Leukotrienes, IL-13, and chemokines cooperate to induce BHR and mucus in allergic mouse lungs
Unité de Pharmacologie Cellulaire, Unité Associée Institut Pasteur-Institut National de la Santé et de la Recherche Médicale U485, Institut Pasteur, 75015 Paris, France In mice, intratracheal challenges with antigen (ovalbumin) or recombinant murine interleukin-13 (IL-13) induce lung inflammation, b...
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| Veröffentlicht in: | American journal of physiology. Lung cellular and molecular physiology 2003-02, Vol.284 (2), p.260-L269 |
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| container_title | American journal of physiology. Lung cellular and molecular physiology |
| container_volume | 284 |
| creator | Vargaftig, B. Boris Singer, Monique |
| description | Unité de Pharmacologie Cellulaire, Unité
Associée Institut Pasteur-Institut National de la Santé
et de la Recherche Médicale U485, Institut Pasteur, 75015 Paris,
France
In mice, intratracheal challenges
with antigen (ovalbumin) or recombinant murine interleukin-13
(IL-13) induce lung inflammation, bronchial hyperreactivity (BHR), and
mucus accumulation as independent events (Singer M, Lefort J, and
Vargaftig BB. Am J Respir Cell Mol Biol 26: 74-84,
2002), largely mediated by leukotrienes (LT). We previously showed that
LTC 4 was released 15 min after ovalbumin, and we show that
it induces the expression of monocyte chemoattractant proteins 1 and 5 and KC in the lungs, as well as IL-13 mRNA. Instilled intratracheally,
these chemokines induced BHR and mucus accumulation, which were
inhibited by the 5-lipoxygenase inhibitor zileuton and by the
cysteinyl-LT receptor antagonist MK-571, suggesting mediation by
cysteinyl-LT. Because these chemokines also induced release of LT into
the bronchoalveolar lavage fluid and IL-13 into the lungs, we
hypothesize that LT- and chemokine-based loops for positive-feedback
regulations cooperate to maintain and amplify BHR and lung mucus
accumulation after allergic challenge and in situations where IL-13,
LT, or chemokines are generated.
inflammation; asthma; MUC; leukotriene; cytokine/chemokine; bronchial hyperreactivity |
| doi_str_mv | 10.1152/ajplung.00226.2002 |
| format | Article |
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Associée Institut Pasteur-Institut National de la Santé
et de la Recherche Médicale U485, Institut Pasteur, 75015 Paris,
France
In mice, intratracheal challenges
with antigen (ovalbumin) or recombinant murine interleukin-13
(IL-13) induce lung inflammation, bronchial hyperreactivity (BHR), and
mucus accumulation as independent events (Singer M, Lefort J, and
Vargaftig BB. Am J Respir Cell Mol Biol 26: 74-84,
2002), largely mediated by leukotrienes (LT). We previously showed that
LTC 4 was released 15 min after ovalbumin, and we show that
it induces the expression of monocyte chemoattractant proteins 1 and 5 and KC in the lungs, as well as IL-13 mRNA. Instilled intratracheally,
these chemokines induced BHR and mucus accumulation, which were
inhibited by the 5-lipoxygenase inhibitor zileuton and by the
cysteinyl-LT receptor antagonist MK-571, suggesting mediation by
cysteinyl-LT. Because these chemokines also induced release of LT into
the bronchoalveolar lavage fluid and IL-13 into the lungs, we
hypothesize that LT- and chemokine-based loops for positive-feedback
regulations cooperate to maintain and amplify BHR and lung mucus
accumulation after allergic challenge and in situations where IL-13,
LT, or chemokines are generated.
