Balamuthia mandrillaris is a causative agent of granulomatous amebic encephalitis, a rare but often fatal condition. To investigate the role of T helper (Th) cell subsets in the immune response against B. mandrillaris, we examined 3 mouse strains with distinct immunological profiles: C57BL/6 (Th1-dominant), BALB/c (Th2-dominant), and ICR (balanced Th1/Th2). Mice were infected intranasally with 1×105 amoebae. Body weight and neurologic symtoms were monitored weekly, and cytokine expression was assessed biweekly over 6 weeks. Minimal weight loss and no mortality were observed in C57BL/6 mice, whereas BALB/c and ICR mice exhibited significant early and delayed mortality, respectively. Interleukin-17A expression was notably elevated in C57BL/6 mice compared with the other strains. These findings indicate that a robust Th17 response, particularly interleukin-17A production, is a critical component of the host defense against B. mandrillaris infection.
Innate lymphoid cells (ILCs) are key players during an immune response at the mucosal surfaces, such as lung, skin, and gastrointestinal tract. Giardia lamblia is an extracellular protozoan pathogen that inhabits the human small intestine. In this study, ILCs prepared from the lamina propria of mouse small intestine were incubated with G. lamblia trophozoites. Transcriptional changes in G. lamblia-exposed ILCs resulted in identification of activation of several immune pathways. Secretion of interleukin (IL)-17A, IL-17F, IL-1β, and interferon-γ was increased, whereas levels of IL-13, IL-5, and IL22, was maintained or reduced upon exposure to G. lamblia. Goup 3 ILC (ILC3) was found to be dominant amongst the ILCs, and increased significantly upon co-cultivation with G. lamblia trophozoites. Oral inoculation of G. lamblia trophozoites into mice resulted in their presence in the small intestine, of which, the highest number of parasites was detected at the 5 days-post infection. Increased ILC3 was observed amongst the ILC population at the 5 days-post infection. These findings indicate that ILC3 from the lamina propria secretes IL-17 in response to G. lamblia, leading to the intestinal pathology observed in giardiasis.
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