article · Biomedicines
Cryptosporidiosis is a significant diarrhoeal disease affecting humans and animals globally. This study examined the therapeutic potential of s-Methylcysteine against Cryptosporidium parvum infection in Swiss albino mice. Infected mice were treated with low or high doses of the compound over two weeks. The results showed that treatment led to lower parasite oocyst counts in faeces compared to untreated infected mice. Furthermore, s-Methylcysteine mitigated intestinal inflammation, reduced liver damage, and improved splenic tissue health in a dose-dependent manner. Treated animals demonstrated reduced levels of inflammatory cytokines, including tumour necrosis factor alpha, interleukin 6, and interferon gamma, alongside normalised liver enzymes. The compound also counteracted oxidative stress in the intestines by raising antioxidant levels such as glutathione and superoxide dismutase. Overall, the compound demonstrated protective effects across multiple organs during parasitic infection.
Cryptosporidium parvum causes severe diarrhoeal illness in humans and livestock, presenting substantial public health and veterinary challenges. Finding effective therapeutic candidates is critical because treatment options remain limited. Demonstrating that s-Methylcysteine can suppress parasite counts, reduce tissue pathology, and mitigate severe inflammatory and oxidative damage in an animal model provides a foundation for exploring new therapeutic strategies against this zoonotic infection.
This research could support the development of novel anti-parasitic therapeutics or supportive treatments for cryptosporidiosis in veterinary and human medicine. Pharmaceutical developers and animal health companies are the primary prospective users. Currently, the work represents early-stage in vivo research in a mouse model, meaning extensive pre-clinical testing, formulation optimisation, and formal clinical trials will be necessary before any real-world therapeutic application is realised.
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Cryptosporidiosis has been proposed to be one of the major causes of diarrhoeal disease in humans worldwide that possesses zoonotic concern. Thereby, this study investigated the potential effects of s-Methylcysteine (SMC) on the parasite in vivo followed by the measurement of cytokines, oxidative stress parameters, and an investigation of the major histopathological changes. Sixty male Swiss albino mice weighing 20-25 g were allocated equally into five groups and orally administered saline only (control), SMC only (SMC50) (50 mg/kg b.w.), and 10<sup>4</sup><i>Cryptosporidium parvum</i> oocysts per mouse via an esophageal tube (C + ve untreated). The fourth and fifth groups (C + SMC25, C + SMC50) administrated 10<sup>4</sup><i>C. parvum</i> oocysts combined with SMC25 (low dose) and 50 (high dose) mg/kg b.w., respectively. At days 7 and 14 post-infection (PI), the feces was collected from each group in order to count <i>C. parvum</i> oocysts. After two weeks of treatment, the animals were euthanized and the serum was collected for biochemical analysis. Next, the intestinal, spleen, and liver sections were dissected for histopathological examination. The results revealed lower oocyst numbers in the C + SMC25 and C + SMC50 groups compared to the infected untreated group. Moreover, higher doses of SMC treatment significantly reduced the enteritis induced by <i>C. parvum</i> in a dose-dependent manner. The hepatic lesions were also mitigated as demonstrated in C + SMC25 and C + SMC50 groups unlike the infected group via lowering the serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) enzymes and increasing albumin and globulin serum levels. SMC administration also reduced cytokines production (SAP, TNF-α, IL-6, and IFN-γ) mediated by <i>Cryptosporidium</i> infection in contrast to the infected untreated group. There were marked lymphoid depletion and amyloidosis observed in the infected untreated group, while the treated groups showed obvious increase in the lymphoid elements. Moreover, the scoring of intestinal parasites, hepatic, and splenic lesions in the SMC-treated groups exhibited significantly lower pathological lesions in different organs in a dose-dependent manner, compared to the infected untreated group. Our results also revealed a significant change in the malondialdehyde content with an elevation of glutathione and superoxide dismutase in the intestines collected from C + SMC25 and C + SMC50 mice relative to the untreated group. Taken together, our results indicated that SMC could be a promising effective compound for treating and declining <i>C. parvum</i> infestation via restoring structural alterations in different tissues, enhancing antioxidant enzymes, and suppressing the cytokines liberation.
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DOI: 10.3390/biomedicines8100423
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