title: Immune response and inhibitory effect of ketotifen on the BALB/c and C3H/HeN mice infected with Echinostoma hortense.
abstract: Although Echinostoma hortense is one of the intestinal trematodes with a high infection rate in South Korea, the exact immune response against E. hortense infection has yet to be fully investigated. In the present study, we investigated differential susceptibilities in two different strains of micenamely, BALB/c (H-2d) and C3H/HeN (H-2k) mice. Likewise, we investigated the effects of ketotifen, an antiallergic drug, on the immune response against E. hortense infection. The worm recovery rate of the C3H/HeN mice was much higher than that of the BALB/c mice. The messenger ribonucleic acid (mRNA) expressions of interleukin (IL)-4 and IL-5 in the BALB/c mice were stronger than that of the C3H/HeN mice after E. hortense infection, but IL-1beta and tumor necrosis factor (TNF)-alpha expressions in the BALB/c mice were weaker than that of the C3H/HeN mice after E. hortense infection. The number of goblet cells and eosinophils increased after E. hortense infection in the BALB/c and the C3H/HeN mice. The worm recovery rate was higher and lasted longer in the ketotifen-treated mice in comparison to the untreated mice. Ketotifen suppressed the mRNA expression of IL-4 and IL-5 in the BALB/c mice, but did not in the C3H/HeN mice. The IL-1beta expressions were inhibited by ketotifen in the two strains, but TNF-alpha expression was inhibited in the C3H/HeN mice after ketotifen treatment. In addition, ketotifen inhibited the increase in eosinophils and goblet cells in varying degrees, depending on the strain. In summary, the immune sensitivity against E. hortense depends on the species of the host. The ketotifen treatment administered on the infected mice differently blocked the immune response against E. hortense infection.
authors.affiliation: Department of Biomedical Laboratory Science, Institute of Health Science, College of Health Science, Yonsei University, Wonju, 220-701, Republic of Korea.
authors.forename: Yong Suk
authors.initials: YS
authors.lastname: Ryang
authors.forename: Eun Ju
authors.initials: EJ
authors.lastname: Yang
authors.forename: Jeong-Lye
authors.initials: JL
authors.lastname: Kim
authors.forename: Kyu-Jae
authors.initials: KJ
authors.lastname: Lee
authors.forename: Ho-Joong
authors.initials: HJ
authors.lastname: Sung
authors.forename: Jong-Bae
authors.initials: JB
authors.lastname: Kim
authors.forename: In Sik
authors.initials: IS
authors.lastname: Kim
mesh_terms: D000818:Animals; D018926:Anti-Allergic Agents / Q000008:administration & dosage / Q000627:therapeutic use; D016207:Cytokines / Q000378:metabolism; D004449:Echinostoma / Q000302:isolation & purification / Q000472:pathogenicity*; D004451:Echinostomiasis / Q000188:drug therapy* / Q000276:immunology* / Q000469:parasitology; D004804:Eosinophils / Q000276:immunology; D005260:Female; D020397:Goblet Cells / Q000276:immunology; D007665:Ketotifen / Q000008:administration & dosage / Q000627:therapeutic use; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D013045:Species Specificity; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D016896:Treatment Outcome
chemical_list: D018926:Anti-Allergic Agents; D016207:Cytokines; D007665:Ketotifen