Ozone Inhalation Stimulates Expression of a Neutrophil Chemotactic Protein, Macrophage Inflammatory Protein 2
Short-term exposure of humans and animals to ozone results in increased lung neutrophils; however, the mechanisms underlying this response are not completely understood. We examined the potential involvement of the neutrophil chemotactic factor, macrophage inflammatory protein 2 (MIP-2), in ozone-in...
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| Veröffentlicht in: | Toxicology and applied pharmacology 1993-04, Vol.119 (2), p.306-309 |
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| creator | Driscoll, K.E. Simpson, L. Carter, J. Hassenbein, D. Leikauf, G.D. |
| description | Short-term exposure of humans and animals to ozone results in increased lung neutrophils; however, the mechanisms underlying this response are not completely understood. We examined the potential involvement of the neutrophil chemotactic factor, macrophage inflammatory protein 2 (MIP-2), in ozone-induced inflammation. Exposure-response relationships for ozone and MIP-2 expression were characterized by exposing C57B1/6 mice to 0.1-2 ppm ozone for 3 hr and determining lung levels of MIP-2 mRNA 6 hr after exposure. Temporal relationships between ozone and MIP-2 were determined by exposing mice (2 ppm ozone × 3 hr) and characterizing MIP-2 mRNA expression 0, 2, 6, and 24 hr after exposure. Neutrophils in lung lavage fluid were determined in both exposure-response and time course studies. Ozone concentrations ≥1.0 ppm increased MIP-2 mRNA and this increase corresponded with recruitment of neutrophils. MIP-2 mRNA was increased immediately after ozone exposure and decreased to control levels by 24 hr. To examine the role of direct oxidant effects in ozone-induced MIP-2 expression, alveolar macrophages were exposed
in vitro for 4 hr to 10
−10-10
−5 M hydrogen peroxide and MIP-2 expression was characterized. MIP-2 mRNA levels in lung macrophages were increased by ≥10
−9 M hydrogen peroxide. In summary, our findings suggest the chemotactic protein MIP-2 may be responsible, at least in part, for ozone-induced increases in lung neutrophils and indicate that direct exposure of alveolar macrophages to an oxidant is sufficient to induce MIP-2 expression. |
| doi_str_mv | 10.1006/taap.1993.1074 |
| format | Article |
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in vitro for 4 hr to 10
−10-10
−5 M hydrogen peroxide and MIP-2 expression was characterized. MIP-2 mRNA levels in lung macrophages were increased by ≥10
−9 M hydrogen peroxide. In summary, our findings suggest the chemotactic protein MIP-2 may be responsible, at least in part, for ozone-induced increases in lung neutrophils and indicate that direct exposure of alveolar macrophages to an oxidant is sufficient to induce MIP-2 expression.</description><identifier>ISSN: 0041-008X</identifier><identifier>EISSN: 1096-0333</identifier><identifier>DOI: 10.1006/taap.1993.1074</identifier><identifier>PMID: 8480341</identifier><identifier>CODEN: TXAPA9</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>550200 -- Biochemistry ; 550300 -- Cytology ; Administration, Inhalation ; Air ; ANIMAL CELLS ; ANIMALS ; Base Sequence ; BASIC BIOLOGICAL SCIENCES ; BIOCHEMICAL REACTION KINETICS ; BIOCHEMISTRY ; Biological and medical sciences ; BIOLOGICAL MATERIALS ; BLOOD ; BLOOD CELLS ; BODY ; BODY FLUIDS ; CHEMISTRY ; Chemokine CXCL2 ; CONNECTIVE TISSUE CELLS ; CYTOCHEMISTRY ; Cytokines - drug effects ; Cytokines - genetics ; DOSE-RESPONSE RELATIONSHIPS ; Environmental pollutants toxicology ; Gene Expression - drug