Upregulated expression of substance P (SP) and NK1R in eczema and SP-induced mast cell accumulation
Substance P (SP) was reported to be associated with eczema and acts as a potent skin mast cell secretagogue. However, little is known of its expression in inflammatory cells in eczema and its ability in induction of mast cell accumulation. In the present study, we investigated expression of SP and n...
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| Veröffentlicht in: | Cell biology and toxicology 2017-08, Vol.33 (4), p.389-405 |
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| description | Substance P (SP) was reported to be associated with eczema and acts as a potent skin mast cell secretagogue. However, little is known of its expression in inflammatory cells in eczema and its ability in induction of mast cell accumulation. In the present study, we investigated expression of SP and neurokinin-1 receptor (NK1R) on peripheral blood leukocytes and mast cells from patients with eczema and influence of SP on mast cell accumulation by using flow cytometry analysis, trans-epithelial cell migration assay and mouse peritoneal model. The results showed that plasma SP and IL-17A levels in eczema patients were higher than that in healthy control subject. The percentages of SP+ and NK1R+ expression populations of monocytes, helper T cells, natural killer T cells and basophils in peripheral blood of eczema patients were markedly elevated. It was observed that not only absolute number of mast cells but also SP+ and NK1R+ mast cells are enhanced in the lesion skin of eczema. SP showed a potent chemoattractant action on mast cells as assessed by a mouse peritoneal model and a trans-endothelium cell migration assay. SP-induced mast cell accumulation appears a CD18/CD11a complex,
l
-selectin and ICAM-1-dependent event which can be blocked by a NK-1R antagonist RP67580. In conclusion, elevated expression of SP in patients with eczema and the ability of SP in induction of mast cell accumulation indicate strongly that SP is a potent proinflammatory mediator, which contributes to the pathogenesis of eczema. Inhibitors of SP and blockers of NK1R are likely useful agents for treatment of eczema. |
| doi_str_mv | 10.1007/s10565-016-9379-0 |
| format | Article |
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l
-selectin and ICAM-1-dependent event which can be blocked by a NK-1R antagonist RP67580. In conclusion, elevated expression of SP in patients with eczema and the ability of SP in induction of mast cell accumulation indicate strongly that SP is a potent proinflammatory mediator, which contributes to the pathogenesis of eczema. Inhibitors of SP and blockers of NK1R are likely useful agents for treatment of eczema.</description><identifier>ISSN: 0742-2091</identifier><identifier>EISSN: 1573-6822</identifier><identifier>DOI: 10.1007/s10565-016-9379-0</identifier><identifier>PMID: 28154998</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Accumulation ; Adolescent ; Adult ; Aged ; Animals ; Assaying ; Biochemistry ; Biomedical and Life Sciences ; Case-Control Studies ; CD11a antigen ; CD18 antigen ; Cell Biology ; Cells, Cultured ; Cytometry ; Disease Models, Animal ; Eczema ; Eczema - blood ; Eczema - genetics ; Eczema - metabolism ; Eczema - pathology ; Endothelium ; Female ; Flow cytometry ; Humans ; Inflammation ; Inhibitors ; Intercellular adhesion molecule 1 ; Intercellular Adhesion Molecule-1 - metabolism ; Interleukin-17 - blood ; L-selectin ; Leukocyte migration ; Leukocytes ; Leukocytes (basophilic) ; Life Sciences ; Lymphocytes ; Lymphocytes T ; Male ; Mast cells ; Mast Cells - drug effects ; Mast Cells - metabolism ; Mast Cells - pathology ; Mice ; Mice, Inbred BALB C ; Middle Aged ; Monocytes ; Natural killer cells ; Neurokinin ; Neurokinin NK1 receptors ; Original Article ; Pathogenesis ; Patients ; Peptides ; Peripheral blood ; Peritoneum ; Pharmacology/Toxicology ; Populations ; Protein expression ; Receptors, Neurokinin-1 - biosynthesis ; Receptors, Neurokinin-1 - blood ; Receptors, Neurokinin-1 - genetics ; Signal Transduction ; Skin diseases ; Substance P ; Substance P - biosynthesis ; Substance P - blood ; Substance P - genetics ; Substance P - pharmacology ; Transcriptional Activation ; Up-Regulation ; Young Adult</subject><ispartof>Cell biology and toxicology, 2017-08, Vol.33 (4), p.389-405</ispartof><rights>Springer Science+Business Media Dordrecht 2017</rights><rights>Cell Biology and Toxicology is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-c4fea1f1bba0b7fe0bd80cc89d0586851e1de1220b0d9b75f9fb500c02787df23</citedby><cites>FETCH-LOGICAL-c438t-c4fea1f1bba0b7fe0bd80cc89d0586851e1de1220b0d9b75f9fb500c02787df23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10565-016-9379-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10565-016-9379-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28154998$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhan, Mengmeng</creatorcontrib><creatorcontrib>Zheng, Wenjiao</creatorcontrib><creatorcontrib>Jiang, Qijun</creatorcontrib><creatorcontrib>Zhao, Zuotao</creatorcontrib><creatorcontrib>Wang, Zhiyun</creatorcontrib><creatorcontrib>Wang, Junling</creatorcontrib><creatorcontrib>Zhang, Huiyun</creatorcontrib><creatorcontrib>He, Shaoheng</creatorcontrib><title>Upregulated expression of substance P (SP) and NK1R in eczema and SP-induced mast cell accumulation</title><title>Cell biology and toxicology</title><addtitle>Cell Biol Toxicol</addtitle><addtitle>Cell Biol Toxicol</addtitle><description>Substance P (SP) was reported to be associated with eczema and acts as a potent skin mast cell secretagogue. However, little is known of its expression in inflammatory cells in eczema and its ability in induction of mast cell accumulation. In the present study, we investigated expression of SP and neurokinin-1 receptor (NK1R) on peripheral blood leukocytes and mast cells from patients with eczema and influence of SP on mast cell accumulation by using flow cytometry analysis, trans-epithelial cell migration assay and mouse peritoneal model. The results showed that plasma SP and IL-17A levels in eczema patients were higher than that in healthy control subject. The percentages of SP+ and NK1R+ expression populations of monocytes, helper T cells, natural killer T cells and basophils in peripheral blood of eczema patients were markedly elevated. It was observed that not only absolute number of mast cells but also SP+ and NK1R+ mast cells are enhanced in the lesion skin of eczema. SP showed a potent chemoattractant action on mast cells as assessed by a mouse peritoneal model and a trans-endothelium cell migration assay. SP-induced mast cell accumulation appears a CD18/CD11a complex,
l
-selectin and ICAM-1-dependent event which can be blocked by a NK-1R antagonist RP67580. In conclusion, elevated expression of SP in patients with eczema and the ability of SP in induction of mast cell accumulation indicate strongly that SP is a potent proinflammatory mediator, which contributes to the pathogenesis of eczema. Inhibitors of SP and blockers of NK1R are likely useful agents for treatment of eczema.</description><subject>Accumulation</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Animals</subject><subject>Assaying</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Case-Control Studies</subject><subject>CD11a antigen</subject><subject>CD18 antigen</subject><subject>Cell Biology</subject><subject>Cells, Cultured</subject><subject>Cytometry</subject><subject>Disease Models, Animal</subject><subject>Eczema</subject><subject>Eczema - blood</subject><subject>Eczema - genetics</subject><subject>Eczema - metabolism</subject><subject>Eczema - pathology</subject><subject>Endothelium</subject><subject>Female</subject><subject>Flow cytometry</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inhibitors</subject><subject>Intercellular adhesion molecule 1</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Interleukin-17 - blood</subject><subject>L-selectin</subject><subject>Leukocyte migration</subject><subject>Leukocytes</subject><subject>Leukocytes (basophilic)</subject><subject>Life Sciences</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Mast cells</subject><subject>Mast Cells - drug effects</subject><subject>Mast Cells - metabolism</subject><subject>Mast Cells - pathology</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Middle Aged</subject><subject>Monocytes</subject><subject>Natural killer cells</subject><subject>Neurokinin</subject><subject>Neurokinin NK1 