type 1 receptor [TNFR1
knockout (KO)] or both TNF type 1 and IL-1 receptors (TNFR1/IL-1R KO).
In lung tissue, NF- B activation was similar among the groups after
exposure to aerosolized LPS. After intraperitoneal injection of LPS,
NF- B activation in liver was attenuated in TNFR1 KO mice and further
diminished in TNFR1/IL-1R KO mice; however, in lung tissue, no
impairment in NF- B activation was found in TNFR1 KO mice and only a
modest decrease was found in TNFR1/IL-1R KO mice. Lung concentrations
of KC and macrophage-inflammatory peptide 2 were lower in TNFR1 KO and
TNFR1/IL-1R KO mice after aerosolized and intraperitoneal LPS. We
conclude that LPS-induced NF- B activation in liver is mediated
through TNF- - and IL-1 receptor-dependent pathways, but, in the
lung, LPS-induced NF- B activation is largely independent of these receptors.
sepsis; macrophage; neutrophil; cytokines; chemokines</description><subject>Aerosols</subject><subject>Animals</subject><subject>Antigens, CD - physiology</subject><subject>Endotoxins - pharmacology</subject><subject>Injections, Intraperitoneal</subject><subject>Lipopolysaccharides - administration & dosage</subject><subject>Liver - metabolism</subject><subject>Lung - metabolism</subject><subject>Mice</subject><subject>Mice, Knockout - genetics</subject><subject>NF-kappa B - physiology</subject><subject>Pneumonia - chemically induced</subject><subject>Receptors, Interleukin-1 - physiology</subject><subject>Receptors, Tumor Necrosis Factor - physiology</subject><subject>Receptors, Tumor Necrosis Factor, Type I</subject><issn>1040-0605</issn><issn>1522-1504</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNp1kN1OwyAYQInROJ2-gBeGF-j8gNK13unidMmcN_OasEJXZlcIbef69nY__tx4Bcl3zgc5CN0QGBDC6Z1cuaIplwMAYNGAAtATdNENaEA4hKfdHUIIIALeQ5dVteo4DhCdox6hLI4Zjy7Q-tWqppC1sSW2GdalsrXdmjIwpWpSrfBsHHxI5yR-xDKtzeaAmhLvnsayVLgwG-1xnXvbLHM8n41x3TqNyX44mQYEe51qV1tfXaGzTBaVvj6effQ-fpqPXoLp2_Nk9DANUhYndfd9rmgCLGWSMJmwMFxkkPBYAVWcDIcyHULIFad6QbgOE0lVxyuQWquYJYT1ET3sTb2tKq8z4bxZS98KAmLXThzbiX07sWvXSbcHyTWLtVa_yjFWBwwOQG6W-afxWri8rYwt7LL9WUhjJiIxJTQcdsL9_8K4KYq53tbf5h9ROJWxLw0bkUo</recordid><startdate>20021201</startdate><enddate>20021201</enddate><creator>Koay, M. Audrey</creator><creator>Christman, John W</creator><creator>Wudel, L. James</creator><creator>Allos, Tara</creator><creator>Cheng, Dong-Sheng</creator><creator>Chapman, William C</creator><creator>Blackwell, Timothy S</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></search><sort><creationdate>20021201</creationdate><title>Modulation of endotoxin-induced NF-kappa B activation in lung and liver through TNF type 1 and IL-1 receptors</title><author>Koay, M. Audrey ; Christman, John W ; Wudel, L. James ; Allos, Tara ; Cheng, Dong-Sheng ; Chapman, William C ; Blackwell, Timothy S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-155d2903c3a13a9344bf0958d02d5177ac7045d52eb15e49a2dd29d0aeed83913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Aerosols</topic><topic>Animals</topic><topic>Antigens, CD - physiology</topic><topic>Endotoxins - pharmacology</topic><topic>Injections, Intraperitoneal</topic><topic>Lipopolysaccharides - administration & dosage</topic><topic>Liver - metabolism</topic><topic>Lung - metabolism</topic><topic>Mice</topic><topic>Mice, Knockout - genetics</topic><topic>NF-kappa B - physiology</topic><topic>Pneumonia - chemically induced</topic><topic>Receptors, Interleukin-1 - physiology</topic><topic>Receptors, Tumor Necrosis Factor - physiology</topic><topic>Receptors, Tumor