We previously demonstrated that mice subjected to a hypoproteinic diet showed milder chronic lesions on infection with Schistosoma mansoni than normally fed mice. Here we compare the immune response of well-nourished and undernourished mice with chronic S. mansoni infection. The proliferative response and cytokine (IFN-gamma and IL-5) production of splenocytes from undernourished mice against the soluble egg antigen (SEA) of S. mansoni or concanavalin A was similar to that of well-nourished mice. The levels of SEA-specific IgG1, IgG2b and IgG3 antibodies were significantly higher in the sera of well-nourished mice in comparison with undernourished mice. Undernourished animals also exhibited diminished periovular granuloma size compared to well-nourished infected controls. Our results support the importance of host nutritional status in the humoral immune response of mice and its effects on the development of periovular granulomas in malnourished animals infected with S. mansoni.

A histological, morphometric and immunocytochemical study of schistosomal periovular granulomas in the liver and intestines of mice revealed that intestinal granulomas are smaller and contain less collagen than those in the liver. After curative treatment intestinal granulomas undergo a relatively more rapid resorption, although the general pattern of collagen degradation apparently does not differ from that observed in the liver. Tendency to form scattered, usually isolated granulomas that are only mildly fibrogenic, coupled with a well-balanced process of resorption appear as the explanation why intestinal fibrosis is not an outstanding feature of schistosomiasis as it is in the liver.

Resumo Objetivou-se avaliar novos biomateriais fosfatados para regeneração de defeito ósseo crítico. Distribuíram-se 45 ratos Wistar em três grupos: CON (sem implantação de biomaterial), FCB (grânulos de fosfato de cálcio bifásico: fosfato tricálcico tipo β, β-TCP/pirofosfato de cálcio) e FCB/BV (FCB/vidro bioativo fosfatado), avaliados aos 15, 45 e 120 dias de pós-operatório. No grupo CON, observaram-se neoformação óssea restrita às bordas ósseas e preenchimento do defeito por delgado tecido conjuntivo fibroso. Em FCB e FCB/BV, os grânulos preencheram toda a extensão do defeito e apresentaram maior fragmentação em FCB/BV. A neoformação óssea foi mais evidente no FCB. De permeio às partículas dos biomateriais formou-se um tecido conjuntivo frouxo, que evoluiu para fibroso em FCB. Os biomateriais desencadearam discreta reação inflamatória crônica granulomatosa, que se tornou inconspícua. Conclui-se que os materiais foram biocompatíveis, atuaram como arcabouços tridimensionais, apresentaram potencial osteocondutor e favoreceram a regeneração óssea, principalmente FCB. A adição do vidro bioativo aumentou a biodegradabilidade de FCB/BV.

Introduction: The pathogenesis of septal hepatic fibrosis, induced in rats by Capillaria hepatica infection, was studied with the aid of a large collection of stored paraffin blocks, representative of the different evolutive phases of fibrosis which appeared in 100% of infected rats. Methods: Studies were conducted involving histology, immunohistochemistry, immunofluorescence and morphometric methods, in order to observe the dynamic behavior of the cellular and matrix components of fibrosis, over a one year period of evolution. Results: Observation verified that septal fibrosis originates from several portal spaces simultaneously. Its origin and progression involve blood vessel proliferation (angiogenesis), multiplication of actinpositive cells (pericytes and myofibroblasts) and progressive collagen deposition. By the end of 4-5 months, a progressive decrease in all these components was observed, when signs of regression of septal fibrosis became more evident over time. Conclusions: Besides indicating the fundamental role played by angiogenesis in the pathogenesis of fibrosis, these morphological data concerning the dynamics of this C. hepatica experimental model proved to be adequate for future investigations regarding the functional aspects of fibrosis induction, progression and regression.