Periportal fibrosis in schistosomiasis has been associated to the host immune response to parasite antigens. We evaluated the immune response in S. mansoni infected individuals with different degrees of periportal fibrosis. Cytokine and chemokines were measured in serum and in supernatants of PBMC cultures stimulated with the soluble adult worm (SWAP) or egg (SEA) antigens, using a sandwich ELISA. The levels of IL-5 in response to SEA were higher in individuals with moderate to severe fibrosis (310.9？pg/mL) compared to individuals without fibrosis (36.8？pg/mL; ). There was also a higher production of TNF-α in cultures stimulated with SWAP in patients with insipient fibrosis (1446？pg/mL) compared to those without fibrosis (756.1？pg/mL; ). The serum levels of IL-13 and MIP-1α were higher in subjects without fibrosis than in those with moderate to severe fibrosis. However a positive association between serum levels of IL-13, TNF-α, MIP-1α, and RANTES and S. mansoni parasite burden was found. From these data we conclude that IL-5 and TNF-α may participate in liver pathology in schistosomiasis. The positive association between IL-13, TNF-α, MIP-1α, and RANTES with parasite burden, however, might predict the development of liver pathology. 1. Introduction Schistosomiasis is a chronic parasitic infection that affects 200 million people in Africa, South America, and Asia and it is estimated that roughly 700 million people in the world live at risk of infection [1, 2]. In Brazil, the only species described is Schistosoma mansoni, and it is estimated that seven million people are infected by the parasite and about 25 million are at risk of infection [3]. The liver pathology results from the host immune response to parasite antigens from the eggs that become trapped in the portal venous system, and it is associated to the morbidity and mortality described in schistosomiasis [4]. The granuloma formation around S. mansoni eggs is complex and represents an interaction between products secreted by the miracidia, which are released from the egg and the host immune response [5]. Consequently, the granulomas formed act as barriers that prevent the dispersion of egg antigens of S. mansoni, and the consequent damage to the liver parenchyma. However, when caused by deposition of large numbers of eggs, the inflammatory process may progress to severe fibrosis, which leads to interruption of normal blood flow in the venous system to the sinusoids resulting in portal hypertension, hepatosplenomegaly, and formation of gastric and esophageal varices that can lead to bleeding and
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