About this Research Topic
Liver fibrosis is characterized by the excessive accumulation of extracellular matrix components, leading to scarring and impaired liver function. Traditionally linked to viral infections, alcohol abuse, and metabolic disorders, recent evidence highlights the significant role parasitic infections play in the development and progression of liver fibrosis. This Special issue will highlight how these infections contribute to fibrosis and discuss new therapeutic pathways for management.
Parasitic diseases such as schistosomiasis, caused by Schistosoma species, are particularly relevant due to their global prevalence and association with chronic liver disease. Schistosoma mansoni and Schistosoma japonicum primarily affect the hepatic portal system, leading to portal hypertension and fibrotic changes in the liver. The immune response triggered by these parasites is complex; while it aims to control infection, it can also result in tissue damage through chronic inflammation.
Schistosome eggs deposited in the liver induce a robust inflammatory response characterized by lymphocyte infiltration, macrophage activation, and cytokine release. Key pro-fibrotic cytokines like transforming growth factor-beta (TGF-β) promote stellate cell activation—crucial players in collagen deposition during fibrogenesis. Chronic exposure to these inflammatory mediators perpetuates a cycle of tissue injury that culminates in fibrosis.
Other parasitic diseases such as echinococcosis (caused by Echinococcus granulosus) can also lead to significant hepatic complications. Hydatid cysts formed in the liver may cause mechanical obstruction or rupture, resulting in acute inflammation and potential secondary fibrosis.
Understanding this interplay between parasitic infections and liver fibrosis opens avenues for innovative therapeutic strategies. Traditional management focuses on antiparasitic treatments but often fails to address persistent fibrotic changes after eradication. One promising approach involves targeting the host's immune response with anti-inflammatory agents to mitigate tissue damage from chronic infection. Additionally, antifibrotic therapies like pirfenidone or nintedanib could be repurposed for treating liver fibrosis associated with parasitic infections.
In conclusion, recognizing the role of parasitic infections like schistosomiasis and echinococcosis in liver fibrosis is crucial for developing comprehensive management strategies. Future research should delve deeper into host-parasite interactions while exploring therapeutic avenues addressing both infection control and fibrotic processes simultaneously.
Researchers and practitioners are invited to join this critical conversation, sharing insights and solutions for advancing our understanding of liver fibrosis linked to parasitic infections.
Parasitic diseases such as schistosomiasis, caused by Schistosoma species, are particularly relevant due to their global prevalence and association with chronic liver disease. Schistosoma mansoni and Schistosoma japonicum primarily affect the hepatic portal system, leading to portal hypertension and fibrotic changes in the liver. The immune response triggered by these parasites is complex; while it aims to control infection, it can also result in tissue damage through chronic inflammation.
Schistosome eggs deposited in the liver induce a robust inflammatory response characterized by lymphocyte infiltration, macrophage activation, and cytokine release. Key pro-fibrotic cytokines like transforming growth factor-beta (TGF-β) promote stellate cell activation—crucial players in collagen deposition during fibrogenesis. Chronic exposure to these inflammatory mediators perpetuates a cycle of tissue injury that culminates in fibrosis.
Other parasitic diseases such as echinococcosis (caused by Echinococcus granulosus) can also lead to significant hepatic complications. Hydatid cysts formed in the liver may cause mechanical obstruction or rupture, resulting in acute inflammation and potential secondary fibrosis.
Understanding this interplay between parasitic infections and liver fibrosis opens avenues for innovative therapeutic strategies. Traditional management focuses on antiparasitic treatments but often fails to address persistent fibrotic changes after eradication. One promising approach involves targeting the host's immune response with anti-inflammatory agents to mitigate tissue damage from chronic infection. Additionally, antifibrotic therapies like pirfenidone or nintedanib could be repurposed for treating liver fibrosis associated with parasitic infections.
In conclusion, recognizing the role of parasitic infections like schistosomiasis and echinococcosis in liver fibrosis is crucial for developing comprehensive management strategies. Future research should delve deeper into host-parasite interactions while exploring therapeutic avenues addressing both infection control and fibrotic processes simultaneously.
Researchers and practitioners are invited to join this critical conversation, sharing insights and solutions for advancing our understanding of liver fibrosis linked to parasitic infections.
Keywords: Schistosomiasis, liver fibrosis, hepatocellular carcinoma, HCC, portal hypertension, bile ducts, nematodes, epidemiology, TGF-beta, PDGF, cytokines, chemokines, experimental models, clinics
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