{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T13:10:15Z","timestamp":1773321015627,"version":"3.50.1"},"reference-count":22,"publisher":"Cambridge University Press (CUP)","issue":"2","license":[{"start":{"date-parts":[[2024,4,12]],"date-time":"2024-04-12T00:00:00Z","timestamp":1712880000000},"content-version":"unspecified","delay-in-days":7621,"URL":"https:\/\/www.cambridge.org\/core\/terms"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Helminthol."],"published-print":{"date-parts":[[2003,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Comparisons were made of the immune and inflammatory responses of four strains of inbred mice to infection with the intestinal nematodes <jats:italic>Trichinella spiralis<\/jats:italic> and <jats:italic>Nippostrongylus brasiliensis<\/jats:italic> to determine whether genetically determined \u2018high responsiveness\u2019 to infection, seen most clearly in intestinal responses, is independent of the parasite concerned and necessarily correlated with protection. The time course of infection was followed by counting adult worms at intervals after infection. Mucosal mast cells and Paneth cell numbers were determined as indices of the intestinal inflammatory response. Levels of IgG2a and IgG1 antibodies and of the cytokines IFN-\u03b3 and IL-5 released from <jats:italic>in vitro<\/jats:italic>-stimulated mesenteric node lymphocytes were measured to assess type 1 and type 2 responses. NIH and CBA mice were the most resistant to <jats:italic>T. spiralis<\/jats:italic> and <jats:italic>N. brasiliensis<\/jats:italic> respectively, resistance in each case being correlated with the most intense intestinal inflammatory responses. C57BL\/10 (B10) and B10.BR were the least resistant to <jats:italic>T. spiralis<\/jats:italic>, but were as resistant as CBA to <jats:italic>N. brasiliensis<\/jats:italic>, despite their intestinal inflammatory responses to both parasites being much lower than the other two strains. Mice infected with <jats:italic>T. spiralis<\/jats:italic> made the expected switch from a type 1 (IFN-\u03b3) to a type 2 (IL-5) response between days 2 and 8, and there were no significant differences in levels of these cytokines between the strains. In contrast, when infected with <jats:italic>N. brasiliensis<\/jats:italic>, CBA showed an IFN-\u03b3 response at day 4, all strains switching to IL-5 by day 8 and NIH mice releasing the greatest amount of IL-5. The results indicate that the \u2018high responder\u2019 phenotype to intestinal nematode infection is in part determined by host characteristics, but is also determined by the parasite concerned \u2013 seen most clearly by the differences between NIH and CBA when infected with <jats:italic>T. spiralis<\/jats:italic> and <jats:italic>N. brasiliensis<\/jats:italic>. The fact that \u2018low responder\u2019 B10 background mice were more resistant to <jats:italic>N. brasiliensis<\/jats:italic> than \u2018high responder\u2019 NIH implies that each parasite elicits a particular pattern of protective host responses, rather than parasites being differentially susceptible to the same response profile.<\/jats:p>","DOI":"10.1079\/joh2003175","type":"journal-article","created":{"date-parts":[[2003,5,22]],"date-time":"2003-05-22T21:50:12Z","timestamp":1053640212000},"page":"119-124","source":"Crossref","is-referenced-by-count":9,"title":["Responses of inbred mouse strains to infection with intestinal nematodes"],"prefix":"10.1017","volume":"77","author":[{"given":"M.S.","family":"Dehlawi","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P.K.","family":"Goyal","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"56","published-online":{"date-parts":[[2024,4,12]]},"reference":[{"key":"S0022149X00702343_ref012","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.147.4.1387"},{"key":"S0022149X00702343_ref010","doi-asserted-by":"publisher","DOI":"10.1079\/9780851994239.0373"},{"key":"S0022149X00702343_ref003","doi-asserted-by":"publisher","DOI":"10.1079\/JOH2001111"},{"key":"S0022149X00702343_ref021","doi-asserted-by":"publisher","DOI":"10.1017\/S0031182000048472"},{"key":"S0022149X00702343_ref011","doi-asserted-by":"publisher","DOI":"10.1159\/000233037"},{"key":"S0022149X00702343_ref004","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830271011"},{"key":"S0022149X00702343_ref001","first-page":"331","article-title":"Genetic factors controlling the intestinal mast cell response in mice infected with Trichinella spiralis","volume":"49","author":"Alizadeh","year":"1983","journal-title":"Clinical and Experimental Immunology"},{"key":"S0022149X00702343_ref016","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.164.4.2046"},{"key":"S0022149X00702343_ref006","doi-asserted-by":"publisher","DOI":"10.1016\/S1383-5769(02)00002-8"},{"key":"S0022149X00702343_ref017","first-page":"343","article-title":"Immunological relationships during primary infection with Heligmosomoides polygyrus","volume":"107","author":"Wahid","year":"1993","journal-title":"Regulation of fast responder phenotype by H-2 and non-H-2 genes. Parasitology"},{"key":"S0022149X00702343_ref020","first-page":"239","article-title":"Genetic control of eosinophilia","volume":"51","author":"Wakelin","year":"1983","journal-title":"Mouse strain variation in response to antigens of parasite origin. Clinical and Experimental Immunology"},{"key":"S0022149X00702343_ref002","doi-asserted-by":"publisher","DOI":"10.1079\/9780851994239.0331"},{"key":"S0022149X00702343_ref013","doi-asserted-by":"publisher","DOI":"10.1017\/S0031182000081063"},{"key":"S0022149X00702343_ref018","first-page":"85","article-title":"Genetic control of immunity to parasites","volume":"2","author":"Wakelin","year":"1980","journal-title":"Infection with Trichinella spiralis in inbred and congenic mice showing rapid and slow responses to infection. Parasite Immunology"},{"key":"S0022149X00702343_ref014","doi-asserted-by":"publisher","DOI":"10.1017\/S0031182000059758"},{"key":"S0022149X00702343_ref015","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)80477-X"},{"key":"S0022149X00702343_ref008","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2567.1998.00412.x"},{"key":"S0022149X00702343_ref022","doi-asserted-by":"publisher","DOI":"10.2307\/3280858"},{"key":"S0022149X00702343_ref007","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-3024.1994.tb00330.x"},{"key":"S0022149X00702343_ref009","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2249.2001.01589.x"},{"key":"S0022149X00702343_ref005","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.15.1.505"},{"key":"S0022149X00702343_ref019","first-page":"153","volume-title":"(Eds) Genetics of resistance to bacterial and parasitic infection","author":"Wakelin","year":"1988"}],"container-title":["Journal of Helminthology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.cambridge.org\/core\/services\/aop-cambridge-core\/content\/view\/S0022149X00702343","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,4,12]],"date-time":"2024-04-12T02:20:53Z","timestamp":1712888453000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.cambridge.org\/core\/product\/identifier\/S0022149X00702343\/type\/journal_article"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2003,6]]},"references-count":22,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2003,6]]}},"alternative-id":["S0022149X00702343"],"URL":"https:\/\/doi.org\/10.1079\/joh2003175","relation":{},"ISSN":["0022-149X","1475-2697"],"issn-type":[{"value":"0022-149X","type":"print"},{"value":"1475-2697","type":"electronic"}],"subject":[],"published":{"date-parts":[[2003,6]]}}}