Recurrent infection progressively disables host protection against intestinal inflammation
Intestinal inflammation is the central pathological feature of colitis and the inflammatory bowel diseases. These syndromes arise from unidentified environmental factors. We found that recurrent nonlethal gastric infections of Gram-negative Typhimurium (ST), a major source of human food poisoning, c...
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| Veröffentlicht in: | Science (American Association for the Advancement of Science) 2017-12, Vol.358 (6370), p.1588-1588 |
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| container_title | Science (American Association for the Advancement of Science) |
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| creator | Yang, Won Ho Heithoff, Douglas M. Aziz, Peter V. Sperandio, Markus Nizet, Victor Mahan, Michael J. Marth, Jamey D. |
| description | Intestinal inflammation is the central pathological feature of colitis and the inflammatory bowel diseases. These syndromes arise from unidentified environmental factors. We found that recurrent nonlethal gastric infections of Gram-negative
Typhimurium (ST), a major source of human food poisoning, caused inflammation of murine intestinal tissue, predominantly the colon, which persisted after pathogen clearance and irreversibly escalated in severity with repeated infections. ST progressively disabled a host mechanism of protection by inducing endogenous neuraminidase activity, which accelerated the molecular aging and clearance of intestinal alkaline phosphatase (IAP). Disease was linked to a Toll-like receptor 4 (TLR4)-dependent mechanism of IAP desialylation with accumulation of the IAP substrate and TLR4 ligand, lipopolysaccharide-phosphate. The administration of IAP or the antiviral neuraminidase inhibitor zanamivir was therapeutic by maintaining IAP abundance and function. |
| doi_str_mv | 10.1126/science.aao5610 |
| format | Article |
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Typhimurium (ST), a major source of human food poisoning, caused inflammation of murine intestinal tissue, predominantly the colon, which persisted after pathogen clearance and irreversibly escalated in severity with repeated infections. ST progressively disabled a host mechanism of protection by inducing endogenous neuraminidase activity, which accelerated the molecular aging and clearance of intestinal alkaline phosphatase (IAP). Disease was linked to a Toll-like receptor 4 (TLR4)-dependent mechanism of IAP desialylation with accumulation of the IAP substrate and TLR4 ligand, lipopolysaccharide-phosphate. The administration of IAP or the antiviral neuraminidase inhibitor zanamivir was therapeutic by maintaining IAP abundance and function.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.aao5610</identifier><identifier>PMID: 29269445</identifier><language>eng</language><publisher>United States: American Association for the Advancement of Science</publisher><subject>Accumulation ; Aging ; Alkaline phosphatase ; Animal tissues ; Augmentation ; Bacteria ; Bacterial infections ; Biodegradation ; Chronic infection ; Colon ; Crohn's Disease ; Diseases ; Disorders ; Duodenum ; Enterocytes ; Environmental factors ; Environmental Influences ; Exo-a-sialidase ; Food contamination ; Food contamination & poisoning ; Food poisoning ; Food production ; Food sources ; Foodborne diseases ; Human behavior ; Human populations ; Infections ; Inflammation ; Inflammatory bowel disease ; Inflammatory bowel diseases ; Ingestion ; Inhibition ; Inhibitors ; Life span ; Lipopolysaccharides ; Pathogens ; Phosphatase ; Phosphates ; Poisoning ; Recurrent infection ; RESEARCH ARTICLE SUMMARY ; Salmonella ; Salmonella enterica ; Salmonella Typhimurium ; Small intestine ; Substrates ; TLR4 protein ; Toll-like receptors ; Ulcerative colitis ; Zanamivir</subject><ispartof>Science (American Association for the Advancement of Science), 2017-12, Vol.358 (6370), p.1588-1588</ispartof><rights>Copyright © 2017 by the American Association for the Advancement of Science</rights><rights>Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.