Lack of a Functioning P2X7 Receptor Leads to Increased Susceptibility to Toxoplasmic Ileitis
Oral infection of C57BL/6J mice with the protozoan parasite Toxoplasma gondii leads to a lethal inflammatory ileitis. Mice lacking the purinergic receptor P2X7R are acutely susceptible to toxoplasmic ileitis, losing significantly more weight than C57BL/6J mice and exhibiting much greater intestinal...
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| creator | Miller, Catherine M Zakrzewski, Alana M Robinson, Dionne P Fuller, Stephen J Walker, Robert A Ikin, Rowan J Bao, Shisan J Grigg, Michael E Wiley, James S Smith, Nicholas C |
| description | Oral infection of C57BL/6J mice with the protozoan parasite Toxoplasma gondii leads to a lethal inflammatory ileitis.
Mice lacking the purinergic receptor P2X7R are acutely susceptible to toxoplasmic ileitis, losing significantly more weight than C57BL/6J mice and exhibiting much greater intestinal inflammatory pathology in response to infection with only 10 cysts of T. gondii. This susceptibility is not dependent on the ability of P2X7R-deficient mice to control the parasite, which they accomplish just as efficiently as C57BL/6J mice. Rather, susceptibility is associated with elevated ileal concentrations of pro-inflammatory cytokines, reactive nitrogen intermediates and altered regulation of elements of NFκB activation in P2X7R-deficient mice.
Our data support the thesis that P2X7R, a well-documented activator of pro-inflammatory cytokine production, also plays an important role in the regulation of intestinal inflammation. |
| doi_str_mv | 10.1371/journal.pone.0129048 |
| format | Article |
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Mice lacking the purinergic receptor P2X7R are acutely susceptible to toxoplasmic ileitis, losing significantly more weight than C57BL/6J mice and exhibiting much greater intestinal inflammatory pathology in response to infection with only 10 cysts of T. gondii. This susceptibility is not dependent on the ability of P2X7R-deficient mice to control the parasite, which they accomplish just as efficiently as C57BL/6J mice. Rather, susceptibility is associated with elevated ileal concentrations of pro-inflammatory cytokines, reactive nitrogen intermediates and altered regulation of elements of NFκB activation in P2X7R-deficient mice.
Our data support the thesis that P2X7R, a well-documented activator of pro-inflammatory cytokine production, also plays an important role in the regulation of intestinal inflammation.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0129048</identifier><identifier>PMID: 26053862</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Cysts ; Cytokines ; Cytokines - metabolism ; Disease Models, Animal ; Disease Progression ; Disease Susceptibility ; Health aspects ; House mouse ; Ileitis ; Ileitis - genetics ; Ileitis - metabolism ; Ileitis - parasitology ; Ileitis - pathology ; Infection ; Inflammation ; Inflammation Mediators - metabolism ; Inflammatory bowel disease ; Intermediates ; Intestine ; Male ; MAP Kinase Signaling System ; Mice ; Mice, Knockout ; NF-kappa B - metabolism ; NF-κB protein ; Oral infection ; Parasites ; Parasitic diseases ; Protozoa ; Reactive nitrogen species ; Reactive Nitrogen Species - metabolism ; Receptors, Purinergic P2X7 - deficiency ; Risk factors ; Rodents ; Toxoplasma ; Toxoplasma gondii ; Toxoplasmosis, Animal - genetics ; Toxoplasmosis, Animal - metabolism ; Toxoplasmosis, Animal - parasitology</subject><ispartof>PloS one, 2015-06, Vol.10 (6), p.e0129048-e0129048</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication: https://creativecommons.org/publicdomain/zero/1.0/ (the “License”) Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-964e362c106b5ad7be79cf016732547b5a8a631363f16f9a8e14be1715f359813</citedby><cites>FETCH-LOGICAL-c692t-964e362c106b5ad7be79cf016732547b5a8a631363f16f9a8e14be1715f359813</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4460092/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4460092/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26053862$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Miller, Catherine M</creatorcontrib><creatorcontrib>Zakrzewski, Alana M</creatorcontrib><creatorcontrib>Robinson, Dionne P</creatorcontrib><creatorcontrib>Fuller, Stephen J</creatorcontrib><creatorcontrib>Walker, Robert A</creatorcontrib><creatorcontrib>Ikin, Rowan J</creatorcontrib><creatorcontrib>Bao, Shisan J</creatorcontrib><creatorcontrib>Grigg, Michael E</creatorcontrib><creatorcontrib>Wiley, James S</creatorcontrib><creatorcontrib>Smith, Nicholas C</creatorcontrib><title>Lack of a Functioning P2X7 Receptor Leads to Increased Susceptibility to Toxoplasmic Ileitis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Oral infection of C57BL/6J mice with the protozoan parasite Toxoplasma gondii leads to a lethal inflammatory ileitis.
