Regulation of cytokine expression in murine macrophages stimulated by excretory/secretory products from Trichinella spiralis in vitro
Trichinella spiralis is a zoonotic nematode and food borne parasite and infection with T. spiralis leads to suppression of the host immune response and other immunopathologies. The excretory/secretory (ES) products of T. spiralis play important roles in the process of immunomodulation. However, the...
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creator | Bai, Xue Wu, Xiuping Wang, Xuelin Guan, Zhenhong Gao, Fei Yu, Jianli Yu, Lu Tang, Bin Liu, Xiaolei Song, Yanxia Wang, Xinrui Radu, Blaga Boireau, Pascal Wang, Feng Liu, Mingyuan |
description | Trichinella spiralis
is a zoonotic nematode and food borne parasite and infection with
T. spiralis
leads to suppression of the host immune response and other immunopathologies. The excretory/secretory (ES) products of
T. spiralis
play important roles in the process of immunomodulation. However, the mechanisms and related molecules are unknown. Macrophages, a target for immunomodulation by the helminth parasite, play a critical role in initiating and modulating the host immune response to parasite infection. In this study, we examined the effect of ES products from different stages of
T. spiralis
on modulating J774A.1 macrophage activities
.
ES products from different stages of
T. spiralis
reduced the capacity of macrophages to express pro-inflammatory cytokines (tumor necrosis factor α, interleukin-1β , interleukin-6 , and interleukin-12) in response to lipopolysaccharide (LPS) challenge. However, only ES products from 3-day-old adult worms and 5-day-old adult worms/new-born larvae significantly inhibited inducible nitric oxide synthase gene expression in LPS-induced macrophages. In addition, ES products alone boosted the expression of anti-inflammatory cytokines interleukin-10 and transforming growth factor-β and effector molecule arginase 1 in J774A.1 macrophages. Signal transduction studies showed that ES products significantly inhibited nuclear factor-κB translocation into the nucleus and the phosphorylation of both extracellular signal-regulated protein kinase 1/2 and p38 mitogen-activated protein kinase in LPS-stimulated J774A.1 macrophages. These results suggest that ES products regulate host immune response at the macrophage level through inhibition of pro-inflammatory cytokines production and induction of macrophage toward the alternative phenotype, which maybe important for worm survival and host health. |
doi_str_mv | 10.1007/s11010-011-1046-4 |
format | Article |
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is a zoonotic nematode and food borne parasite and infection with
T. spiralis
leads to suppression of the host immune response and other immunopathologies. The excretory/secretory (ES) products of
T. spiralis
play important roles in the process of immunomodulation. However, the mechanisms and related molecules are unknown. Macrophages, a target for immunomodulation by the helminth parasite, play a critical role in initiating and modulating the host immune response to parasite infection. In this study, we examined the effect of ES products from different stages of
T. spiralis
on modulating J774A.1 macrophage activities
.
ES products from different stages of
T. spiralis
reduced the capacity of macrophages to express pro-inflammatory cytokines (tumor necrosis factor α, interleukin-1β , interleukin-6 , and interleukin-12) in response to lipopolysaccharide (LPS) challenge. However, only ES products from 3-day-old adult worms and 5-day-old adult worms/new-born larvae significantly inhibited inducible nitric oxide synthase gene expression in LPS-induced macrophages. In addition, ES products alone boosted the expression of anti-inflammatory cytokines interleukin-10 and transforming growth factor-β and effector molecule arginase 1 in J774A.1 macrophages. Signal transduction studies showed that ES products significantly inhibited nuclear factor-κB translocation into the nucleus and the phosphorylation of both extracellular signal-regulated protein kinase 1/2 and p38 mitogen-activated protein kinase in LPS-stimulated J774A.1 macrophages. These results suggest that ES products regulate host immune response at the macrophage level through inhibition of pro-inflammatory cytokines production and induction of macrophage toward the alternative phenotype, which maybe important for worm survival and host health.