Coccidial infections are known to cause cytotoxicity and oxidative damage within intestinal tissues in their hosts. The current work was designed to study the protective effects of palm pollen aqueous extract (PPE) against Eimeria papillata-induced intestinal damage in mice. Coccidiosis was induced in male albino mice via oral inoculation with 1.5×103 sporulated E. papillata oocysts. Infected mice were administered PPE as daily dose of 150 mg/kg for five successive days. On day 5 p.i., animals were scarified and jejunum samples were prepared for paraffin embedded histological sections and jejunal homogenate was used for determination of oxidative damage biomarkers. The data show that E. papillata infection in mice induced marked histological alterations within jejunum tissue in the form of inflammation, vacuolation of the epithelium and destruction of some villi with concurrent decrease in goblet cell number. Upon treatment of infected mice with PPE, the histological injury score within infected jejunum tissue was reduced by 60% and goblet cell number was significantly restored near its control values. Also, the results showed that E. papillata induced a state of oxidative damage and disturbance in antioxidant system within jejunum tissue. The infection enhanced lipid peroxidation and protein oxidation processes as evidenced by the significant increase in hydrogen peroxide, malondialdehyde and protein carbonyl contents. The antioxidant enzymes, catalse and glutathione peroxidase were decreased in their activities as a consequence of the infection with concurrent reduction in reduced glutathione level and total antioxidant capacity within infected jejunum tissue. Moreover, mediators of nitric oxide pathway of inflammation (tumor necrosis factor-α, inducible nitric oxide synthase and nitric oxide) were significantly increased after infection. Collectively, treatment of E. papillata infected mice with PPE led to reduction in lipid peroxidation and protein oxidation processes, with concureent decrease in the activities of mediators of nitric oxide pathway of inflammation; in addition to the significant enhancement of the jejunal antioxidant system.