Interleukin 5 (IL-5) is not required for expression of a Th2 response or host resistance mechanisms during murine schistosomiasis mansoni but does play a role in development of IL-4-producing non-T, non-B cells - PubMed (original) (raw)
Interleukin 5 (IL-5) is not required for expression of a Th2 response or host resistance mechanisms during murine schistosomiasis mansoni but does play a role in development of IL-4-producing non-T, non-B cells
L R Brunet et al. Infect Immun. 1999 Jun.
Abstract
During schistosomiasis, interleukin-5 (IL-5)-dependent eosinophil responses have been implicated in immunopathology, resistance to superinfection, synergistic interactions with chemotherapeutic agents, and the inductive phase of the egg-induced Th2 response. We examined these issues in IL-5-deficient (IL-5(-/-)) mice. IL-5(-/-) and wild-type (WT) mice were indistinguishable in terms of susceptibility to primary infections and the ability to resist secondary infections. Moreover, hepatic pathology was similar in both strains apart from a relative lack of eosinophils and, during chronic infection, a significantly larger mast cell component in the granulomas of IL-5(-/-) mice. Splenocyte cytokine production in response to soluble egg antigen (SEA) or anti-CD3 revealed no significant differences except for heightened tumor necrosis factor alpha production by cells from chronically infected IL-5(-/-) mice compared to WT animals. In contrast, ionomycin-stimulated non-B, non-T (NBNT) cells from IL-5(-/-) mice produced significantly smaller IL-4 amounts than did NBNT cells from WT animals. This difference was not apparent following plate-bound anti-immunoglobulin E or SEA stimulation. The absence of IL-5 failed to affect the induction of Th2 responses in naive mice. Peritoneal exudate cells recovered from egg-injected IL-5(-/-) or WT mice produced equivalent levels of IL-4 following restimulation with SEA or anti-CD3.
Figures
FIG. 1
Comparison of IL-4 cytokine levels from PEC of WT and IL-5−/− mice (three animals per group) injected 10 days earlier with either S. mansoni eggs or PBS. PEC were pooled and cultured for 72 h in duplicate wells in the presence of anti-IL-4R either alone, with SEA, or with plate-bound anti-CD3. Data are from one experiment; the experiment was repeated three times with similar results. Data are expressed as means ± standard errors.
FIG. 2
Comparison of IL-4 levels produced by NBNT cells of WT and IL-5−/− mice (at least three animals per group) infected with S. mansoni (8 weeks postinfection). NBNT cells were cultured for 24 h with PBS, SEA, plate-bound anti-IgE, or ionomycin. Results are from one experiment and are representative of data from three separate experiments. Data are expressed as means ± standard errors. An asterisk indicates P < 0.05 compared with WT animals.
FIG. 3
Comparison of resistance to superinfection in WT and IL-5−/− mice. Worm burdens in infected WT and IL-5−/− mice were determined after perfusion. Mice received a primary infection (group A; four WT and six IL-5−/− mice) primary and secondary infections (group B; five WT and five IL-5−/− mice), or a secondary infection (group C; six WT and six IL-5−/− mice). Resistance to reinfection was observed in both WT (61.4% ± 4.1%) and IL-5−/− (53.6% ± 10.2%) mice in group B. Data are expressed as means ± standard errors. An asterisk indicates P < 0.05 compared with groups receiving a challenge infection alone.
FIG. 4
Effect of praziquantel on worm burden in IL-5−/− and WT mice. Mice (three animals per group) were treated with praziquantel in carrier or with carrier alone. Data are expressed as means ± standard errors. Results are representative of two separate experiments. An asterisk indicates P < 0.05 compared with untreated groups.
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