Immunomodulatory and anti-fibrotic effects of Toxocara canis infection in a murine model of thioacetamide-induced chronic hepatic fibrosis.

Chronic hepatic fibrosis is a serious result of chronic extracellular matrix (ECM) accumulation due to repeated liver injury from varied causes such as viruses, alcohol and chemicals. Toxocaral hepatitis, however, is brought about by inflammation resulting from migrating larvae of Toxocara canis (T. canis). Researchers have not yet explored the interaction between thioacetamide (TAA) induced and hepatic toxocariasis. In this experiment, the effect of these larvae as a potential safe vector that carries glycoconjugate antigens for treatment of liver fibrosis investigated in a model of chronic TAA intoxication. Chronic hepatic fibrosis induced in mice by 8 weeks intraperitoneal treatment with TAA. Hepatic larva migrans established over two weeks by oral administration of 1000 third-stage larvated eggs. In T. canis infected groups after establishment of hepatic fibrosis (TAA/T. canis), alternatively activated M2 macrophage polarization against fibrosis retained. However, compared to TAA injected groups, the M2 macrophage clusters significantly decreased (p-value <0.001).. Furthermore, TAA/T. canis groups had a significant decrease in hepatic collagen I and III fiber depositions compared to TAA injected groups (p value <0.001). By Batts-Ludwig scoring system, histopathological alterations observed in liver grading and staging. Thus, T. canis larvae can exhibit anti-inflammatory and antifibrotic activity in chronic liver injury. Such achievement is most likely influenced by immunomodulatory mechanisms, possibly through macrophage phenotypes modulation and suppression of ECM buildup. More studies will be necessary to advance novel antifibrotic strategies by means of parasite antigens.