extract protects pigeons from-like-triggered inflammatory dysregulation.

Abstract

BACKGROUND: Coccidiosis, caused byspecies, is a major enteric disease in birds, with-like isolates frequently inducing severe intestinal lesions, diarrhea, and reduced weight gain in pigeons. Conventional anticoccidial drugs face limitations due to resistance, residue concerns, and environmental impact, highlighting the need for alternative strategies.(myrrh) is a resinous plant extract rich in bioactive compounds with antioxidant, antimicrobial, antiparasitic, and anti-inflammatory properties. This study evaluated the protective effects ofresin in pigeons experimentally infected with-like isolates. METHODS: Resin ofwas collected from Riyadh, Saudi Arabia, authenticated, and extracted with 70% methanol to prepare a crude extract (MyE). Its chemical composition was characterized using GC-MS. A laboratory strain of-like oocysts was propagated in pigeons, sporulated, and used for experimental infection. Twenty-five pigeons were randomly assigned to five groups: uninfected control, uninfected + myrrh extract (MyE), infected control, infected + MyE, and infected + amprolium (standard drug). MyE and amprolium treatments were administered orally for 5 days post-infection. Parasitological, histological, immunohistochemical (NF-κB and IFN-γ), gene expression (MUC2, IL-1β, IL-10, IFN-γ, and TNF-α), and cytokine (IL-10 and TNF-α) analyses were conducted. RESULTS: In this study, myrrh resin was methanol-extracted and characterized by GC-MS, revealing 29 phytochemical components. Experimental infection of pigeons with-like oocysts resulted in peak fecal oocyst shedding (~5.25 × 10oocysts/g.feces), extensive development of intracellular parasite stages (meronts, gamonts, and developing oocysts), a marked reduction in goblet cell numbers, and elevated intestinal inflammatory responses, including increased NF-κB and IFN-γ immunoreactivity, as well as upregulated mRNA expression of IL-1β, IL-10, IFN-γ, and TNF-α. Oral administration of MyE significantly suppressed oocyst shedding by 60%, reduced the number of intracellular parasitic stages, restored goblet cell counts, and downregulated both gene and protein levels of pro-inflammatory markers while enhancing MUC2 expression, indicating effective modulation of-induced intestinal damage and inflammatory dysregulation. CONCLUSION: These findings demonstrate thatextract effectively mitigates-induced intestinal damage, inflammation, and immune dysregulation, highlighting its potential as a natural, plant-based intervention for managing pigeon coccidiosis.