Interaction and involvement of cellular adhesion molecules in the pathogenesis of Schistosomiasis mansoni

Parasites from genus Schistosoma currently infect more than 200 million people worldwide. Infection with Schistosoma mansoni causes intestinal schistosomiasis with geographical distribution across Africa, Middle East, Caribbean, Brazil, Venezuela and Suriname. People with Schistosomiasis mansoni suffer from a chronic disease as result of an exacerbated immune response to the eggs deposited in hepatic tissue. The presence of eggs in the tissue triggers the recruitment and activation of immune cells to wall off and isolate them from the rest of the organism. In this context, immune cells turn activated and increase the expression of cellular adhesion molecules (CAM), such as l-selectin and LFA-1, and DC-SIGN which through interaction with CAM expressed on activated endothelial vessels, help moving leukocytes quickly to the sites of infection (inflammation around the eggs), as a strategy to defend the organism from foreign invaders. Since the vertebrate host is not able to eliminate the foreign invader a granuloma formation take place in the tissue where the eggs are trapped, originating granulomas. Patients and mice with chronic schistosomiasis have increased levels of CAM in their circulation and egg-trapped tissue, which may contribute to the inflammatory process, granuloma formation and pathology aggravation. Here we systematically reviewed the findings raised over the last two decades that addressed the involvement of cellular adhesion molecules in the intestinal and hepatic inflammatory response and liver granuloma formation during Schistosomiasis mansoni. This review intends to contribute to the understanding of Schistosomiasis mansoni pathogenesis by discussing alterations and interactions in cellular adhesion molecules during the disease.