effects ; Glyceraldehyde-3-Phosphate Dehydrogenases - drug effects ; Glyceraldehyde-3-Phosphate Dehydrogenases - genetics ; HYDROGEN COMPOUNDS ; HYDROGEN PEROXIDE ; Hydrogen Peroxide - pharmacology ; IN VITRO ; In Vitro Techniques ; INFLAMMATION ; KINETICS ; LAVAGE ; LEUKOCYTES ; LUNGS ; MACROPHAGES ; Macrophages, Alveolar - drug effects ; MAMMALS ; MATERIALS ; Medical sciences ; MICE ; Mice, Inbred C57BL ; Molecular Sequence Data ; Monokines - drug effects ; Monokines - genetics ; NEUTROPHILS ; ORGANS ; OXYGEN COMPOUNDS ; OZONE ; Ozone - administration & dosage ; Ozone - pharmacology ; PATHOLOGICAL CHANGES ; Peptide Fragments - drug effects ; Peptide Fragments - genetics ; PEROXIDES ; PHAGOCYTES ; Polymerase Chain Reaction ; RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT ; RATS ; Rats, Inbred F344 ; REACTION KINETICS ; RESPIRATORY SYSTEM ; RNA, Messenger - analysis ; RODENTS ; SOMATIC CELLS ; SYMPTOMS ; Toxicology ; VERTEBRATES 560300 -- Chemicals Metabolism & Toxicology</subject><ispartof>Toxicology and applied pharmacology, 1993-04, Vol.119 (2), p.306-309</ispartof><rights>1993 Academic Press</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c426t-83b0ae9bfd243a4dcdaf872d02752e2ada654adbcf2003ce5f7d600d5c70fc513</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/taap.1993.1074$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4772025$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8480341$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/6773382$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Driscoll, K.E.</creatorcontrib><creatorcontrib>Simpson, L.</creatorcontrib><creatorcontrib>Carter, J.</creatorcontrib><creatorcontrib>Hassenbein, D.</creatorcontrib><creatorcontrib>Leikauf, G.D.</creatorcontrib><title>Ozone Inhalation Stimulates Expression of a Neutrophil Chemotactic Protein, Macrophage Inflammatory Protein 2</title><title>Toxicology and applied pharmacology</title><addtitle>Toxicol Appl Pharmacol</addtitle><description>Short-term exposure of humans and animals to ozone results in increased lung neutrophils; however, the mechanisms underlying this response are not completely understood. We examined the potential involvement of the neutrophil chemotactic factor, macrophage inflammatory protein 2 (MIP-2), in ozone-induced inflammation. Exposure-response relationships for ozone and MIP-2 expression were characterized by exposing C57B1/6 mice to 0.1-2 ppm ozone for 3 hr and determining lung levels of MIP-2 mRNA 6 hr after exposure. Temporal relationships between ozone and MIP-2 were determined by exposing mice (2 ppm ozone × 3 hr) and characterizing MIP-2 mRNA expression 0, 2, 6, and 24 hr after exposure. Neutrophils in lung lavage fluid were determined in both exposure-response and time course studies. Ozone concentrations ≥1.0 ppm increased MIP-2 mRNA and this increase corresponded with recruitment of neutrophils. MIP-2 mRNA was increased immediately after ozone exposure and decreased to control levels by 24 hr. To examine the role of direct oxidant effects in ozone-induced MIP-2 expression, alveolar macrophages were exposed
in vitro for 4 hr to 10
−10-10
−5 M hydrogen peroxide and MIP-2 expression was characterized. MIP-2 mRNA levels in lung macrophages were increased by ≥10
