Complementarily, given the advancement of high-throughput analysis tools such as next-generation sequencing, the comprehensive identification and clinical validation of host factors that might regulate hepatic fibrosis individually and/or collectively in some schistosomiasis-diseased individuals should be further pursued to provide more candidates for therapeutic evaluation

Complementarily, given the advancement of high-throughput analysis tools such as next-generation sequencing, the comprehensive identification and clinical validation of host factors that might regulate hepatic fibrosis individually and/or collectively in some schistosomiasis-diseased individuals should be further pursued to provide more candidates for therapeutic evaluation. Author contributions JN and SK defined the topic and designed the search strategy. mesenteric veins of the intestinal tract causing hepatosplenic schistosomiasis leading to Eslicarbazepine Acetate progressive liver fibrosis and portal hypertension (6). The immunology of schistosomiasis has progressed through the use of murine and non-human primate animal models, Eslicarbazepine Acetate corroborating in many cases with human data (7, 8). The disease morbidity is driven by schistosome eggs and not directly by adult worms (9). Upon infection, a fraction of the produced eggs is not excreted by the host and become permanently lodged in organs such as the intestines and liver (and or in the bladder and urogenital system (worms, particularly, reside within the mesenteric veins where females release on average 340 eggs per female per day with rates ranging between 190 and 658 eggs depending of the strain; this rate is higher for (22). More than 50% of eggs are carried to the liver by the portal circulation where they become trapped in the liver sinusoids (13). This is associated with the production of profibrotic Eslicarbazepine Acetate cytokines (23, 24). Both murine and human infections with or reveal aHSCs as the key drivers of hepatic fibrosis (25, 26). In the context of hepatosplenic schistosomiasis, an accumulating number of studies have reported Rabbit polyclonal to ZNF346 disparities between prevalence of infection and levels of tissue morbidity, characterized by the stage of advancement of hepatic fibrosis and the presence/absence of periportal fibrosis (11, 27C30). For example, despite a higher prevalence and intensity of infections, in Kenya (31, 32) and Mali (33) compared to Egypt (31, 32) and Sudan (34, 35), the prevalence of periportal fibrosis in endemic sites is considerably higher in the latter countries. Furthermore, even adjacent communities with comparable levels of infection, exhibit considerable differences in their prevalence of periportal fibrosis (11). Although some possible explanations for these observed differential morbidity patterns could well be the different duration, intensity of infection (32, 35), the host genetic background (36, 37) has been increasingly suggested as a central basis for these discrepancies (11, 30, 38C42) as it Eslicarbazepine Acetate appears that hepatic fibrosis occurs and progresses dissimilarly in schistosomiasis-diseased individuals with the same extrinsic and biosocial risk factors. In fact, in another recent study conducted in a village of rural Cameroon endemic for hepatosplenic schistosomiasis, participants with similar egg excretion profiles, similar age/gender distribution, same length of residence in the area, same frequency and Eslicarbazepine Acetate duration of daily exposure to contaminated water, same social status and within similar dates of reinfection (i.e., previously treated with Praziquantel at the same time) as judged by the average number of eggs excreted in the feces, displayed a strikingly different stage of advancement of schistosomiasis-driven hepatic fibrosis (43). This indicated that, although the presence of the parasite eggs prompt the onset of liver lesions, host factors might indeed play a defining role in the regulation of liver fibrosis during hepatosplenic schistosomiasis. With the well documented and successful concept of host-directed therapies against diseases now including infectious diseases (37, 39, 42, 44, 45), the recollection of known host-derived factors that potentially play a role in the control of liver fibrosis during human schistosomiasis (pro- or anti-fibrotic) is long overdue for research on schistosomiasis in particular and all fibroproliferative diseases in general. Humans factors associated with liver fibrosis during schistosomiasis The present compilation of host factors reported to associate with the progression/resistance to hepatic fibrosis during Human hepatosplenic schistosomiasis (Table ?(Table11 and Figure ?Figure1)1) should facilitate subsequent investigations aimed at validating their role as hepatic fibrosis monitoring tools.