Mechanism Anti-Tumor of IgA-based Delivery System on the Human Colostral Mononuclear Cells via Fcα Receptor

This study investigated the effect of anti-tumor of the IgA-based delivery system on the human colostral mononuclear cells via the Fcα receptor co-cultured with breast cancer cell lines (MCF-7-ATCC) and the colostrum mononuclear (MN) cells were collected from healthy mothers'.. MN cells and co-...

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Bibliographic Details
Published inBiointerface Research in Applied Chemistry Vol. 11; no. 6; pp. 14906 - 14917
Format Journal Article
LanguageEnglish
Published 15.12.2021
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Summary:This study investigated the effect of anti-tumor of the IgA-based delivery system on the human colostral mononuclear cells via the Fcα receptor co-cultured with breast cancer cell lines (MCF-7-ATCC) and the colostrum mononuclear (MN) cells were collected from healthy mothers'.. MN cells and co-culture (MN plus MCF-7 cells) were pre-incubated for 24 h with or without 100 ng. mL-1 secretory immunoglobulin A (SIgA), PEG microspheres (PEG), or 100 ng. mL-1 SIgA adsorbed to PEG microspheres (PEG-SIgA). Cells subsets of MN cells, chemokines (colostrum or culture supernatant), and apoptosis in the MN cells and co-culture were determined by flow cytometry. The highest percentage of mononuclear cells present in the colostrum was macrophages; approximately 80% of the cells expressed CD14+. There was an increase in the release of MIG in the co-culture of MN cells and MCF-7 cells and reduced IL-8 and MCP-1 in the presence of PEG-SIgA. The MN cells in co-culture with the MCF-7 cells, independent of treatment, showed the highest apoptosis index. The addition of a MoAb anti-human Fcreceptor resulted in a significant increase of IL-8 and MCP-1 release in co-culture and higher apoptosis rates, suggesting an interaction between sIgA and FcR mechanism anti-tumor of IgA-based delivery system. These data suggest that the control of chemokines release and apoptosis in co-culture incubated of PEG-SIgA may be one alternative mechanism involved in protection against the breast tumor.
ISSN:2069-5837
2069-5837
DOI:10.33263/BRIAC116.1490614917