Mice lacking the purinergic receptor P2X7R are acutely susceptible to toxoplasmic ileitis, losing significantly more weight than C57BL/6J mice and exhibiting much greater intestinal inflammatory pathology in response to infection with only 10 cysts of T. gondii. This susceptibility is not dependent on the ability of P2X7R-deficient mice to control the parasite, which they accomplish just as efficiently as C57BL/6J mice. Rather, susceptibility is associated with elevated ileal concentrations of pro-inflammatory cytokines, reactive nitrogen intermediates and altered regulation of elements of NFκB activation in P2X7R-deficient mice.
Our data support the thesis that P2X7R, a well-documented activator of pro-inflammatory cytokine production, also plays an important role in the regulation of intestinal inflammation.</description><subject>Animals</subject><subject>Cysts</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Disease Susceptibility</subject><subject>Health aspects</subject><subject>House mouse</subject><subject>Ileitis</subject><subject>Ileitis - genetics</subject><subject>Ileitis - metabolism</subject><subject>Ileitis - parasitology</subject><subject>Ileitis - pathology</subject><subject>Infection</subject><subject>Inflammation</subject><subject>Inflammation Mediators - metabolism</subject><subject>Inflammatory bowel disease</subject><subject>Intermediates</subject><subject>Intestine</subject><subject>Male</subject><subject>MAP Kinase Signaling System</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Oral infection</subject><subject>Parasites</subject><subject>Parasitic diseases</subject><subject>Protozoa</subject><subject>Reactive nitrogen species</subject><subject>Reactive Nitrogen Species - metabolism</subject><subject>Receptors, Purinergic P2X7 - deficiency</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Toxoplasma</subject><subject>Toxoplasma gondii</subject><subject>Toxoplasmosis, Animal - genetics</subject><subject>Toxoplasmosis, Animal - metabolism</subject><subject>Toxoplasmosis, Animal - parasitology</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11v0zAUhiMEYlvhHyCIhITgosVfceIbpGliUKnS0DYQF0iW45y0Lm5cYmfa_j1Om00N2gXJRaxznvM6fn1OkrzCaIZpjj-uXdc2ys62roEZwkQgVjxJjrGgZMoJok8P1kfJifdrhDJacP48OSJ8tyTHya-F0r9TV6cqPe8aHYxrTLNMv5GfeXoJGrbBtekCVOXT4NJ5o1tQHqr0qvN90pTGmnDX567drdta5TdGp3MLJhj_InlWK-vh5fCdJN_PP1-ffZ0uLr7Mz04XU80FCVPBGVBONEa8zFSVl5ALXSPMc0oylsdYoTjFlNMa81qoAjArAec4q2kmCkwnyZu97tY6LwdjvMS84HmBWcYjMd8TlVNruW3NRrV30ikjdwHXLqVqg9EWJEFlLoBkGSIFI6wQnEPGM0YzjpkgELU-Dbt15QYqDU1olR2JjjONWcmlu5GMcYQEiQLvB4HW_enAB7kx0U1rVQOu2_13Tjmm8Zkkb_9BHz_dQC1VPIBpahf31b2oPGXRJ5ZzJCI1e4SKbwXxzmIX1SbGRwUfRgWRCXAblqrzXs6vLv-fvfgxZt8dsCtQNqy8s13ffH4Msj2oW-d9C_WDyRjJfgju3ZD9EMhhCGLZ68MLeii673r6FwhN_jc</recordid><startdate>20150608</startdate><enddate>20150608</enddate><creator>Miller, Catherine M</creator><creator>Zakrzewski, Alana M</creator><creator>Robinson, Dionne P</creator><creator>Fuller, Stephen J</creator><creator>Walker, Robert A</creator><creator>Ikin, Rowan J</creator><creator>Bao, Shisan J</creator><creator>Grigg, Michael E</creator><creator>Wiley, James S</creator><creator>Smith, Nicholas C</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150608</creationdate><title>Lack