Differential development of oil granulomas induced by pristane injection in galectin-3 deficient mice. (December 2015)

• Record Type: Journal Article
• Authors: Brand, Camila; da Costa, Thayse; Bernardes, Emerson; Machado, Camila; Andrade, Leonardo; Chammas, Roger; de Oliveira, Felipe; El-Cheikh, Márcia
• Is Part Of: BMC immunology. Volume 16:Number 1(2015)
• Page Start: 1
• Page End: 13
• Publication Date: 2015-12
• Subjects: Pristane -- Oil granuloma -- Bone marrow -- Peritoneal cavity -- Inflammation; Immunology -- Periodicals; Immune System -- Periodicals; Immunity -- Periodicals; Immune System Diseases -- Periodicals; Immunologic Techniques -- Periodicals; 616.07905
• DOI: 10.1186/s12865-015-0133-9
• Languages: English
• ISSNs: 1471-2172

Abstract

Abstract Background 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. 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. Results In 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. Conclusions Our 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.