Dynamics Of IL-10 Levels Among Trichinella Spiralis-Infected Mice

Background: Trichinellosis is a foodborne zoonotic disease caused by nematodes (roundworms) of the genus Trichinella, mainly Trichinella spiralis. It possesses the capability of infecting humans and a wide range of animals, including domestic pigs, wild boars, rats, and horses.Objective: This study aimed to elucidate the temporal dynamics of interleukin-10 (IL-10) during Trichinella spiralis infection in an experimental murine model. Methods: A total of 40 female Swiss albino mice (CD1 strain), aged 6–8 weeks and weighing 20–25 grams, were randomly divided into five equal groups (n = 8 per group): a non-infected control group (G1) and four infected groups (G2–G5) that each received a standardized dose of larvae. Infected groups were euthanized at different time points—Day 3 (G2), Day 7 (G3), Day 14 (G4), and Day 28 (G5) post-infection. At each endpoint, comprehensive evaluations were performed, including parasitological quantification of adult worms from the intestine and muscle-stage larvae, detailed histopathological examination of intestinal and skeletal muscle tissues, and quantitative measurement of serum interleukin-10 (IL-10) to assess host immune response during infection.Results: Infected mice exhibited a significant, time-dependent increase in serum IL-10 levels, with a marked early rise at 3 days post-infection (PI) that peaked by day 28 (P < 0.001), followed by a tendency toward plateauing during the chronic phase, indicating early immune activation with subsequent regulatory modulation. Parasitological assessment revealed a progressive increase in adult intestinal worm burden during the enteral phase, followed by the establishment of a substantial muscle larval load by day 28 PI. Histopathological examination corroborated these findings, demonstrating progressive intestinal mucosal damage in the early phase of infection and extensive larval encystation with prominent inflammatory infiltration in skeletal muscle during the chronic stage.