Substance P increases neutrophil adhesion to bronchial epithelial cells
Polymorphonuclear neutrophils (PMNs) accumulate within the airways during acute and chronic bronchitis and can adhere to bronchial epithelium. Substance P (SP), a neuropeptide released from the primary afferent nerve endings, has been shown to have a proinflammatory effect on PMNs. To test the hypot...
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| Veröffentlicht in: | The Journal of immunology (1950) 1994-02, Vol.152 (3), p.1339-1346 |
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| container_title | The Journal of immunology (1950) |
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| creator | DeRose, V Robbins, RA Snider, RM Spurzem, JR Thiele, GM Rennard, SI Rubinstein, I |
| description | Polymorphonuclear neutrophils (PMNs) accumulate within the airways during acute and chronic bronchitis and can adhere to bronchial epithelium. Substance P (SP), a neuropeptide released from the primary afferent nerve endings, has been shown to have a proinflammatory effect on PMNs. To test the hypothesis that SP could modulate PMN bronchial epithelial cell adherence, bovine bronchial epithelial cells (BBECs) were isolated and cultured, and the capacity of SP to modulate PMN-BBEC adherence was evaluated. SP interacted with BBECs to induce an increase in PMN adhesion (14.7 +/- 1.2% vs 5.3 +/- 0.7% adherence, p < 0.01). The effect of SP was both time- and dose-dependent with maximal responses at 6 h and 10(-10) M. The effect was reproduced by the carboxyl-terminal sequence of the molecule (SP 6-11). Importantly, pretreatment of the BBECs with the tachykinin SP receptor (NK1) antagonist, CP-96,345, significantly reduced the increase in adhesion induced by SP (p < 0.01). Furthermore, treatment of the BBECs with antibodies against CD11a (LFA-1), CD11b (MAC-1), or ICAM-1 significantly decreased SP-induced adherence (p < 0.01 all comparisons). Conversely, SP stimulation of PMN induced a dose-dependent, rapid (within 5 min) increase in adherence. This effect was also mediated by the carboxy end of the molecule and was decreased by CP-96,345, again suggesting that this effect was NK1 mediated. These data demonstrate the SP has the capacity for modulating PMN-BBEC interactions and suggest an important role for SP in modulating airway inflammation. |
| doi_str_mv | 10.4049/jimmunol.152.3.1339 |
| format | Article |
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Substance P (SP), a neuropeptide released from the primary afferent nerve endings, has been shown to have a proinflammatory effect on PMNs. To test the hypothesis that SP could modulate PMN bronchial epithelial cell adherence, bovine bronchial epithelial cells (BBECs) were isolated and cultured, and the capacity of SP to modulate PMN-BBEC adherence was evaluated. SP interacted with BBECs to induce an increase in PMN adhesion (14.7 +/- 1.2% vs 5.3 +/- 0.7% adherence, p < 0.01). The effect of SP was both time- and dose-dependent with maximal responses at 6 h and 10(-10) M. The effect was reproduced by the carboxyl-terminal sequence of the molecule (SP 6-11). Importantly, pretreatment of the BBECs with the tachykinin SP receptor (NK1) antagonist, CP-96,345, significantly reduced the increase in adhesion induced by SP (p < 0.01). Furthermore, treatment of the BBECs with antibodies against CD11a (LFA-1), CD11b (MAC-1), or ICAM-1 significantly decreased SP-induced adherence (p < 0.01 all comparisons). Conversely, SP stimulation of PMN induced a dose-dependent, rapid (within 5 min) increase in adherence. This effect was also mediated by the carboxy end of the molecule and was decreased by CP-96,345, again suggesting that this effect was NK1 mediated. These data demonstrate the SP has the capacity for modulating PMN-BBEC interactions and suggest an important role for SP in modulating airway inflammation.