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-011-1046-4</identifier><identifier>PMID: 21909996</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Active Transport, Cell Nucleus - drug effects ; Animals ; Arginase ; Biochemistry ; Biomedical and Life Sciences ; Bone morphogenetic proteins ; Cardiology ; Cell Line ; Cell Nucleus - metabolism ; Cell Survival - drug effects ; Culture Media, Conditioned - pharmacology ; Cytokines ; Cytokines - genetics ; Cytokines - metabolism ; Gene expression ; Gene Expression - drug effects ; Gene Expression Regulation ; Health aspects ; Host-Parasite Interactions ; Inflammation - chemically induced ; Inflammation - metabolism ; Larva - metabolism ; Life Sciences ; Lipopolysaccharides ; Macrophages ; Macrophages - drug effects ; Macrophages - enzymology ; Macrophages - metabolism ; Medical Biochemistry ; Mice ; Mitogen-Activated Protein Kinases - metabolism ; Mitogens ; Nematoda ; NF-kappa B - metabolism ; Nitric oxide ; Nitric Oxide Synthase Type II - metabolism ; Oncology ; Phosphorylation ; Rats ; Rats, Wistar ; Trichinella spiralis - metabolism</subject><ispartof>Molecular and cellular biochemistry, 2012-01, Vol.360 (1-2), p.79-88</ispartof><rights>Springer Science+Business Media, LLC. 2011</rights><rights>COPYRIGHT 2012 Springer</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c576t-50a7d04be2d3ba07399774530d75248bbb62631431311f1cf5199380ec70f11d3</citedby><cites>FETCH-LOGICAL-c576t-50a7d04be2d3ba07399774530d75248bbb62631431311f1cf5199380ec70f11d3</cites><orcidid>0000-0002-3998-7792 ; 0000-0003-0873-4423</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-011-1046-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-011-1046-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21909996$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-04537898$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Bai, Xue</creatorcontrib><creatorcontrib>Wu, Xiuping</creatorcontrib><creatorcontrib>Wang, Xuelin</creatorcontrib><creatorcontrib>Guan, Zhenhong</creatorcontrib><creatorcontrib>Gao, Fei</creatorcontrib><creatorcontrib>Yu, Jianli</creatorcontrib><creatorcontrib>Yu, Lu</creatorcontrib><creatorcontrib>Tang, Bin</creatorcontrib><creatorcontrib>Liu, Xiaolei</creatorcontrib><creatorcontrib>Song, Yanxia</creatorcontrib><creatorcontrib>Wang, Xinrui</creatorcontrib><creatorcontrib>Radu, Blaga</creatorcontrib><creatorcontrib>Boireau, Pascal</creatorcontrib><creatorcontrib>Wang, Feng</creatorcontrib><creatorcontrib>Liu, Mingyuan</creatorcontrib><title>Regulation of cytokine expression in murine macrophages stimulated by excretory/secretory products from Trichinella spiralis in vitro</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>Trichinella spiralis
is a zoonotic nematode and food borne parasite and infection with
T. spiralis
leads to suppression of the host immune response and other immunopathologies. The excretory/secretory (ES) products of
T. spiralis
play important roles in the process of immunomodulation. However, the mechanisms and related molecules are unknown. Macrophages, a target for immunomodulation by the helminth parasite, play a critical role in initiating and modulating the host immune response to parasite infection. In this study, we examined the effect of ES products from different stages of
T. spiralis
on modulating J774A.1 macrophage activities
.
ES products from different stages of
T. spiralis
reduced the capacity of macrophages to express pro-inflammatory cytokines (tumor necrosis factor α, interleukin-1β , interleukin-6 , and interleukin-12) in response to lipopolysaccharide (LPS) challenge. However, only ES products from 3-day-old adult worms and 5-day-old adult worms/new-born larvae significantly inhibited inducible nitric oxide synthase gene expression in LPS-induced macrophages. In addition, ES products alone boosted the expression of anti-inflammatory cytokines interleukin-10 and transforming growth factor-β and effector molecule arginase 1 in J774A.1 macrophages. Signal transduction studies showed that ES products significantly inhibited nuclear factor-κB translocation into the nucleus and the phosphorylation of both extracellular signal-regulated protein kinase 1/2 and p38 mitogen-activated protein kinase in LPS-stimulated J774A.1 macrophages. These results suggest that ES products regulate host immune response at the macrophage level through inhibition of pro-inflammatory cytokines production and induction of macrophage toward the alternative phenotype, which maybe important for worm survival and host health.