Regulation of Human Alveolar Macrophage Inflammatory Cytokine Production by Interleukin-10
Alveolar macrophages are the primary source of inflammatory cytokine production in the lung. Both site-specific and differentiation-specific factors play a role in cytokine production, and regulation of this activity in alveolar macrophages is distinctly different from that of circulating blood mono...
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| Veröffentlicht in: | Clinical immunology and immunopathology 1996-09, Vol.80 (3), p.321-324 |
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| container_title | Clinical immunology and immunopathology |
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| creator | Thomassen, Mary Jane Divis, Lisa T. Fisher, Charles J. |
| description | Alveolar macrophages are the primary source of inflammatory cytokine production in the lung. Both site-specific and differentiation-specific factors play a role in cytokine production, and regulation of this activity in alveolar macrophages is distinctly different from that of circulating blood monocytes. Interleukin-10 (IL-10) inhibits the production of inflammatory cytokines [tumor necrosis factor (TNF)-α, interleukin-1 (IL-1), interleukin-6 (IL-6), and interleukin-8 (IL-8)] and enhances production of interleukin-1-receptor antagonist (IL-1ra) from endotoxin-stimulated human monocytes, but the effect of IL-10 on such activity in alveolar macrophages is unknown. This study was undertaken to determine the effect of recombinant IL-10 on endotoxin-stimulated cytokine production by human alveolar macrophages. TNF, IL-1, IL-6, and IL-8 secretions were significantly (P< 0.05) stimulated by endotoxin [lipopolysaccharide (LPS)] and were all significantly (P< 0.05) inhibited (median inhibition = 43%) by IL-10 (10 ng/ml). In contrast, IL-1ra was not stimulated by LPS and basal levels were not affected by IL-10. LPS also did not significantly elevate alveolar macrophage IL-10 secretion ( |
| doi_str_mv | 10.1006/clin.1996.0130 |
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Both site-specific and differentiation-specific factors play a role in cytokine production, and regulation of this activity in alveolar macrophages is distinctly different from that of circulating blood monocytes. Interleukin-10 (IL-10) inhibits the production of inflammatory cytokines [tumor necrosis factor (TNF)-α, interleukin-1 (IL-1), interleukin-6 (IL-6), and interleukin-8 (IL-8)] and enhances production of interleukin-1-receptor antagonist (IL-1ra) from endotoxin-stimulated human monocytes, but the effect of IL-10 on such activity in alveolar macrophages is unknown. This study was undertaken to determine the effect of recombinant IL-10 on endotoxin-stimulated cytokine production by human alveolar macrophages. TNF, IL-1, IL-6, and IL-8 secretions were significantly (P< 0.05) stimulated by endotoxin [lipopolysaccharide (LPS)] and were all significantly (P< 0.05) inhibited (median inhibition = 43%) by IL-10 (10 ng/ml). In contrast, IL-1ra was not stimulated by LPS and basal levels were not affected by IL-10. LPS also did not significantly elevate alveolar macrophage IL-10 secretion (<100 pg/ml) and basal levels were undetectable (<15 pg/ml). This potent inhibitory activity of IL-10 on inflammatory cytokine production by human alveolar macrophages suggests that exogenous IL-10 may be useful in treatment of inflammatory lung diseases such as adult respiratory distress syndrome.</description><identifier>ISSN: 0090-1229</identifier><identifier>EISSN: 1090-2341</identifier><identifier>DOI: 10.1006/clin.1996.0130</identifier><identifier>PMID: 8811054</identifier><identifier>CODEN: CLIIAT</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>Analysis of the immune response. Humoral and cellular immunity ; Biological and medical sciences ; Cytokines - biosynthesis ; Fundamental and applied biological sciences. 