Abstract
Undernourished mice infected (UI) submitted to low and long-lasting infections by Schistosoma mansoni are unable to develop the hepatic periportal fibrosis that is equivalent to Symmers’ fibrosis in humans. In this report, the effects of the host’s nutritional status on parasite (worm load, egg viability and maturation) and host (growth curves, biology, collagen synthesis and characteristics of the immunological response) were studied and these are considered as interdependent factors influencing the amount and distribution of fibrous tissue in hepatic periovular granulomas and portal spaces. The nutritional status of the host influenced the low body weight and low parasite burden detected in UI mice as well as the number, viability and maturation of released eggs. The reduced oviposition and increased number of degenerated or dead eggs were associated with low protein synthesis detected in deficient hosts, which likely induced the observed decrease in transformation growth factor (TGF)-β1 and liver collagen. Despite the reduced number of mature eggs in UI mice, the activation of TGF-β1 and hepatic stellate cells occurred regardless of the unviability of most miracidia, due to stimulation by fibrogenic proteins and eggshell glycoproteins. However, changes in the repair mechanisms influenced by the nutritional status in deficient animals may account for the decreased liver collagen detected in the present study.
Highlights
Mice that were experimentally infected by Schistosoma mansoni can develop two distinct and sometimes mixed histopathological patterns during the chronic stage of schistosomiasis: scattered small periovular granulomas with mild nonspecific reactive hepatitis and/or a concentration of circumoval granulomas causing fibrotic expansion and the development of thin fibrous tracts connecting portal spaces
Due to fibrogenic stimuli from antigens derived from miracidia bodies (Hang et al 1974) and, to a lesser extent, from the eggshells themselves, inflammatory cells and macrophages are activated and secrete fibrogenic cytokines such as transformation growth factor (TGF)-β1, interleukin (IL)-13 and other mediators, which contribute to the regulation of the inflammatory response as well as stimulate the activation of hepatic stellate cells (HSCs) known as pericytes, fat-storing cells or Ito’s cells (Geerts 2001, Gressner et al 2002)
Andreia Ferreira Barros et al Investigations of the interrelationships between schistosomiasis and host nutritional status have demonstrated that mice infected by S. mansoni and fed a low-protein diet develop, in the acute stage of the disease, small periovular granulomas with fewer inflammatory cells, reduced amounts of fibrous tissue in the liver and an inability to develop the murine “pipestem”-like fibrosis or periportal fibrosis (Coutinho et al 1997, 2003, 2007) as was seen in 30-50% of well-fed animals submitted to low and long-lasting infections (Warren 1966, Andrade & Cheever 1993)
Summary
Mice that were experimentally infected by Schistosoma mansoni can develop two distinct and sometimes mixed histopathological patterns during the chronic stage of schistosomiasis: scattered small periovular granulomas with mild nonspecific reactive hepatitis and/or a concentration of circumoval granulomas causing fibrotic expansion and the development of thin fibrous tracts connecting portal spaces (murine periportal fibrosis). All these variables (nutritional status, egg unviability, low fibrogenic cytokine response, low collagen synthesis) are likely interdependent factors that influence the amount and distribution of fibrous (collagen) tissue in the liver periovular granulomas and portal spaces, explaining the absence of development of the murine type of periportal schistosomal fibrosis in UI mice.
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