title: Differential expression of interleukin-5 mRNA+ cells and eosinophils in Nippostrongylus brasiliensis infection in resistant and susceptible strains of mice.
abstract: Interleukin (IL)-5 is produced by both T cells and eosinophils and has been implicated in lymphocyte and eosinophil differentiation and maturation. The extent to which differences in IL-5 expression contribute to genetic variability in parasite immunity was investigated by comparing eosinophilia, IgE production, mastocytosis and IL-5 mRNA+ cells following Nippostrongylus brasiliensis infection of resistant (BALB/c) and susceptible (C57BL/6) mice. In uninfected mice, IL-5 mRNA+ cells detected by in situ hybridization were distributed throughout the lamina propria and crypt regions of the small intestine in both strains, but were 1.5-fold higher in BALB/c than in C57BL/6 mice. Following N. brasiliensis infection, the numbers of IL-5 mRNA+ cells in BALB/c mice continued to increase until day 11 post-infection at which time they were more than 4-fold more numerous than in uninfected control mice of the same strain. In C57BL/6 mice, IL-5 mRNA+ cells reached peak numbers on day 7 post-infection, only 1.5-fold higher than uninfected controls, but the numbers began to decline thereafter. At all time points after day 5, the numbers of IL-5 mRNA+ cells in the gut of C57BL/6 mice were significantly lower than BALB/c mice. The differences in numbers of IL-5 mRNA+ cells induced by infection in each strain of mice correlated with changes in blood and intestinal eosinophilia, mastocytosis and IgE production and was reflected in differences in worm expulsion and egg counts. Although numbers of intestinal IgA-containing cells increased in both strains after infection, there was no difference between strains except at day 11 when there were significantly higher numbers in BALB/c mice than in C57BL/6 mice. These results suggest that IL-5 is an important regulatory factor determining host immunity to parasite infection and that differential regulation of IL-5 expression explains in part the observed strain differences with respect to parasite resistance.
authors.affiliation: Department of Veterinary Pathology, University of Sydney, Australia.
authors.forename: Y
authors.initials: Y
authors.lastname: Zhou
authors.forename: S
authors.initials: S
authors.lastname: Bao
authors.forename: T L
authors.initials: TL
authors.lastname: Rothwell
authors.forename: A J
authors.initials: AJ
authors.lastname: Husband
mesh_terms: D000818:Animals; D004804:Eosinophils / Q000502:physiology*; D005243:Feces / Q000469:parasitology; D007070:Immunoglobulin A / Q000032:analysis; D007073:Immunoglobulin E / Q000032:analysis; D015848:Interleukin-5 / Q000235:genetics*; D007422:Intestines / Q000276:immunology / Q000473:pathology; D008407:Mast Cells; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009559:Nippostrongylus; D012333:RNA, Messenger / Q000032:analysis*; D017206:Strongylida Infections / Q000276:immunology*
chemical_list: D007070:Immunoglobulin A; D015848:Interleukin-5; D012333:RNA, Messenger; D007073:Immunoglobulin E