</rights><rights>Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-514d1d8c24f8debc14368564731348375b5b0ebc7742111542e547b85f4a7e093</citedby><cites>FETCH-LOGICAL-c509t-514d1d8c24f8debc14368564731348375b5b0ebc7742111542e547b85f4a7e093</cites><orcidid>0000-0001-9323-1649 ; 0000-0001-8954-2516 ; 0000-0002-7689-3613 ; 0000-0001-8957-100X ; 0000-0002-6090-7101 ; 0000-0003-3847-0422</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/26401157$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/26401157$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,780,784,803,885,2882,2883,27922,27923,58015,58248</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29269445$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Won Ho</creatorcontrib><creatorcontrib>Heithoff, Douglas M.</creatorcontrib><creatorcontrib>Aziz, Peter V.</creatorcontrib><creatorcontrib>Sperandio, Markus</creatorcontrib><creatorcontrib>Nizet, Victor</creatorcontrib><creatorcontrib>Mahan, Michael J.</creatorcontrib><creatorcontrib>Marth, Jamey D.</creatorcontrib><title>Recurrent infection progressively disables host protection against intestinal inflammation</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>Intestinal inflammation is the central pathological feature of colitis and the inflammatory bowel diseases. These syndromes arise from unidentified environmental factors. We found that recurrent nonlethal gastric infections of Gram-negative
Typhimurium (ST), a major source of human food poisoning, caused inflammation of murine intestinal tissue, predominantly the colon, which persisted after pathogen clearance and irreversibly escalated in severity with repeated infections. ST progressively disabled a host mechanism of protection by inducing endogenous neuraminidase activity, which accelerated the molecular aging and clearance of intestinal alkaline phosphatase (IAP). Disease was linked to a Toll-like receptor 4 (TLR4)-dependent mechanism of IAP desialylation with accumulation of the IAP substrate and TLR4 ligand, lipopolysaccharide-phosphate. The administration of IAP or the antiviral neuraminidase inhibitor zanamivir was therapeutic by maintaining IAP abundance and function.</description><subject>Accumulation</subject><subject>Aging</subject><subject>Alkaline phosphatase</subject><subject>Animal tissues</subject><subject>Augmentation</subject><subject>Bacteria</subject><subject>Bacterial infections</subject><subject>Biodegradation</subject><subject>Chronic infection</subject><subject>Colon</subject><subject>Crohn's Disease</subject><subject>Diseases</subject><subject>Disorders</subject><subject>Duodenum</subject><subject>Enterocytes</subject><subject>Environmental factors</subject><subject>Environmental Influences</subject><subject>Exo-a-sialidase</subject><subject>Food contamination</subject><subject>Food contamination & poisoning</subject><subject>Food poisoning</subject><subject>Food production</subject><subject>Food sources</subject><subject>Foodborne diseases</subject><subject>Human behavior</subject><subject>Human populations</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Inflammatory bowel disease</subject><subject>Inflammatory bowel diseases</subject><subject>Ingestion</subject><subject>Inhibition</subject><subject>Inhibitors</subject><subject>Life span</subject><subject>Lipopolysaccharides</subject><subject>Pathogens</subject><subject>Phosphatase</subject><subject>Phosphates</subject><subject>Poisoning</subject><subject>Recurrent infection</subject><subject>RESEARCH ARTICLE SUMMARY</subject><subject>Salmonella</subject><subject>Salmonella enterica</subject><subject>Salmonella Typhimurium</subject><subject>Small intestine</subject><subject>Substrates</subject><subject>TLR4 protein</subject><subject>Toll-like receptors</subject><subject>Ulcerative 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infection progressively disables host protection against intestinal inflammation</title><author>Yang, Won Ho ; Heithoff, Douglas M. ; Aziz, Peter V. ; Sperandio, Markus ; Nizet, Victor ; Mahan, Michael J. ; Marth, Jamey D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c509t-514d1d8c24f8debc14368564731348375b5b0ebc7742111542e547b85f4a7e093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Accumulation</topic><topic>Aging</topic><topic>Alkaline phosphatase</topic><topic>Animal tissues</topic><topic>Augmentation</topic><topic>Bacteria</topic><topic>Bacterial infections</topic><topic>Biodegradation</topic><topic>Chronic infection</topic><topic>Colon</topic><topic>Crohn's Disease</topic><topic>Diseases</topic><topic>Disorders</topic><topic>Duodenum</topic><topic>Enterocytes</topic><topic>Environmental