Schistosome Egg Migration: Mechanisms, Pathogenesis and Host Immune Responses

Abstract

Many parasitic worms possess complex and intriguing life cycles, and schistosomes are no exception. To exit the human body and progress to their successive snail host, Schistosoma mansoni eggs must migrate from the mesenteric vessels, across the intestinal wall and into the feces. This process is complex and not always successful. A vast proportion of eggs fail to leave their definite host, instead becoming lodged within intestinal or hepatic tissue, where they can evoke potentially life-threatening pathology. Thus, to maximize the likelihood of successful egg passage whilst minimizing host pathology, intriguing egg exit strategies have evolved. Notably, schistosomes actively exert counter-inflammatory influences on the host immune system, discreetly compromise endothelial and epithelial barriers, and modulate granuloma formation around transiting eggs, which is instrumental to their migration. In this review, we discuss new developments in our understanding of schistosome egg migration, with an emphasis on S. mansoni and the intestine, and outline the host-parasite interactions that are thought to make this process possible. In addition, we explore the potential immune implications of egg penetration and discuss the long-term consequences for the host of unsuccessful egg transit, such as fibrosis, co-infection and cancer development.

Uncovering Biological Application of Brazilian Green Propolis: A Phenotypic Screening againstSchistosoma mansoni

“…The obtained concentrations of artepillin C (1), caffeic acid (2), coumaric acid (3) and drupanin (4) were 115.87 μg mL À 1 , 35.10 μg mL À 1 , 19.89 μg mL À 1 and 42.36 μg mL À 1 , respectively, which corresponded to 14.67 %, 4.29 %, 2.50 % and 5.29 % confirming the previously reported high contents of these compounds in Brazilian green propolis. [29] The RSD values for artepillin C (1), caffeic acid (2), coumaric acid (3) and drupanin (4) concentrations were below 5 % and the means obtained in different days did not differ statistically (p < 0.05). .…”

“…[2] The intestinal form of the disease is mainly caused by Schistosoma mansoni and Schistosoma japonicum parasites, which is characterized by a process of granulomatous inflammation in response to the trapped eggs in the intestine and liver of the host. [3] Although 90 % of infected individuals are asymptomatic, [4] another portion of the infected individuals shows a typical chronic condition characterized by liver fibrosis, portal hypertension and hepatosplenomegaly. [5] In 2017, the World Health Organization estimated that approximately 220 million people worldwide needed preventive treatment, and that praziquantel (PZQ) is the only treatment effective against schistosomiasis.…”

TLR7 Modulated T Cell Response in the Mesenteric Lymph Node of Schistosoma japonicum-Infected C57BL/6 Mice

“…Schistosoma eggs must migrate from the mesenteric vessels, across the intestinal wall and into the feces. A vast proportion of eggs fail to leave their definite host, instead becoming lodged within intestinal or hepatic tissue, where they could evoke potentially lifethreatening pathology [7].…”

Soluble CD83 alleviates experimental allergic rhinitis through modulating antigen-specific Th2 cell property

“…Current understanding about the pathogenesis of Th2 polarization is that this disorder is caused by multiple factors. For example, nematode infection is a common cause of Th2 polarization [23]. Microbial products are another cause to induce Th2 polarization, such as cholera toxin is used in the development of food allergy animal model [24].…”