Abstract
BackgroundGalectin-3 is known to be a lectin that plays an important role in inflammatory processes, acting as pro-inflammatory mediator in activation and migration of neutrophils and macrophages, as well as in the phagocytic function of these cells. The injection of mineral oils into the peritoneal cavity of mice, such as 2, 6, 10, 14-tetramethylpentadecane (pristane), induce a chronic granulomatous inflammatory reaction which is rich in macrophages, B cells and peritoneal plasma cells known as oil granuloma. In addition, this inflammatory microenvironment provided by oil granulomas is also an important site of plasmacytoma induction, which are dependent on cytokine production and cellular mobilization.Here, we have analyzed the role of galectin-3 in inflammatory cells mobilization and organization after pristane injection characterizing granulomatous reaction through the formation of oil granulomas.ResultsIn galectin-3 deficient mice (gal-3−/−), the mobilization of inflammatory cells, between peritoneal cavity and bone marrow, was responsible for the formation of disorganized oil granulomas, which presented scattered cells, large necrotic areas and low amounts of extracellular matrix. The production of inflammatory cytokines partially explained the distribution of cells through peritoneal cavity, since high levels of IL-6 in gal-3−/− mice led to drastically reduction of B1 cells. The previous pro-inflammatory status of these animals also explains the excess of cell death and disruption of oil granulomas architecture.ConclusionsOur data indicate, for the first time, that the disruption in the inflammatory cells migration in the absence of galectin-3 is a crucial event in the formation and organization of oil granulomas.Electronic supplementary materialThe online version of this article (doi:10.1186/s12865-015-0133-9) contains supplementary material, which is available to authorized users.
Highlights
Galectin-3 is known to be a lectin that plays an important role in inflammatory processes, acting as pro-inflammatory mediator in activation and migration of neutrophils and macrophages, as well as in the phagocytic function of these cells
Considering that galectin-3 deficient mice present a delay in hematopoietic cells differentiation and mobilization, we investigated the bone marrow and peritoneal cavity at 7 days and 60 days after pristane injection, comparing to noninjected control animals
In contrast to gal-3−/−, wild type (WT) animals presented an increase in CD5 + CD4+ T lymphocytes in bone marrow (Fig. 1c), accompanied by the increase of this population in the peritoneal cavity (Fig. 1d)
Summary
Galectin-3 is known to be a lectin that plays an important role in inflammatory processes, acting as pro-inflammatory mediator in activation and migration of neutrophils and macrophages, as well as in the phagocytic function of these cells. The injection of mineral oils into the peritoneal cavity of mice, such as 2, 6, 10, 14-tetramethylpentadecane (pristane), induce a chronic granulomatous inflammatory reaction which is rich in macrophages, B cells and peritoneal plasma cells known as oil granuloma This inflammatory microenvironment provided by oil granulomas is an important site of plasmacytoma induction, which are dependent on cytokine production and cellular mobilization. Pristane induces a continuous intraperitoneal chronic inflammation followed by oil-granuloma formation and plasma cell tumors, known as plasmacytoma [10,11,12] These granulomas are frequently adhered to peritoneal structures correlated to vigorous immune response, autoantibody production and clinical manifestations resembling systemic lupus erythematous [13]
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