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Both site-specific and differentiation-specific factors play a role in cytokine production, and regulation of this activity in alveolar macrophages is distinctly different from that of circulating blood monocytes. Interleukin-10 (IL-10) inhibits the production of inflammatory cytokines [tumor necrosis factor (TNF)-α, interleukin-1 (IL-1), interleukin-6 (IL-6), and interleukin-8 (IL-8)] and enhances production of interleukin-1-receptor antagonist (IL-1ra) from endotoxin-stimulated human monocytes, but the effect of IL-10 on such activity in alveolar macrophages is unknown. This study was undertaken to determine the effect of recombinant IL-10 on endotoxin-stimulated cytokine production by human alveolar macrophages. TNF, IL-1, IL-6, and IL-8 secretions were significantly (P< 0.05) stimulated by endotoxin [lipopolysaccharide (LPS)] and were all significantly (P< 0.05) inhibited (median inhibition = 43%) by IL-10 (10 ng/ml). In contrast, IL-1ra was not stimulated by LPS and basal levels were not affected by IL-10. LPS also did not significantly elevate alveolar macrophage IL-10 secretion (<100 pg/ml) and basal levels were undetectable (<15 pg/ml). This potent inhibitory activity of IL-10 on inflammatory cytokine production by human alveolar macrophages suggests that exogenous IL-10 may be useful in treatment of inflammatory lung diseases such as adult respiratory distress syndrome.</description><subject>Analysis of the immune response. Humoral and cellular immunity</subject><subject>Biological and medical sciences</subject><subject>Cytokines - biosynthesis</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Humans</subject><subject>Immunobiology</subject><subject>Inflammation - metabolism</subject><subject>Interleukin-10 - biosynthesis</subject><subject>Interleukin-10 - metabolism</subject><subject>Interleukin-10 - pharmacology</subject><subject>Interleukin-2 - biosynthesis</subject><subject>Lymphokines, interleukins ( function, expression)</subject><subject>Macrophages, Alveolar - drug effects</subject><subject>Macrophages, Alveolar - metabolism</subject><subject>Regulatory factors and their cellular receptors</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><issn>0090-1229</issn><issn>1090-2341</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUGP1CAYhonRrOPq1ZtJD8ZbRz5gWjhuJupuskZj9OKFAP1YUVpGaDeZfy91JnszniB5n_cDHgh5CXQLlHZvXQzTFpTqthQ4fUQ2QBVtGRfwmGzougfG1FPyrJSftBYE7S_IhZQAdCc25PsXvFuimUOamuSb62U0U3MV7zFFk5uPxuV0-GHusLmZfDTjaOaUj83-OKdfYcLmc07D4v627bEyM-aIS41aoM_JE29iwRfn9ZJ8e__u6_66vf304WZ_dds6rtTcYmehY4pJBKeoBddLZgUVjlMnBm-FE50fwPbSek57tWOKcu6tEVaanev5JXlzmnvI6feCZdZjKA5jNBOmpehe8noQsP-C0AFI1qkKbk9gfX0pGb0-5DCafNRA9Wpdr9b1al2v1mvh1XnyYkccHvCz5pq_PuemOBN9NpML5QHjrP5TzysmTxhWXfcBsy4u4ORwCBndrIcU_nWDPxr_nYY</recordid><startdate>19960901</startdate><enddate>19960901</enddate><creator>Thomassen, Mary Jane</creator><creator>Divis, Lisa T.</creator><creator>Fisher, Charles J.</creator><general>Elsevier Inc</general><general>Academic Press</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19960901</creationdate><title>Regulation of Human Alveolar Macrophage Inflammatory Cytokine Production by Interleukin-10</title><author>Thomassen, Mary Jane ; Divis, Lisa T. ; Fisher, Charles J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c399t-e6b162928e1c90b1c782b404c30c4dfb4c46fd1b78bf3079529033fba4b8a5c73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Analysis of the immune response. Humoral and cellular immunity</topic><topic>Biological and medical sciences</topic><topic>Cytokines - biosynthesis</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Humans</topic><topic>Immunobiology</topic><topic>Inflammation - metabolism</topic><topic>Interleukin-10 - biosynthesis</topic><topic>Interleukin-10 - metabolism</topic><topic>Interleukin-10 - pharmacology</topic><topic>Interleukin-2 - biosynthesis</topic><topic>Lymphokines, interleukins ( function, expression)</topic><topic>Macrophages, Alveolar - drug effects</topic><topic>Macrophages, Alveolar - metabolism</topic><topic>Regulatory factors and their cellular receptors</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><toplevel>online_resources</toplevel><creatorcontrib>Thomassen, Mary Jane</creatorcontrib><creatorcontrib>Divis, Lisa T.