Necrosis Factor, Type I</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Koay, M. Audrey</creatorcontrib><creatorcontrib>Christman, John W</creatorcontrib><creatorcontrib>Wudel, L. James</creatorcontrib><creatorcontrib>Allos, Tara</creatorcontrib><creatorcontrib>Cheng, Dong-Sheng</creatorcontrib><creatorcontrib>Chapman, William C</creatorcontrib><creatorcontrib>Blackwell, Timothy S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</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>Koay, M. Audrey</au><au>Christman, John W</au><au>Wudel, L. James</au><au>Allos, Tara</au><au>Cheng, Dong-Sheng</au><au>Chapman, William C</au><au>Blackwell, Timothy S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of endotoxin-induced NF-kappa B activation in lung and liver through TNF type 1 and IL-1 receptors</atitle><jtitle>American journal of physiology. Lung cellular and molecular physiology</jtitle><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><date>2002-12-01</date><risdate>2002</risdate><volume>283</volume><issue>6</issue><spage>1247</spage><epage>L1254</epage><pages>1247-L1254</pages><issn>1040-0605</issn><eissn>1522-1504</eissn><abstract>Departments of 1 Medicine and
2 Surgery, Vanderbilt University School of Medicine,
Nashville 37232-2650; and 3 Department of Veterans
Affairs Medical Center, Nashville, Tennessee 37203
We investigated the requirement
for tumor necrosis factor- (TNF- ) and interleukin (IL)-1
receptors in the pathogenesis of the pulmonary and hepatic responses to
Escherichia coli lipopolysaccharide (LPS) by studying
wild-type mice and mice deficient in TNF type 1 receptor [TNFR1
knockout (KO)] or both TNF type 1 and IL-1 receptors (TNFR1/IL-1R KO).
In lung tissue, NF- B activation was similar among the groups after
exposure to aerosolized LPS. After intraperitoneal injection of LPS,
NF- B activation in liver was attenuated in TNFR1 KO mice and further
diminished in TNFR1/IL-1R KO mice; however, in lung tissue, no
impairment in NF- B activation was found in TNFR1 KO mice and only a
modest decrease was found in TNFR1/IL-1R KO mice. Lung concentrations
of KC and macrophage-inflammatory peptide 2 were lower in TNFR1 KO and
TNFR1/IL-1R KO mice after aerosolized and intraperitoneal LPS. We
conclude that LPS-induced NF- B activation in liver is mediated
through TNF- - and IL-1 receptor-dependent pathways, but, in the
lung, LPS-induced NF- B activation is largely independent of these receptors.
sepsis; macrophage; neutrophil; cytokines; chemokines</abstract><cop>United States</cop><pmid>12388356</pmid><doi>10.1152/ajplung.00036.2002</doi></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1040-0605 |
| ispartof | American journal of physiology. Lung cellular and molecular physiology, 2002-12, Vol.283 (6), p.1247-L1254 |
| issn | 1040-0605 1522-1504 |
| language | eng |
| recordid | cdi_pubmed_primary_12388356 |
| source | American Physiological Society Journals |
| subjects | Aerosols Animals Antigens, CD - physiology Endotoxins - pharmacology Injections, Intraperitoneal Lipopolysaccharides - administration & dosage Liver - metabolism Lung - metabolism Mice Mice, Knockout - genetics NF-kappa B - physiology Pneumonia - chemically induced Receptors, Interleukin-1 - physiology Receptors, Tumor Necrosis Factor - physiology Receptors, Tumor Necrosis Factor, Type I |
| title | Modulation of endotoxin-induced NF-kappa B activation in lung and liver through TNF type 1 and IL-1 receptors |
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