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.152.3.1339</identifier><identifier>PMID: 7507964</identifier><identifier>CODEN: JOIMA3</identifier><language>eng</language><publisher>Bethesda, MD: Am Assoc Immnol</publisher><subject>Animals ; Biological and medical sciences ; Biphenyl Compounds - pharmacology ; Bronchi - cytology ; Bronchi - immunology ; Cattle ; Cell Adhesion - drug effects ; Cell Adhesion Molecules - metabolism ; Epithelium - immunology ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Humans ; Immunobiology ; In Vitro Techniques ; Intercellular Adhesion Molecule-1 ; Lymphocyte Function-Associated Antigen-1 - metabolism ; Macrophage-1 Antigen - metabolism ; Myeloid cells: ontogeny, maturation, markers, receptors ; Neurokinin-1 Receptor Antagonists ; Neutrophils - cytology ; Peptide Fragments - pharmacology ; Polynuclears ; Rosette Formation ; Substance P - pharmacology ; Time Factors</subject><ispartof>The Journal of immunology (1950), 1994-02, Vol.152 (3), p.1339-1346</ispartof><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-cb2aa9e74ef0da12bfc86890ffbcd11679eac3503c3a282123fc944e40bb42b33</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3949936$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7507964$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>DeRose, V</creatorcontrib><creatorcontrib>Robbins, RA</creatorcontrib><creatorcontrib>Snider, RM</creatorcontrib><creatorcontrib>Spurzem, JR</creatorcontrib><creatorcontrib>Thiele, GM</creatorcontrib><creatorcontrib>Rennard, SI</creatorcontrib><creatorcontrib>Rubinstein, I</creatorcontrib><title>Substance P increases neutrophil adhesion to bronchial epithelial cells</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Polymorphonuclear neutrophils (PMNs) accumulate within the airways during acute and chronic bronchitis and can adhere to bronchial epithelium. Substance P (SP), a neuropeptide released from the primary afferent nerve endings, has been shown to have a proinflammatory effect on PMNs. To test the hypothesis that SP could modulate PMN bronchial epithelial cell adherence, bovine bronchial epithelial cells (BBECs) were isolated and cultured, and the capacity of SP to modulate PMN-BBEC adherence was evaluated. SP interacted with BBECs to induce an increase in PMN adhesion (14.7 +/- 1.2% vs 5.3 +/- 0.7% adherence, p < 0.01). The effect of SP was both time- and dose-dependent with maximal responses at 6 h and 10(-10) M. The effect was reproduced by the carboxyl-terminal sequence of the molecule (SP 6-11). Importantly, pretreatment of the BBECs with the tachykinin SP receptor (NK1) antagonist, CP-96,345, significantly reduced the increase in adhesion induced by SP (p < 0.01). Furthermore, treatment of the BBECs with antibodies against CD11a (LFA-1), CD11b (MAC-1), or ICAM-1 significantly decreased SP-induced adherence (p < 0.01 all comparisons). Conversely, SP stimulation of PMN induced a dose-dependent, rapid (within 5 min) increase in adherence. This effect was also mediated by the carboxy end of the molecule and was decreased by CP-96,345, again suggesting that this effect was NK1 mediated. These data demonstrate the SP has the capacity for modulating PMN-BBEC interactions and suggest an important role for SP in modulating airway inflammation.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biphenyl Compounds - pharmacology</subject><subject>Bronchi - cytology</subject><subject>Bronchi - immunology</subject><subject>Cattle</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Epithelium - immunology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Humans</subject><subject>Immunobiology</subject><subject>In Vitro Techniques</subject><subject>Intercellular Adhesion Molecule-1</subject><subject>Lymphocyte Function-Associated Antigen-1 - metabolism</subject><subject>Macrophage-1 Antigen - metabolism</subject><subject>Myeloid cells: ontogeny, maturation, markers, receptors</subject><subject>Neurokinin-1 Receptor Antagonists</subject><subject>Neutrophils - cytology</subject><subject>Peptide Fragments - pharmacology</subject><subject>Polynuclears</subject><subject>Rosette Formation</subject><subject>Substance P - pharmacology</subject><subject>Time Factors</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1r3DAQhkVoSLZJfkEp-FCak7ejD0urYwjNtrCQQJqzkLTjWkG2N5KNyb-Pl92G3HqagXnmneEh5AuFpQChfzyHth27Pi5pxZZ8STnXJ2RBqwpKKUF-IgsAxkqqpDonn3N-BgAJTJyRM1WB0lIsyPpxdHmwncfioQidT2gz5qLDcUj9rgmxsNsGc-i7YugLl_rON8HGAndhaDDuW48x5ktyWtuY8epYL8jT3c8_t7_Kzf369-3NpvQV8KH0jlmrUQmsYWspc7VfyZWGunZ-S6lUGq3nM-q5ZStGGa-9FgIFOCeY4_yCfD_k7lL_MmIeTBvy_gPbYT9moySvqNbqvyCVWikhYQb5AfSpzzlhbXYptDa9Ggpm79n882xmz4abved56-sxfnQtbt93jmLn-bfj3GZvY51mxSG_Y1wLrbmcsesD1oS_zRQSmtzaGOdQaqZp-nDwDa8Glmw</recordid><startdate>19940201</startdate><enddate>19940201</enddate><creator>DeRose, V</creator><creator>Robbins, RA</creator><creator>Snider, RM</creator><creator>Spurzem, JR</creator><creator>Thiele, GM</creator><creator>Rennard, SI</creator><creator>Rubinstein, I</creator><general>Am Assoc Immnol</general><general>American Association of Immunologists</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>19940201</creationdate><title>Substance P increases neutrophil adhesion to bronchial epithelial