receptors</subject><subject>Original Article</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>Peptides</subject><subject>Peripheral blood</subject><subject>Peritoneum</subject><subject>Pharmacology/Toxicology</subject><subject>Populations</subject><subject>Protein expression</subject><subject>Receptors, Neurokinin-1 - biosynthesis</subject><subject>Receptors, Neurokinin-1 - blood</subject><subject>Receptors, Neurokinin-1 - genetics</subject><subject>Signal Transduction</subject><subject>Skin diseases</subject><subject>Substance P</subject><subject>Substance P - biosynthesis</subject><subject>Substance P - blood</subject><subject>Substance P - genetics</subject><subject>Substance P - pharmacology</subject><subject>Transcriptional Activation</subject><subject>Up-Regulation</subject><subject>Young Adult</subject><issn>0742-2091</issn><issn>1573-6822</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kE1LAzEQhoMoWj9-gBcJeNHD6kzabJKjiF8oWqw9h3xKpbtbN7ug_npTq-LFS4bMvPMMPITsI5wggDhNCLzkBWBZqKFQBayRAXIxLErJ2DoZgBixgoHCLbKd0gsAlCj4JtliEvlIKTkgbrpow3M_N13wNLzlT0qzpqZNpKm3qTO1C3RMjybjY2pqT-9v8ZHOahrcR6jMV2syLma1710GVCZ11IX5nBrn-mqJzbBdshHNPIW977pDppcXT-fXxd3D1c352V3hRkPZ5TcGgxGtNWBFDGC9BOek8sBlKTkG9AEZAwteWcGjipYDOGBCCh_ZcIccrriLtnntQ-r0S9O3dT6pUeFIlbwsZU7hKuXaJqU2RL1oZ5Vp3zWCXmrVK606a9VLrRryzsE3ubdV8L8bPx5zgK0CKY_q59D-Of0v9RPc0YIg</recordid><startdate>20170801</startdate><enddate>20170801</enddate><creator>Zhan, Mengmeng</creator><creator>Zheng, Wenjiao</creator><creator>Jiang, Qijun</creator><creator>Zhao, Zuotao</creator><creator>Wang, Zhiyun</creator><creator>Wang, Junling</creator><creator>Zhang, Huiyun</creator><creator>He, Shaoheng</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7TM</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20170801</creationdate><title>Upregulated expression of substance P (SP) and NK1R in eczema and SP-induced mast cell accumulation</title><author>Zhan, Mengmeng ; Zheng, Wenjiao ; Jiang, Qijun ; Zhao, Zuotao ; Wang, Zhiyun ; Wang, Junling ; Zhang, Huiyun ; He, Shaoheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-c4fea1f1bba0b7fe0bd80cc89d0586851e1de1220b0d9b75f9fb500c02787df23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Accumulation</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Animals</topic><topic>Assaying</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Case-Control Studies</topic><topic>CD11a antigen</topic><topic>CD18 antigen</topic><topic>Cell Biology</topic><topic>Cells, Cultured</topic><topic>Cytometry</topic><topic>Disease Models, Animal</topic><topic>Eczema</topic><topic>Eczema - blood</topic><topic>Eczema - genetics</topic><topic>Eczema - metabolism</topic><topic>Eczema - pathology</topic><topic>Endothelium</topic><topic>Female</topic><topic>Flow cytometry</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inhibitors</topic><topic>Intercellular adhesion molecule 1</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Interleukin-17 - blood</topic><topic>L-selectin</topic><topic>Leukocyte migration</topic><topic>Leukocytes</topic><topic>Leukocytes (basophilic)</topic><topic>Life Sciences</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Mast cells</topic><topic>Mast Cells - drug effects</topic><topic>Mast Cells - metabolism</topic><topic>Mast Cells - pathology</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Middle Aged</topic><topic>Monocytes</topic><topic>Natural killer cells</topic><topic>Neurokinin</topic><topic>Neurokinin NK1 receptors</topic><topic>Original Article</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>Peptides</topic><topic>Peripheral blood</topic><topic>Peritoneum</topic><topic>Pharmacology/Toxicology</topic><topic>Populations</topic><topic>Protein expression</topic><topic>Receptors, Neurokinin-1 - biosynthesis</topic><topic>Receptors, Neurokinin-1 - blood</topic><topic>Receptors, Neurokinin-1 - genetics</topic><topic>Signal Transduction</topic><topic>Skin diseases</topic><topic>Substance P</topic><topic>Substance P - biosynthesis</topic><topic>Substance P - blood</topic><topic>Substance P - genetics</topic><topic>Substance P - pharmacology</topic><topic>Transcriptional