−9 M hydrogen peroxide. In summary, our findings suggest the chemotactic protein MIP-2 may be responsible, at least in part, for ozone-induced increases in lung neutrophils and indicate that direct exposure of alveolar macrophages to an oxidant is sufficient to induce MIP-2 expression.</description><subject>550200 -- Biochemistry</subject><subject>550300 -- Cytology</subject><subject>Administration, Inhalation</subject><subject>Air</subject><subject>ANIMAL CELLS</subject><subject>ANIMALS</subject><subject>Base Sequence</subject><subject>BASIC BIOLOGICAL SCIENCES</subject><subject>BIOCHEMICAL REACTION KINETICS</subject><subject>BIOCHEMISTRY</subject><subject>Biological and medical sciences</subject><subject>BIOLOGICAL MATERIALS</subject><subject>BLOOD</subject><subject>BLOOD CELLS</subject><subject>BODY</subject><subject>BODY FLUIDS</subject><subject>CHEMISTRY</subject><subject>Chemokine CXCL2</subject><subject>CONNECTIVE TISSUE CELLS</subject><subject>CYTOCHEMISTRY</subject><subject>Cytokines - drug effects</subject><subject>Cytokines - genetics</subject><subject>DOSE-RESPONSE RELATIONSHIPS</subject><subject>Environmental pollutants toxicology</subject><subject>Gene Expression - drug effects</subject><subject>Glyceraldehyde-3-Phosphate Dehydrogenases - drug effects</subject><subject>Glyceraldehyde-3-Phosphate Dehydrogenases - genetics</subject><subject>HYDROGEN COMPOUNDS</subject><subject>HYDROGEN PEROXIDE</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>IN VITRO</subject><subject>In Vitro Techniques</subject><subject>INFLAMMATION</subject><subject>KINETICS</subject><subject>LAVAGE</subject><subject>LEUKOCYTES</subject><subject>LUNGS</subject><subject>MACROPHAGES</subject><subject>Macrophages, Alveolar - drug effects</subject><subject>MAMMALS</subject><subject>MATERIALS</subject><subject>Medical sciences</subject><subject>MICE</subject><subject>Mice, Inbred C57BL</subject><subject>Molecular Sequence Data</subject><subject>Monokines - drug effects</subject><subject>Monokines - genetics</subject><subject>NEUTROPHILS</subject><subject>ORGANS</subject><subject>OXYGEN COMPOUNDS</subject><subject>OZONE</subject><subject>Ozone - administration & dosage</subject><subject>Ozone - pharmacology</subject><subject>PATHOLOGICAL CHANGES</subject><subject>Peptide Fragments - drug effects</subject><subject>Peptide Fragments - genetics</subject><subject>PEROXIDES</subject><subject>PHAGOCYTES</subject><subject>Polymerase Chain Reaction</subject><subject>RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT</subject><subject>RATS</subject><subject>Rats, Inbred F344</subject><subject>REACTION KINETICS</subject><subject>RESPIRATORY SYSTEM</subject><subject>RNA, Messenger - analysis</subject><subject>RODENTS</subject><subject>SOMATIC CELLS</subject><subject>SYMPTOMS</subject><subject>Toxicology</subject><subject>VERTEBRATES 560300 -- Chemicals Metabolism & Toxicology</subject><issn>0041-008X</issn><issn>1096-0333</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1v1DAQxS0EKtuFKzekCKGeyDL-SJwc0apApUKRAIlbNGuPWaMk3toOovz1JNqlN8TJ9ryfn2bmMfaMw4YD1K8z4mHD21bOT60esBWHti5BSvmQrQAULwGab4_ZeUo_AKBVip-xs0Y1IBVfseHmdxipuBr32GP2YSw-Zz9M851ScfnrECmlpRpcgcVHmnIMh73vi-2ehpDRZG-KTzFk8uOr4gOaRcbvi6HrcRgwh3j3FyjEE_bIYZ_o6elcs69vL79s35fXN--utm-uS6NEnctG7gCp3TkrlERljUXXaGFB6EqQQIt1pdDujBMA0lDltK0BbGU0OFNxuWYvjr4hZd8l4zOZvQnjSCZ3tdZSNmKGLo7QIYbbiVLuBp8M9T2OFKbU6UpDxRX8F-R1JWQ7t7pmmyM4ryGlSK47RD9gvOs4dEta3ZJWt6TVLWnNH56fnKfdQPYeP8Uz6y9POiaDvYs4Gp_uMaW1AFHNWHPEaN7pT09xGZlGQ9bHZWIb_L86-AOkULGr</recordid><startdate>19930401</startdate><enddate>19930401</enddate><creator>Driscoll, K.E.</creator><creator>Simpson, L.</creator><creator>Carter, J.</creator><creator>Hassenbein, D.</creator><creator>Leikauf, G.D.