cells</title><author>DeRose, V ; Robbins, RA ; Snider, RM ; Spurzem, JR ; Thiele, GM ; Rennard, SI ; Rubinstein, I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-cb2aa9e74ef0da12bfc86890ffbcd11679eac3503c3a282123fc944e40bb42b33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biphenyl Compounds - pharmacology</topic><topic>Bronchi - cytology</topic><topic>Bronchi - immunology</topic><topic>Cattle</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Epithelium - immunology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Humans</topic><topic>Immunobiology</topic><topic>In Vitro Techniques</topic><topic>Intercellular Adhesion Molecule-1</topic><topic>Lymphocyte Function-Associated Antigen-1 - metabolism</topic><topic>Macrophage-1 Antigen - metabolism</topic><topic>Myeloid cells: ontogeny, maturation, markers, receptors</topic><topic>Neurokinin-1 Receptor Antagonists</topic><topic>Neutrophils - cytology</topic><topic>Peptide Fragments - pharmacology</topic><topic>Polynuclears</topic><topic>Rosette Formation</topic><topic>Substance P - pharmacology</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DeRose, V</creatorcontrib><creatorcontrib>Robbins, RA</creatorcontrib><creatorcontrib>Snider, RM</creatorcontrib><creatorcontrib>Spurzem, JR</creatorcontrib><creatorcontrib>Thiele, GM</creatorcontrib><creatorcontrib>Rennard, SI</creatorcontrib><creatorcontrib>Rubinstein, I</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>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>DeRose, V</au><au>Robbins, RA</au><au>Snider, RM</au><au>Spurzem, JR</au><au>Thiele, GM</au><au>Rennard, SI</au><au>Rubinstein, I</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Substance P increases neutrophil adhesion to bronchial epithelial cells</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>1994-02-01</date><risdate>1994</risdate><volume>152</volume><issue>3</issue><spage>1339</spage><epage>1346</epage><pages>1339-1346</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><coden>JOIMA3</coden><abstract>Polymorphonuclear neutrophils (PMNs) accumulate within the airways during acute and chronic bronchitis and can adhere to bronchial epithelium. Substance P (SP), a neuropeptide released from the primary afferent nerve endings, has been shown to have a proinflammatory effect on PMNs. To test the hypothesis that SP could modulate PMN bronchial epithelial cell adherence, bovine bronchial epithelial cells (BBECs) were isolated and cultured, and the capacity of SP to modulate PMN-BBEC adherence was evaluated. SP interacted with BBECs to induce an increase in PMN adhesion (14.7 +/- 1.2% vs 5.3 +/- 0.7% adherence, p < 0.01). The effect of SP was both time- and dose-dependent with maximal responses at 6 h and 10(-10) M. The effect was reproduced by the carboxyl-terminal sequence of the molecule (SP 6-11). Importantly, pretreatment of the BBECs with the tachykinin SP receptor (NK1) antagonist, CP-96,345, significantly reduced the increase in adhesion induced by SP (p < 0.01). Furthermore, treatment of the BBECs with antibodies against CD11a (LFA-1), CD11b (MAC-1), or ICAM-1 significantly decreased SP-induced adherence (p < 0.01 all comparisons). Conversely, SP stimulation of PMN induced a dose-dependent, rapid (within 5 min) increase in adherence. This effect was also mediated by the carboxy end of the molecule and was decreased by CP-96,345, again suggesting that this effect was NK1 mediated. These data demonstrate the SP has the capacity for modulating PMN-BBEC interactions and suggest an important role for SP in modulating airway inflammation.</abstract><cop>Bethesda, MD</cop><pub>Am Assoc Immnol</pub><pmid>7507964</pmid><doi>10.4049/jimmunol.152.3.1339</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Animals Biological and medical sciences Biphenyl Compounds - pharmacology Bronchi - cytology Bronchi - immunology Cattle Cell Adhesion - drug effects Cell Adhesion Molecules - metabolism Epithelium - immunology Fundamental and applied biological sciences. Psychology Fundamental immunology Humans Immunobiology In Vitro Techniques Intercellular Adhesion Molecule-1 Lymphocyte Function-Associated Antigen-1 - metabolism Macrophage-1 Antigen - metabolism Myeloid cells: ontogeny, maturation, markers, receptors Neurokinin-1 Receptor Antagonists Neutrophils - cytology Peptide Fragments - pharmacology Polynuclears Rosette Formation Substance P - pharmacology Time Factors |
| title | Substance P increases neutrophil adhesion to bronchial epithelial cells |
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