factors</topic><topic>Environmental Influences</topic><topic>Exo-a-sialidase</topic><topic>Food contamination</topic><topic>Food contamination & poisoning</topic><topic>Food poisoning</topic><topic>Food production</topic><topic>Food sources</topic><topic>Foodborne diseases</topic><topic>Human behavior</topic><topic>Human populations</topic><topic>Infections</topic><topic>Inflammation</topic><topic>Inflammatory bowel disease</topic><topic>Inflammatory bowel diseases</topic><topic>Ingestion</topic><topic>Inhibition</topic><topic>Inhibitors</topic><topic>Life span</topic><topic>Lipopolysaccharides</topic><topic>Pathogens</topic><topic>Phosphatase</topic><topic>Phosphates</topic><topic>Poisoning</topic><topic>Recurrent infection</topic><topic>RESEARCH ARTICLE SUMMARY</topic><topic>Salmonella</topic><topic>Salmonella enterica</topic><topic>Salmonella Typhimurium</topic><topic>Small intestine</topic><topic>Substrates</topic><topic>TLR4 protein</topic><topic>Toll-like receptors</topic><topic>Ulcerative 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Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Won Ho</au><au>Heithoff, Douglas M.</au><au>Aziz, Peter V.</au><au>Sperandio, Markus</au><au>Nizet, Victor</au><au>Mahan, Michael J.</au><au>Marth, Jamey D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Recurrent infection progressively disables host protection against intestinal inflammation</atitle><jtitle>Science (American Association for the Advancement of Science)</jtitle><addtitle>Science</addtitle><date>2017-12-22</date><risdate>2017</risdate><volume>358</volume><issue>6370</issue><spage>1588</spage><epage>1588</epage><pages>1588-1588</pages><issn>0036-8075</issn><eissn>1095-9203</eissn><abstract>Intestinal inflammation is the central pathological feature of colitis and the inflammatory bowel diseases. These syndromes arise from unidentified environmental factors. We found that recurrent nonlethal gastric infections of Gram-negative
Typhimurium (ST), a major source of human food poisoning, caused inflammation of murine intestinal tissue, predominantly the colon, which persisted after pathogen clearance and irreversibly escalated in severity with repeated infections. ST progressively disabled a host mechanism of protection by inducing endogenous neuraminidase activity, which accelerated the molecular aging and clearance of intestinal alkaline phosphatase (IAP). Disease was linked to a Toll-like receptor 4 (TLR4)-dependent mechanism of IAP desialylation with accumulation of the IAP substrate and TLR4 ligand, lipopolysaccharide-phosphate. The administration of IAP or the antiviral neuraminidase inhibitor zanamivir was therapeutic by maintaining IAP abundance and function.</abstract><cop>United States</cop><pub>American Association for the Advancement of Science</pub><pmid>29269445</pmid><doi>10.1126/science.aao5610</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-9323-1649</orcidid><orcidid>https://orcid.org/0000-0001-8954-2516</orcidid><orcidid>https://orcid.org/0000-0002-7689-3613</orcidid><orcidid>https://orcid.org/0000-0001-8957-100X</orcidid><orcidid>https://orcid.org/0000-0002-6090-7101</orcidid><orcidid>https://orcid.org/0000-0003-3847-0422</orcidid><oa>free_for_read</oa></addata></record> |
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| source | JSTOR Archive Collection A-Z Listing; American Association for the Advancement of Science |
| subjects | Accumulation Aging Alkaline phosphatase Animal tissues Augmentation Bacteria Bacterial infections Biodegradation Chronic infection Colon Crohn's Disease Diseases Disorders Duodenum Enterocytes Environmental factors Environmental Influences Exo-a-sialidase Food contamination Food contamination & poisoning Food poisoning Food production Food sources Foodborne diseases Human behavior Human populations Infections Inflammation Inflammatory bowel disease Inflammatory bowel diseases Ingestion Inhibition Inhibitors Life span Lipopolysaccharides Pathogens Phosphatase Phosphates Poisoning Recurrent infection RESEARCH ARTICLE SUMMARY Salmonella Salmonella enterica Salmonella Typhimurium Small intestine Substrates TLR4 protein Toll-like receptors Ulcerative colitis Zanamivir |
| title | Recurrent infection progressively disables host protection against intestinal inflammation |
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