</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>7QR</scope><scope>7T5</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope><scope>OTOTI</scope></search><sort><creationdate>19930401</creationdate><title>Ozone Inhalation Stimulates Expression of a Neutrophil Chemotactic Protein, Macrophage Inflammatory Protein 2</title><author>Driscoll, K.E. ; Simpson, L. ; Carter, J. ; Hassenbein, D. ; Leikauf, G.D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c426t-83b0ae9bfd243a4dcdaf872d02752e2ada654adbcf2003ce5f7d600d5c70fc513</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>550200 -- Biochemistry</topic><topic>550300 -- Cytology</topic><topic>Administration, Inhalation</topic><topic>Air</topic><topic>ANIMAL CELLS</topic><topic>ANIMALS</topic><topic>Base Sequence</topic><topic>BASIC BIOLOGICAL SCIENCES</topic><topic>BIOCHEMICAL REACTION KINETICS</topic><topic>BIOCHEMISTRY</topic><topic>Biological and medical sciences</topic><topic>BIOLOGICAL MATERIALS</topic><topic>BLOOD</topic><topic>BLOOD CELLS</topic><topic>BODY</topic><topic>BODY FLUIDS</topic><topic>CHEMISTRY</topic><topic>Chemokine CXCL2</topic><topic>CONNECTIVE TISSUE CELLS</topic><topic>CYTOCHEMISTRY</topic><topic>Cytokines - drug effects</topic><topic>Cytokines - genetics</topic><topic>DOSE-RESPONSE RELATIONSHIPS</topic><topic>Environmental pollutants toxicology</topic><topic>Gene Expression - drug effects</topic><topic>Glyceraldehyde-3-Phosphate Dehydrogenases - drug effects</topic><topic>Glyceraldehyde-3-Phosphate Dehydrogenases - genetics</topic><topic>HYDROGEN COMPOUNDS</topic><topic>HYDROGEN PEROXIDE</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>IN VITRO</topic><topic>In Vitro Techniques</topic><topic>INFLAMMATION</topic><topic>KINETICS</topic><topic>LAVAGE</topic><topic>LEUKOCYTES</topic><topic>LUNGS</topic><topic>MACROPHAGES</topic><topic>Macrophages, Alveolar - drug effects</topic><topic>MAMMALS</topic><topic>MATERIALS</topic><topic>Medical sciences</topic><topic>MICE</topic><topic>Mice, Inbred C57BL</topic><topic>Molecular Sequence Data</topic><topic>Monokines - drug effects</topic><topic>Monokines - genetics</topic><topic>NEUTROPHILS</topic><topic>ORGANS</topic><topic>OXYGEN COMPOUNDS</topic><topic>OZONE</topic><topic>Ozone - administration & dosage</topic><topic>Ozone - pharmacology</topic><topic>PATHOLOGICAL CHANGES</topic><topic>Peptide Fragments - drug effects</topic><topic>Peptide Fragments - genetics</topic><topic>PEROXIDES</topic><topic>PHAGOCYTES</topic><topic>Polymerase Chain Reaction</topic><topic>RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT</topic><topic>RATS</topic><topic>Rats, Inbred F344</topic><topic>REACTION KINETICS</topic><topic>RESPIRATORY SYSTEM</topic><topic>RNA, Messenger - analysis</topic><topic>RODENTS</topic><topic>SOMATIC CELLS</topic><topic>SYMPTOMS</topic><topic>Toxicology</topic><topic>VERTEBRATES 560300 -- Chemicals Metabolism & Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Driscoll, K.E.</creatorcontrib><creatorcontrib>Simpson, L.</creatorcontrib><creatorcontrib>Carter, J.</creatorcontrib><creatorcontrib>Hassenbein, D.</creatorcontrib><creatorcontrib>Leikauf, G.D.</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>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>OSTI.GOV</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Driscoll, K.E.</au><au>Simpson, L.</au><au>Carter, J.</au><au>Hassenbein, D.