Jacalin drives macrophage polarization toward an anti-tumor M1-like phenotype

Abstract

Event Abstract Back to Event Jacalin drives macrophage polarization toward an anti-tumor M1-like phenotype Gabriela Pereira-da-Silva1, 2*, Cláudia D. Polli2, Thais H. Geraldino2, Luciana C. Veronez2, Luciana P. Ruas2 and Maria Cristina Roque-Barreira3 1 Escola de Enfermagem de Ribeirão Preto, Universidade de São Paulo, Enfermagem Materno-Infantil e Saúde Pública, Brazil 2 Programa de Pós-graduação em Imunologia Básica e Aplicada. Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Brazil 3 Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Biologia Celular e Molecular, Brazil Tumor-associated macrophages (TAMs) have an ambiguous and complex role in the carcinogenic process, since these cells can be polarized into different phenotypes by the tumor microenvironment. As the interactions between tumor cells and TAMs involve several players, a better understanding of the function and regulation of TAMs is crucial to drive their differentiation into cells with an anti-tumor phenotype. In this study, we investigated the modulation of macrophage tumoricidal activities by jacalin. The lectin bound to macrophage surface through its carbohydrate recognition domains, and induced cytokine production by these cells. Jacalin stimulation increased the expression of TNF-α, IL-1β and MIP-1α mRNA. As measured by ELISA, higher levels of TNF, IL-6, IL-12, IL-1β and IL-10 were detected in the supernatant from jacalin-stimulated macrophages. Given that pro-inflammatory cytokines were predominantly produced by macrophages in response to stimulation with jacalin, we next investigated whether NF-κB signaling is activated by the lectin. We found that jacalin was able to activate the transcription factor. The results obtained indicate that the lectin polarize macrophages toward the pro-inflammatory, anti-tumor M1-like phenotype. Therefore, we studied the tumoricidal activities of jacalin-stimulated macrophages. Incubation of HT-29 or MCF-7 cells with supernatants from macrophages stimulated with jacalin resulted in a reduction of cell viability, as assessed by MTT assays. Furthermore, flow cytometric analysis showed that the reduction of cell viability was due to apoptosis of tumor cells. Taken together, these results indicate that jacalin, through its ability to exert a pro-inflammatory activity, can direct macrophages to an anti-tumor phenotype. Financial Support: Fundação de Amparo à Pesquisa do Estado de São Paulo – FAPESP.