inflammation; asthma; MUC; leukotriene; cytokine/chemokine; bronchial hyperreactivity</description><identifier>ISSN: 1040-0605</identifier><identifier>EISSN: 1522-1504</identifier><identifier>DOI: 10.1152/ajplung.00226.2002</identifier><identifier>PMID: 12388339</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Bronchial Hyperreactivity - etiology ; Bronchoalveolar Lavage Fluid - chemistry ; Chemokines - genetics ; Chemokines - metabolism ; Chemokines - pharmacology ; Hypersensitivity - complications ; Hypersensitivity - metabolism ; Interleukin-13 - genetics ; Interleukin-13 - metabolism ; Interleukin-13 - pharmacology ; Leukotriene C4 - pharmacology ; Leukotrienes - metabolism ; Lung - secretion ; Male ; Metaplasia ; Mice ; Mice, Inbred Strains ; Mucins - genetics ; Mucus - secretion ; Ovalbumin - pharmacology ; Recombinant Proteins - pharmacology ; Respiratory Mucosa - drug effects ; Respiratory Mucosa - pathology ; RNA, Messenger - metabolism</subject><ispartof>American journal of physiology. Lung cellular and molecular physiology, 2003-02, Vol.284 (2), p.260-L269</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c453t-aefe96db0f06bcc3dac9bfd26d477051994e468a4fd63223f7f29c2e6dc028293</citedby><cites>FETCH-LOGICAL-c453t-aefe96db0f06bcc3dac9bfd26d477051994e468a4fd63223f7f29c2e6dc028293</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3026,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12388339$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vargaftig, B. Boris</creatorcontrib><creatorcontrib>Singer, Monique</creatorcontrib><title>Leukotrienes, IL-13, and chemokines cooperate to induce BHR and mucus in allergic mouse lungs</title><title>American journal of physiology. Lung cellular and molecular physiology</title><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><description>Unité de Pharmacologie Cellulaire, Unité
Associée Institut Pasteur-Institut National de la Santé
et de la Recherche Médicale U485, Institut Pasteur, 75015 Paris,
France
In mice, intratracheal challenges
with antigen (ovalbumin) or recombinant murine interleukin-13
(IL-13) induce lung inflammation, bronchial hyperreactivity (BHR), and
mucus accumulation as independent events (Singer M, Lefort J, and
Vargaftig BB. Am J Respir Cell Mol Biol 26: 74-84,
2002), largely mediated by leukotrienes (LT). We previously showed that
LTC 4 was released 15 min after ovalbumin, and we show that
it induces the expression of monocyte chemoattractant proteins 1 and 5 and KC in the lungs, as well as IL-13 mRNA. Instilled intratracheally,
these chemokines induced BHR and mucus accumulation, which were
inhibited by the 5-lipoxygenase inhibitor zileuton and by the
cysteinyl-LT receptor antagonist MK-571, suggesting mediation by
cysteinyl-LT. Because these chemokines also induced release of LT into
the bronchoalveolar lavage fluid and IL-13 into the lungs, we
hypothesize that LT- and chemokine-based loops for positive-feedback
regulations cooperate to maintain and amplify BHR and lung mucus
accumulation after allergic challenge and in situations where IL-13,
LT, or chemokines are generated.
inflammation; asthma; MUC; leukotriene; cytokine/chemokine; bronchial hyperreactivity</description><subject>Animals</subject><subject>Bronchial Hyperreactivity - etiology</subject><subject>Bronchoalveolar Lavage Fluid - chemistry</subject><subject>Chemokines - genetics</subject><subject>Chemokines - metabolism</subject><subject>Chemokines - pharmacology</subject><subject>Hypersensitivity - complications</subject><subject>Hypersensitivity - metabolism</subject><subject>Interleukin-13 - genetics</subject><subject>Interleukin-13 - metabolism</subject><subject>Interleukin-13 - pharmacology</subject><subject>Leukotriene C4 - pharmacology</subject><subject>Leukotrienes - metabolism</subject><subject>Lung - secretion</subject><subject>Male</subject><subject>Metaplasia</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Mucins - genetics</subject><subject>Mucus - secretion</subject><subject>Ovalbumin - pharmacology</subject><subject>Recombinant Proteins - pharmacology</subject><subject>Respiratory Mucosa - drug effects</subject><subject>Respiratory Mucosa - pathology</subject><subject>RNA, Messenger - metabolism</subject><issn>1040-0605</issn><issn>1522-1504</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEFv1DAQhS0EakvbP8AB-cSpWSbjxEmOUFFaKRISKsfK8tqT3bRJHOxYsP8eb3ernjjNaOa9p6ePsQ85rPK8xM_6cR7itFkBIMoVpvGGnaUHZnkJxdu0QwEZSChP2fsQHgGgBJAn7DRHUddCNGfsoaX45Bbf00Thit-1WS6uuJ4sN1sa3VOfztw4N5PXC_HF8X6y0RD_evvzWTZGE0M6cj0M5De94aOLgfi-Wbhg7zo9BLo8znP26-bb_fVt1v74fnf9pc1MUYol09RRI-0aOpBrY4TVpll3FqUtqgrKvGkKKmSti85KgSi6qsPGIElrAGtsxDn7dMidvfsdKSxq7IOhYdATpTaqwkaKqqiTEA9C410Injo1-37UfqdyUHuo6ghVPUNVe6jJ9PGYHtcj2VfLkWISNAfBtt9s__Se1Lzdhd4NbrNTN3EY7unv8pKMdaFQtShBzbZL3uz_3pcyrx7xD50dmZY</recordid><startdate>20030201</startdate><enddate>20030201</enddate><creator>Vargaftig, B. Boris</creator><creator>Singer, Monique</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>20030201</creationdate><title>Leukotrienes, IL-13, and