title: CD4+ T-cell-dependent goblet cell proliferation and expulsion of Gymnophalloides seoi from the intestine of C57BL/6 mice.
abstract: Mechanisms for the spontaneous worm expulsion from the host intestine are not well understood in gastrointestinal trematode models. We studied the role of CD4+ T-helper cells in mediating goblet cell hyperplasia and expulsion of Gymnophalloides seoi from the intestines of C57BL/6 (resistant) and ICR (susceptible) mice. C57BL/6 mice expelled all G. seoi worms within 4 days post-infection (PI), while ICR mice did not completely expel worms until day 7 PI. This difference in worm expulsion was associated with high numbers of mucosal goblet cells in C57BL/6 mice along with alteration of the mucin quality, with changes in the terminal sugar chain and high levels of IL-4 and IL-5 mRNA expression in mesenteric lymph nodes. Adoptive transfer of mucosal CD4+ T-helper cells to syngeneic mice elicited strong goblet cell hyperplasia and a notably accelerated worm expulsion. However, this T-helper cell transfer had no relationship with the alteration of mucin quality. The results showed that CD4+ T-helper cells play an important role as a mediator of goblet cell hyperplasia, but not for functional activation of goblet cells. It is suggested that both T-cell dependent and independent mechanisms operate for expulsion of G. seoi from the mouse intestine.
authors.affiliation: Department of Parasitology, Korea University College of Medicine, Seoul 136-705, Korea.
authors.forename: Sang-Mee
authors.initials: SM
authors.lastname: Guk
authors.forename: Jun-Haeng
authors.initials: JH
authors.lastname: Lee
authors.forename: Hyo-Jin
authors.initials: HJ
authors.lastname: Kim
authors.forename: Won-Hee
authors.initials: WH
authors.lastname: Kim
authors.forename: Eun-Hee
authors.initials: EH
authors.lastname: Shin
authors.forename: Jong-Yil
authors.initials: JY
authors.lastname: Chai
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D049109:Cell Proliferation; D004198:Disease Susceptibility; D020397:Goblet Cells / Q000276:immunology* / Q000473:pathology; D006965:Hyperplasia / Q000276:immunology; D015847:Interleukin-4 / Q000235:genetics / Q000276:immunology; D015848:Interleukin-5 / Q000235:genetics / Q000276:immunology; D007411:Intestinal Diseases, Parasitic / Q000276:immunology* / Q000628:therapy; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008813:Mice, Inbred ICR; D009077:Mucins / Q000737:chemistry; D009093:Mucus / Q000737:chemistry / Q000276:immunology / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D013047:Specific Pathogen-Free Organisms; D018418:Th2 Cells / Q000276:immunology; D014200:Trematoda / Q000276:immunology*; D014201:Trematode Infections / Q000276:immunology* / Q000628:therapy
chemical_list: D015848:Interleukin-5; D009077:Mucins; D012333:RNA, Messenger; D015847:Interleukin-4