Activation</topic><topic>Up-Regulation</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhan, Mengmeng</creatorcontrib><creatorcontrib>Zheng, Wenjiao</creatorcontrib><creatorcontrib>Jiang, Qijun</creatorcontrib><creatorcontrib>Zhao, Zuotao</creatorcontrib><creatorcontrib>Wang, Zhiyun</creatorcontrib><creatorcontrib>Wang, Junling</creatorcontrib><creatorcontrib>Zhang, Huiyun</creatorcontrib><creatorcontrib>He, Shaoheng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Environmental Science Collection</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Cell biology and toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhan, Mengmeng</au><au>Zheng, Wenjiao</au><au>Jiang, Qijun</au><au>Zhao, Zuotao</au><au>Wang, Zhiyun</au><au>Wang, Junling</au><au>Zhang, Huiyun</au><au>He, Shaoheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulated expression of substance P (SP) and NK1R in eczema and SP-induced mast cell accumulation</atitle><jtitle>Cell biology and toxicology</jtitle><stitle>Cell Biol Toxicol</stitle><addtitle>Cell Biol Toxicol</addtitle><date>2017-08-01</date><risdate>2017</risdate><volume>33</volume><issue>4</issue><spage>389</spage><epage>405</epage><pages>389-405</pages><issn>0742-2091</issn><eissn>1573-6822</eissn><abstract>Substance P (SP) was reported to be associated with eczema and acts as a potent skin mast cell secretagogue. However, little is known of its expression in inflammatory cells in eczema and its ability in induction of mast cell accumulation. In the present study, we investigated expression of SP and neurokinin-1 receptor (NK1R) on peripheral blood leukocytes and mast cells from patients with eczema and influence of SP on mast cell accumulation by using flow cytometry analysis, trans-epithelial cell migration assay and mouse peritoneal model. The results showed that plasma SP and IL-17A levels in eczema patients were higher than that in healthy control subject. The percentages of SP+ and NK1R+ expression populations of monocytes, helper T cells, natural killer T cells and basophils in peripheral blood of eczema patients were markedly elevated. It was observed that not only absolute number of mast cells but also SP+ and NK1R+ mast cells are enhanced in the lesion skin of eczema. SP showed a potent chemoattractant action on mast cells as assessed by a mouse peritoneal model and a trans-endothelium cell migration assay. SP-induced mast cell accumulation appears a CD18/CD11a complex,
l
-selectin and ICAM-1-dependent event which can be blocked by a NK-1R antagonist RP67580. In conclusion, elevated expression of SP in patients with eczema and the ability of SP in induction of mast cell accumulation indicate strongly that SP is a potent proinflammatory mediator, which contributes to the pathogenesis of eczema. Inhibitors of SP and blockers of NK1R are likely useful agents for treatment of eczema.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>28154998</pmid><doi>10.1007/s10565-016-9379-0</doi><tpages>17</tpages></addata></record> |
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| subjects | Accumulation Adolescent Adult Aged Animals Assaying Biochemistry Biomedical and Life Sciences Case-Control Studies CD11a antigen CD18 antigen Cell Biology Cells, Cultured Cytometry Disease Models, Animal Eczema Eczema - blood Eczema - genetics Eczema - metabolism Eczema - pathology Endothelium Female Flow cytometry Humans Inflammation Inhibitors Intercellular adhesion molecule 1 Intercellular Adhesion Molecule-1 - metabolism Interleukin-17 - blood L-selectin Leukocyte migration Leukocytes Leukocytes (basophilic) Life Sciences Lymphocytes Lymphocytes T Male Mast cells Mast Cells - drug effects Mast Cells - metabolism Mast Cells - pathology Mice Mice, Inbred BALB C Middle Aged Monocytes Natural killer cells Neurokinin Neurokinin NK1 receptors Original Article Pathogenesis Patients Peptides Peripheral blood Peritoneum Pharmacology/Toxicology Populations Protein expression Receptors, Neurokinin-1 - biosynthesis Receptors, Neurokinin-1 - blood Receptors, Neurokinin-1 - genetics Signal Transduction Skin diseases Substance P Substance P - biosynthesis Substance P - blood Substance P - genetics Substance P - pharmacology Transcriptional Activation Up-Regulation Young Adult |
| title | Upregulated expression of substance P (SP) and NK1R in eczema and SP-induced mast cell accumulation |
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