chemokines cooperate to induce BHR and mucus in allergic mouse lungs</title><author>Vargaftig, B. Boris ; Singer, Monique</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c453t-aefe96db0f06bcc3dac9bfd26d477051994e468a4fd63223f7f29c2e6dc028293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Bronchial Hyperreactivity - etiology</topic><topic>Bronchoalveolar Lavage Fluid - chemistry</topic><topic>Chemokines - genetics</topic><topic>Chemokines - metabolism</topic><topic>Chemokines - pharmacology</topic><topic>Hypersensitivity - complications</topic><topic>Hypersensitivity - metabolism</topic><topic>Interleukin-13 - genetics</topic><topic>Interleukin-13 - metabolism</topic><topic>Interleukin-13 - pharmacology</topic><topic>Leukotriene C4 - pharmacology</topic><topic>Leukotrienes - metabolism</topic><topic>Lung - secretion</topic><topic>Male</topic><topic>Metaplasia</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Mucins - genetics</topic><topic>Mucus - secretion</topic><topic>Ovalbumin - pharmacology</topic><topic>Recombinant Proteins - pharmacology</topic><topic>Respiratory Mucosa - drug effects</topic><topic>Respiratory Mucosa - pathology</topic><topic>RNA, Messenger - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vargaftig, B. Boris</creatorcontrib><creatorcontrib>Singer, Monique</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>Vargaftig, B. Boris</au><au>Singer, Monique</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Leukotrienes, IL-13, and chemokines cooperate to induce BHR and mucus in allergic mouse lungs</atitle><jtitle>American journal of physiology. Lung cellular and molecular physiology</jtitle><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><date>2003-02-01</date><risdate>2003</risdate><volume>284</volume><issue>2</issue><spage>260</spage><epage>L269</epage><pages>260-L269</pages><issn>1040-0605</issn><eissn>1522-1504</eissn><abstract>Unité de Pharmacologie Cellulaire, Unité
Associée Institut Pasteur-Institut National de la Santé
et de la Recherche Médicale U485, Institut Pasteur, 75015 Paris,
France
In mice, intratracheal challenges
with antigen (ovalbumin) or recombinant murine interleukin-13
(IL-13) induce lung inflammation, bronchial hyperreactivity (BHR), and
mucus accumulation as independent events (Singer M, Lefort J, and
Vargaftig BB. Am J Respir Cell Mol Biol 26: 74-84,
2002), largely mediated by leukotrienes (LT). We previously showed that
LTC 4 was released 15 min after ovalbumin, and we show that
it induces the expression of monocyte chemoattractant proteins 1 and 5 and KC in the lungs, as well as IL-13 mRNA. Instilled intratracheally,
these chemokines induced BHR and mucus accumulation, which were
inhibited by the 5-lipoxygenase inhibitor zileuton and by the
cysteinyl-LT receptor antagonist MK-571, suggesting mediation by
cysteinyl-LT. Because these chemokines also induced release of LT into
the bronchoalveolar lavage fluid and IL-13 into the lungs, we
hypothesize that LT- and chemokine-based loops for positive-feedback
regulations cooperate to maintain and amplify BHR and lung mucus
accumulation after allergic challenge and in situations where IL-13,
LT, or chemokines are generated.
inflammation; asthma; MUC; leukotriene; cytokine/chemokine; bronchial hyperreactivity</abstract><cop>United States</cop><pmid>12388339</pmid><doi>10.1152/ajplung.00226.2002</doi></addata></record> |
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| source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Bronchial Hyperreactivity - etiology Bronchoalveolar Lavage Fluid - chemistry Chemokines - genetics Chemokines - metabolism Chemokines - pharmacology Hypersensitivity - complications Hypersensitivity - metabolism Interleukin-13 - genetics Interleukin-13 - metabolism Interleukin-13 - pharmacology Leukotriene C4 - pharmacology Leukotrienes - metabolism Lung - secretion Male Metaplasia Mice Mice, Inbred Strains Mucins - genetics Mucus - secretion Ovalbumin - pharmacology Recombinant Proteins - pharmacology Respiratory Mucosa - drug effects Respiratory Mucosa - pathology RNA, Messenger - metabolism |
| title | Leukotrienes, IL-13, and chemokines cooperate to induce BHR and mucus in allergic mouse lungs |
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