Juglone as a Therapeutic Agent in Murine Coccidiosis: Enhancing Intestinal Recovery and Regulating Host Immune Responses.

Abstract

Coccidiosis, caused by Eimeria spp., significantly impacts gastrointestinal health and leads to economic losses. This study investigated juglone, a phenolic compound, as a potential treatment for mouse coccidiosis caused by Eimeria papillata. Twenty-five male Swiss albino mice were categorized into five groups: Group 1: non-infected, Group 2: juglone control (JG), Group 3: infected with 1,000 sporulated oocysts, Group 4: infected-treated with juglone (Infected + JG), and Group 5: infected-treated with anticoccidial drug, amprolium (Infected + ACD). Following 5 days of treatment, the mice were euthanized, and numerous analyses were performed such as growth performance, oocyst shedding, oxidative stress, histology, goblet cell response, and inflammation. Results showed that E. papillata infection significantly decreased body weight and feed intake, increased oocyst shedding, and elevated oxidative stress markers while reducing antioxidant enzyme levels. Histopathological analysis indicated severe intestinal damage, with intracellular parasitic stages and reduced goblet cell density and MUC-2 expression. Infection also heightened gene expression of inflammatory cytokines including tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), interleukin 1β (IL1β), and interleukin 10 (IL10). Juglone treatment effectively mitigated these negative effects, improving body weight and feed consumption, lowering oocyst shedding, and restoring antioxidant enzyme activity. It also repaired intestinal structure, enhanced goblet cell density and MUC-2 expression, as well as diminished inflammatory cytokines. The findings indicated that juglone significantly mitigates the pathological effects induced by E. papillata by decreasing parasite shedding, oxidative stress, inflammation, and modulating immune responses while facilitating intestinal recovery and enhancing overall health in infected mice.