</au><au>Leikauf, G.D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ozone Inhalation Stimulates Expression of a Neutrophil Chemotactic Protein, Macrophage Inflammatory Protein 2</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>1993-04-01</date><risdate>1993</risdate><volume>119</volume><issue>2</issue><spage>306</spage><epage>309</epage><pages>306-309</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><coden>TXAPA9</coden><abstract>Short-term exposure of humans and animals to ozone results in increased lung neutrophils; however, the mechanisms underlying this response are not completely understood. We examined the potential involvement of the neutrophil chemotactic factor, macrophage inflammatory protein 2 (MIP-2), in ozone-induced inflammation. Exposure-response relationships for ozone and MIP-2 expression were characterized by exposing C57B1/6 mice to 0.1-2 ppm ozone for 3 hr and determining lung levels of MIP-2 mRNA 6 hr after exposure. Temporal relationships between ozone and MIP-2 were determined by exposing mice (2 ppm ozone × 3 hr) and characterizing MIP-2 mRNA expression 0, 2, 6, and 24 hr after exposure. Neutrophils in lung lavage fluid were determined in both exposure-response and time course studies. Ozone concentrations ≥1.0 ppm increased MIP-2 mRNA and this increase corresponded with recruitment of neutrophils. MIP-2 mRNA was increased immediately after ozone exposure and decreased to control levels by 24 hr. To examine the role of direct oxidant effects in ozone-induced MIP-2 expression, alveolar macrophages were exposed
in vitro for 4 hr to 10
−10-10
−5 M hydrogen peroxide and MIP-2 expression was characterized. MIP-2 mRNA levels in lung macrophages were increased by ≥10
−9 M hydrogen peroxide. In summary, our findings suggest the chemotactic protein MIP-2 may be responsible, at least in part, for ozone-induced increases in lung neutrophils and indicate that direct exposure of alveolar macrophages to an oxidant is sufficient to induce MIP-2 expression.</abstract><cop>San Diego, CA</cop><pub>Elsevier Inc</pub><pmid>8480341</pmid><doi>10.1006/taap.1993.1074</doi><tpages>4</tpages></addata></record> |
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| ispartof | Toxicology and applied pharmacology, 1993-04, Vol.119 (2), p.306-309 |
| issn | 0041-008X 1096-0333 |
| language | eng |
| recordid | cdi_osti_scitechconnect_6773382 |
| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | 550200 -- Biochemistry 550300 -- Cytology Administration, Inhalation Air ANIMAL CELLS ANIMALS Base Sequence BASIC BIOLOGICAL SCIENCES BIOCHEMICAL REACTION KINETICS BIOCHEMISTRY Biological and medical sciences BIOLOGICAL MATERIALS BLOOD BLOOD CELLS BODY BODY FLUIDS CHEMISTRY Chemokine CXCL2 CONNECTIVE TISSUE CELLS CYTOCHEMISTRY Cytokines - drug effects Cytokines - genetics DOSE-RESPONSE RELATIONSHIPS Environmental pollutants toxicology Gene Expression - drug effects Glyceraldehyde-3-Phosphate Dehydrogenases - drug effects Glyceraldehyde-3-Phosphate Dehydrogenases - genetics HYDROGEN COMPOUNDS HYDROGEN PEROXIDE Hydrogen Peroxide - pharmacology IN VITRO In Vitro Techniques INFLAMMATION KINETICS LAVAGE LEUKOCYTES LUNGS MACROPHAGES Macrophages, Alveolar - drug effects MAMMALS MATERIALS Medical sciences MICE Mice, Inbred C57BL Molecular Sequence Data Monokines - drug effects Monokines - genetics NEUTROPHILS ORGANS OXYGEN COMPOUNDS OZONE Ozone - administration & dosage Ozone - pharmacology PATHOLOGICAL CHANGES Peptide Fragments - drug effects Peptide Fragments - genetics PEROXIDES PHAGOCYTES Polymerase Chain Reaction RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT RATS Rats, Inbred F344 REACTION KINETICS RESPIRATORY SYSTEM RNA, Messenger - analysis RODENTS SOMATIC CELLS SYMPTOMS Toxicology VERTEBRATES 560300 -- Chemicals Metabolism & Toxicology |
| title | Ozone Inhalation Stimulates Expression of a Neutrophil Chemotactic Protein, Macrophage Inflammatory Protein 2 |
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