In adults, haemopoiesis is located in the bone marrow, where it is tightly regulated by cytokines and by a physical association of haemopoietic progenitors with the stroma. However, in pathological situations, haemopoiesis can be partly or fully dislodged to peripheral tissues. It is not clear which are the requirements for a given peripheral stroma to sustain haemopoiesis. Using the growth factor-dependent cell line FDC-P1, we have compared the myelopoietic capacities of a murine bone marrow-derived cell line S17, a liver inflammatory granuloma-derived stroma (GR) that sustains haemopoiesis, and normal skin fibroblasts (SF) that sustain neither survival nor proliferation of myeloid cells. All three stromas expressed mRNA for major haemopoietins with the exception of IL-3. Despite the incapacity of SF to sustain FDC-P1 cells, the biologically active GM-CSF could be recovered from all the studied stromas by treatment with high-salt buffers that release non-covalently bound molecules from stroma cells. Glycosaminoglycans purified from stromas had distinct effect on the GM-CSF-mediated proliferation of FDC-P1 cells: those purified from S17 and GR cells were stimulatory, whereas those obtained from SF cells were slightly stimulatory at low concentration, but inhibitory at the higher ones. We conclude that the quality of the stroma pericellular glycoconjugates is determinant for the ability of a given stroma to sustain myelopoiesis, even when biologically active haemopoietins are locally produced.

Galectin-3 is a β-galactoside-binding protein that has been shown to regulate pathophysiological processes, including cellular activation, differentiation and apoptosis. Recently, we showed that galectin-3 acts as a potent inhibitor of B cell differentiation into plasma cells. Here, we have investigated whether galectin-3 interferes with the lymphoid organization of B cell compartments in mesenteric lymph nodes (MLNs) during chronic schistosomiasis, using WT and galectin-3-/- mice. Schistosoma mansoni synthesizes GalNAcβ1-4(Fucα1-3)GlcNAc(Lac-DiNAc) structures (N-acetylgalactosamine β1-4 N-acetylglucosamine), which are known to interact with galectin-3 and elicit an intense humoral response. Antigens derived from the eggs and adult worms are continuously drained to MLNs and induce a polyclonal B cell activation. In the present work, we observed that chronically-infected galectin-3-/- mice exhibited a significant reduced amount of macrophages and B lymphocytes followed by drastic histological changes in B lymphocyte and plasma cell niches in the MLNs. The lack of galectin-3 favored an increase in the lymphoid follicle number, but made follicular cells more susceptible to apoptotic stimuli. There were an excessive quantity of apoptotic bodies, higher number of annexin V+/PI- cells, and reduced clearance of follicular apoptotic cells in the course of schistosomiasis. Here, we observed that galectin-3 was expressed in non-lymphoid follicular cells and its absence was associated with severe damage to tissue architecture. Thus, we convey new information on the role of galectin-3 in regulation of histological events associated with B lymphocyte and plasma cell niches, apoptosis, phagocytosis and cell cycle properties in the MLNs of mice challenged with S.mansoni.

There are several pathologies associated with the peritoneum, such as mesothelioma and peritonitis. Moreover, the peritoneum is widely used in ultrafiltration procedures, i.e., peritoneal dialysis, presenting advantages over hemodialysis. On the other hand, ultrafiltration failure may lead to dialysis-induced fibrosis and hypervolemia. Therefore, the pathophysiological study of this tissue is of extreme biomedical importance. Studies investigating the biology of the cells dwelling in the peritoneum wall provide evidence of their plasticity and progenitor features. For instance, both mesothelial and submesothelial cells present characteristics similar to mesenchymal stem cells, including osteogenic and adipogenic differentiation potential, support of extramedullary hematopoiesis, modulation of inflammatory responses, and regulation of tumor progression. Indeed, the participation of each cell type in peritoneal pathological and physiological phenomena is still under debate, especially regarding a possible differentiation pathway connecting these peritoneal cells. The primary aim of this review is to raise this discussion. In order to do so, we will firstly provide an overview of the peritoneum anatomy, histology, and ontology, and finally we will address how a better understanding of peritoneal cell biology may contribute to future cell therapy and tissue engineering approaches.

Galectin-3 is a β-galactoside-binding protein with an inhibitory role in B cell differentiation into plasma cells in distinct lymphoid tissues. We use a model of chronic schistosomiasis, a well-characterized experimental disease hallmarked by polyclonal B cell activation, in order to investigate the role of galectin-3 in controlling IgA production through peritoneal B1 cells. Chronically infected, galectin-3-deficient mice (Lgals3 −/− ) display peritoneal fluid hypercellularity, increased numbers of atypical peritoneal IgM + /IgA + B1a and B1b lymphocytes and histological disturbances in plasma cell niches when compared with Lgals3 + / + mice. Similar to our infection model, peritoneal B1 cells from uninfected Lgals3 −/− mice show enhanced switching to IgA after in vitro treatment with interleukin-5 plus transforming growth factor-β (IL-5 + TGF-β1). A higher number of IgA + B1a lymphocytes was found in the peritoneal cavity of Lgals3 −/− -uninfected mice at 1 week after i.p. injection of IL-5 + TGF-β1; this correlates with the increased levels of secreted IgA detected in the peritoneal fluid of these mice after cytokine treatment. Interestingly, a higher number of degranulated mast cells is present in the peritoneal cavity of uninfected and Schistosoma mansoni-infected Lgals3 −/− mice, indicating that, at least in part, mast cells account for the enhanced differentiation of B1 into IgAproducing B cells found in the absence of galectin-3. Thus, a novel role is revealed for galectin-3 in controlling the expression of surface IgA by peritoneal B1 lymphocytes; this might have important implications for manipulating the mucosal immune response.