</description><subject>Active Transport, Cell Nucleus - drug effects</subject><subject>Animals</subject><subject>Arginase</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Bone morphogenetic proteins</subject><subject>Cardiology</subject><subject>Cell Line</subject><subject>Cell Nucleus - metabolism</subject><subject>Cell Survival - drug effects</subject><subject>Culture Media, Conditioned - pharmacology</subject><subject>Cytokines</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression - drug effects</subject><subject>Gene Expression Regulation</subject><subject>Health aspects</subject><subject>Host-Parasite Interactions</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - metabolism</subject><subject>Larva - metabolism</subject><subject>Life Sciences</subject><subject>Lipopolysaccharides</subject><subject>Macrophages</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - enzymology</subject><subject>Macrophages - metabolism</subject><subject>Medical Biochemistry</subject><subject>Mice</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Mitogens</subject><subject>Nematoda</subject><subject>NF-kappa B - metabolism</subject><subject>Nitric oxide</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Oncology</subject><subject>Phosphorylation</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Trichinella spiralis - metabolism</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFktGK1DAUhoMo7rj6AN5IwRu96O45Tdo0l8OirjAgyHod0jSdydo2NWmXnQfY996EjguCKLlI-PP9f3I4h5C3CBcIwC8DIiDkgJgjsCpnz8gGS05zJlA8JxugAHmNnJ-RVyHcQoQj-5KcFShACFFtyMN3s196NVs3Zq7L9HF2P-1oMnM_eRNCku2YDYtP4qC0d9NB7U3IwmyHZDRt1hwjrr2ZnT9eBnM6ZZN37aLnkHXeDdmNt_oQQ_peZWGyXvU2pOg7O3v3mrzoVB_Mm9N-Tn58_nRzdZ3vvn35erXd5brk1ZyXoHgLrDFFSxsFnArBOSsptLwsWN00TVVUFBlFitih7koUgtZgNIcOsaXn5OOae1C9nLwdlD9Kp6y83u5k0iCm8VrUdxjZDysb6_i1mDDLwQad_j8atwSJrGIlCEbp_1GAuqaswIS-X9G96o20Y-dmr3TC5ZaWtRB1LCBSF3-h4mrNYLUbTWej_ocBV0NsUAjedE_VIaTnuVxnRcb-yzQrkkXPu9Ovl2Yw7ZPj93BEoFiBEK_GvfHy1i1-jA36R-ojQ-rI4A</recordid><startdate>20120101</startdate><enddate>20120101</enddate><creator>Bai, Xue</creator><creator>Wu, Xiuping</creator><creator>Wang, Xuelin</creator><creator>Guan, Zhenhong</creator><creator>Gao, Fei</creator><creator>Yu, Jianli</creator><creator>Yu, Lu</creator><creator>Tang, Bin</creator><creator>Liu, Xiaolei</creator><creator>Song, Yanxia</creator><creator>Wang, Xinrui</creator><creator>Radu, Blaga</creator><creator>Boireau, Pascal</creator><creator>Wang, Feng</creator><creator>Liu, Mingyuan</creator><general>Springer US</general><general>Springer</general><general>Springer Verlag</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>7T5</scope><scope>H94</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-3998-7792</orcidid><orcidid>https://orcid.org/0000-0003-0873-4423</orcidid></search><sort><creationdate>20120101</creationdate><title>Regulation of cytokine expression in murine macrophages stimulated by excretory/secretory products from Trichinella spiralis in vitro</title><author>Bai, Xue ; Wu, Xiuping ; Wang, Xuelin ; Guan, Zhenhong ; Gao, Fei ; Yu, Jianli ; Yu, Lu ; Tang, Bin ; Liu, Xiaolei ; Song, Yanxia ; Wang, Xinrui ; Radu, Blaga ; Boireau, Pascal ; Wang, Feng ; Liu, Mingyuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c576t-50a7d04be2d3ba07399774530d75248bbb62631431311f1cf5199380ec70f11d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Active Transport, Cell Nucleus - drug effects</topic><topic>Animals</topic><topic>Arginase</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Bone morphogenetic proteins</topic><topic>Cardiology</topic><topic>Cell Line</topic><topic>Cell Nucleus - metabolism</topic><topic>Cell Survival - drug effects</topic><topic>Culture Media, Conditioned - pharmacology</topic><topic>Cytokines</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Gene expression</topic><topic>Gene Expression - drug effects</topic><topic>Gene Expression Regulation</topic><topic>Health aspects</topic><topic>Host-Parasite Interactions</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - metabolism</topic><topic>Larva - metabolism</topic><topic>Life Sciences</topic><topic>Lipopolysaccharides</topic><topic>Macrophages</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - enzymology</topic><topic>Macrophages - metabolism</topic><topic>Medical Biochemistry</topic><topic>Mice</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Mitogens</topic><topic>Nematoda</topic><topic>NF-kappa B - metabolism</topic><topic>Nitric oxide</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Oncology</topic><topic>Phosphorylation</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Trichinella spiralis - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bai, Xue</creatorcontrib><creatorcontrib>Wu, Xiuping</creatorcontrib><creatorcontrib>Wang, Xuelin</creatorcontrib><creatorcontrib>Guan, Zhenhong</creatorcontrib><creatorcontrib>Gao, Fei</creatorcontrib><creatorcontrib>Yu, Jianli</creatorcontrib><creatorcontrib>Yu, Lu</creatorcontrib><creatorcontrib>Tang, Bin</creatorcontrib><creatorcontrib>Liu, Xiaolei</creatorcontrib><creatorcontrib>Song, Yanxia</creatorcontrib><creatorcontrib>Wang, Xinrui</creatorcontrib><creatorcontrib>Radu, Blaga</creatorcontrib><creatorcontrib>Boireau, Pascal</creatorcontrib><creatorcontrib>Wang, Feng</creatorcontrib><creatorcontrib>Liu, Mingyuan</creatorcontrib><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>Hyper Article en Ligne (HAL)</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bai, Xue</au><au>Wu, Xiuping</au><au>Wang, Xuelin</au><au>Guan, Zhenhong</au><au>Gao, Fei</au><au>Yu, Jianli</au><au>Yu, Lu</au><au>Tang, Bin</au><au>Liu, Xiaolei</au><au>Song, Yanxia</au><au>Wang, Xinrui</au><au>Radu, Blaga</au><au>Boireau, Pascal</au><au>Wang, Feng</au><au>Liu, Mingyuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of cytokine expression in murine macrophages stimulated by excretory/secretory products from Trichinella spiralis in vitro</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2012-01-01</date><risdate>2012</risdate><volume>360</volume><issue>1-2</issue><spage>79</spage><epage>88</epage><pages>79-88</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Trichinella spiralis
is a zoonotic nematode and food borne parasite and infection with
T. spiralis
leads to suppression of the host immune response and other immunopathologies. The excretory/secretory (ES) products of
T. spiralis
play important roles in the process of immunomodulation. However, the mechanisms and related molecules are unknown. Macrophages, a target for immunomodulation by the helminth parasite, play a critical role in initiating and modulating the host immune response to parasite infection. In this study, we examined the effect of ES products from different stages of
T. spiralis
on modulating J774A.1 macrophage activities
.
ES products from different stages of
T. spiralis
reduced the capacity of macrophages to express pro-inflammatory cytokines (tumor necrosis factor α, interleukin-1β , interleukin-6 , and interleukin-12) in response to lipopolysaccharide (LPS) challenge. However, only ES products from 3-day-old adult worms and 5-day-old adult worms/new-born larvae significantly inhibited inducible nitric oxide synthase gene expression in LPS-induced macrophages. In addition, ES products alone boosted the expression of anti-inflammatory cytokines interleukin-10 and transforming growth factor-β and effector molecule arginase 1 in J774A.1 macrophages. Signal transduction studies showed that ES products significantly inhibited nuclear factor-κB translocation into the nucleus and the phosphorylation of both extracellular signal-regulated protein kinase 1/2 and p38 mitogen-activated protein kinase in LPS-stimulated J774A.1 macrophages. These results suggest that ES products regulate host immune response at the macrophage level through inhibition of pro-inflammatory cytokines production and induction of macrophage toward the alternative phenotype, which maybe important for worm survival and host health.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>21909996</pmid><doi>10.1007/s11010-011-1046-4</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-3998-7792</orcidid><orcidid>https://orcid.org/0000-0003-0873-4423</orcidid></addata></record> |
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subjects | Active Transport, Cell Nucleus - drug effects Animals Arginase Biochemistry Biomedical and Life Sciences Bone morphogenetic proteins Cardiology Cell Line Cell Nucleus - metabolism Cell Survival - drug effects Culture Media, Conditioned - pharmacology Cytokines Cytokines - genetics Cytokines - metabolism Gene expression Gene Expression - drug effects Gene Expression Regulation Health aspects Host-Parasite Interactions Inflammation - chemically induced Inflammation - metabolism Larva - metabolism Life Sciences Lipopolysaccharides Macrophages Macrophages - drug effects Macrophages - enzymology Macrophages - metabolism Medical Biochemistry Mice Mitogen-Activated Protein Kinases - metabolism Mitogens Nematoda NF-kappa B - metabolism Nitric oxide Nitric Oxide Synthase Type II - metabolism Oncology Phosphorylation Rats Rats, Wistar Trichinella spiralis - metabolism |
title | Regulation of cytokine expression in murine macrophages stimulated by excretory/secretory products from Trichinella spiralis in vitro |
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