of a Functioning P2X7 Receptor Leads to Increased Susceptibility to Toxoplasmic Ileitis</title><author>Miller, Catherine M ; Zakrzewski, Alana M ; Robinson, Dionne P ; Fuller, Stephen J ; Walker, Robert A ; Ikin, Rowan J ; Bao, Shisan J ; Grigg, Michael E ; Wiley, James S ; Smith, Nicholas C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-964e362c106b5ad7be79cf016732547b5a8a631363f16f9a8e14be1715f359813</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Cysts</topic><topic>Cytokines</topic><topic>Cytokines - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Miller, Catherine M</au><au>Zakrzewski, Alana M</au><au>Robinson, Dionne P</au><au>Fuller, Stephen J</au><au>Walker, Robert A</au><au>Ikin, Rowan J</au><au>Bao, Shisan J</au><au>Grigg, Michael E</au><au>Wiley, James S</au><au>Smith, Nicholas C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lack of a Functioning P2X7 Receptor Leads to Increased Susceptibility to Toxoplasmic Ileitis</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-06-08</date><risdate>2015</risdate><volume>10</volume><issue>6</issue><spage>e0129048</spage><epage>e0129048</epage><pages>e0129048-e0129048</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Oral infection of C57BL/6J mice with the protozoan parasite Toxoplasma gondii leads to a lethal inflammatory ileitis.
Mice lacking the purinergic receptor P2X7R are acutely susceptible to toxoplasmic ileitis, losing significantly more weight than C57BL/6J mice and exhibiting much greater intestinal inflammatory pathology in response to infection with only 10 cysts of T. gondii. This susceptibility is not dependent on the ability of P2X7R-deficient mice to control the parasite, which they accomplish just as efficiently as C57BL/6J mice. Rather, susceptibility is associated with elevated ileal concentrations of pro-inflammatory cytokines, reactive nitrogen intermediates and altered regulation of elements of NFκB activation in P2X7R-deficient mice.
Our data support the thesis that P2X7R, a well-documented activator of pro-inflammatory cytokine production, also plays an important role in the regulation of intestinal inflammation.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26053862</pmid><doi>10.1371/journal.pone.0129048</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Cysts Cytokines Cytokines - metabolism Disease Models, Animal Disease Progression Disease Susceptibility Health aspects House mouse Ileitis Ileitis - genetics Ileitis - metabolism Ileitis - parasitology Ileitis - pathology Infection Inflammation Inflammation Mediators - metabolism Inflammatory bowel disease Intermediates Intestine Male MAP Kinase Signaling System Mice Mice, Knockout NF-kappa B - metabolism NF-κB protein Oral infection Parasites Parasitic diseases Protozoa Reactive nitrogen species Reactive Nitrogen Species - metabolism Receptors, Purinergic P2X7 - deficiency Risk factors Rodents Toxoplasma Toxoplasma gondii Toxoplasmosis, Animal - genetics Toxoplasmosis, Animal - metabolism Toxoplasmosis, Animal - parasitology |
| title | Lack of a Functioning P2X7 Receptor Leads to Increased Susceptibility to Toxoplasmic Ileitis |
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