Insights Into Toxocara canis-Induced Liver Fibrosis

Toxocara canis larvae migrate through the liver, where persistent tissue injury and immune-mediated inflammation may promote granuloma formation and fibrosis. This review summarizes the histopathological and imaging features, cellular and molecular mechanisms, clinical assessment, and potential reversibility of T. canis-induced liver fibrosis. Experimental evidence indicates that fibrosis is typically focal or multifocal and progresses from eosinophil-rich inflammation and fibrocellular granulomas to collagen-rich lesions, with a later predominance of collagen type I. Fibrogenesis involves hepatic stellate-cell activation within a TGF-β1-, IL-4/IL-13-, and alternatively activated macrophage-associated microenvironment. Toxocara excretory-secretory products, proteases, extracellular vesicles, and regulatory RNAs may further influence NF-κB/MAPK, NOD1/2-RIP2, JAK/STAT, and IL-33/ST2 signaling, although many proposed links remain indirect or unvalidated in the liver. Human evidence is limited mainly to imaging reports and small case series; the epidemiological contribution of toxocariasis to chronic fibrosis and cirrhosis therefore remains unknown. A preliminary murine study suggesting regression of chemically induced fibrosis after infection highlights the context-dependent nature of parasite-host interactions but requires independent confirmation. Standardized human studies and clinically relevant experimental models are needed to define disease burden, validate biomarkers, and identify safe adjunctive antifibrotic strategies.