</creatorcontrib><creatorcontrib>Fisher, Charles J.</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical immunology and immunopathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Thomassen, Mary Jane</au><au>Divis, Lisa T.</au><au>Fisher, Charles J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of Human Alveolar Macrophage Inflammatory Cytokine Production by Interleukin-10</atitle><jtitle>Clinical immunology and immunopathology</jtitle><addtitle>Clin Immunol Immunopathol</addtitle><date>1996-09-01</date><risdate>1996</risdate><volume>80</volume><issue>3</issue><spage>321</spage><epage>324</epage><pages>321-324</pages><issn>0090-1229</issn><eissn>1090-2341</eissn><coden>CLIIAT</coden><abstract>Alveolar macrophages are the primary source of inflammatory cytokine production in the lung. Both site-specific and differentiation-specific factors play a role in cytokine production, and regulation of this activity in alveolar macrophages is distinctly different from that of circulating blood monocytes. Interleukin-10 (IL-10) inhibits the production of inflammatory cytokines [tumor necrosis factor (TNF)-α, interleukin-1 (IL-1), interleukin-6 (IL-6), and interleukin-8 (IL-8)] and enhances production of interleukin-1-receptor antagonist (IL-1ra) from endotoxin-stimulated human monocytes, but the effect of IL-10 on such activity in alveolar macrophages is unknown. This study was undertaken to determine the effect of recombinant IL-10 on endotoxin-stimulated cytokine production by human alveolar macrophages. TNF, IL-1, IL-6, and IL-8 secretions were significantly (P< 0.05) stimulated by endotoxin [lipopolysaccharide (LPS)] and were all significantly (P< 0.05) inhibited (median inhibition = 43%) by IL-10 (10 ng/ml). In contrast, IL-1ra was not stimulated by LPS and basal levels were not affected by IL-10. LPS also did not significantly elevate alveolar macrophage IL-10 secretion (<100 pg/ml) and basal levels were undetectable (<15 pg/ml). This potent inhibitory activity of IL-10 on inflammatory cytokine production by human alveolar macrophages suggests that exogenous IL-10 may be useful in treatment of inflammatory lung diseases such as adult respiratory distress syndrome.</abstract><cop>San Diego, CA</cop><cop>New York, NY</cop><cop>Boston</cop><pub>Elsevier Inc</pub><pmid>8811054</pmid><doi>10.1006/clin.1996.0130</doi><tpages>4</tpages></addata></record> |
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| ispartof | Clinical immunology and immunopathology, 1996-09, Vol.80 (3), p.321-324 |
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| subjects | Analysis of the immune response. Humoral and cellular immunity Biological and medical sciences Cytokines - biosynthesis Fundamental and applied biological sciences. Psychology Fundamental immunology Humans Immunobiology Inflammation - metabolism Interleukin-10 - biosynthesis Interleukin-10 - metabolism Interleukin-10 - pharmacology Interleukin-2 - biosynthesis Lymphokines, interleukins ( function, expression) Macrophages, Alveolar - drug effects Macrophages, Alveolar - metabolism Regulatory factors and their cellular receptors Tumor Necrosis Factor-alpha - biosynthesis |
| title | Regulation of Human Alveolar Macrophage Inflammatory Cytokine Production by Interleukin-10 |
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