Do Previous Influenza and Mastitis Infections Change the Gene Expressions of Immune T Cell Surface Markers Present in Human Milk?

• Published in: Current developments in nutrition 2021-06, Vol.5 (Supplement_2), p.736-736
• Main Authors: Demers-Mathieu, Veronique, DaPra, Ciera, Medo, Elena
• Format: Article
• Language: English
• Subjects: Maternal, Perinatal and Pediatric Nutrition
• ISSN: 2475-2991; 2475-2991
• DOI: 10.1093/cdn/nzab046_033

The function of neonatal T cells is reduced compared to adult T cells. Human milk T cells may be transferred to the breastfed infant and compensate for their immature T cells. This study investigated the impact of mastitis and influenza post-infections (1–4 months) on T cell surface markers’ gene expressions in human milk. Gene expressions of CD4, CD44, CD8A, CCR6, CCR7, CD62L, CXCR3, CXCR5, and CD25 were determined in milk samples from 7 women with mastitis, 7 women with influenza, and 9 women without infection during the last year. The concentrations of Th cytokines (IL-4, IL-17, IFN-g, IL-2, and TNF-b) were also determined. The gene expression in milk from women with influenza infection had lower CCR7 (naïve T cells) and higher CD8A (cytotoxic T cells), CD44 and CD62L (activated/memory T cells) than mothers without infection. Gene expression in milk from mothers with mastitis had higher CD4 (Th cells) and lower CCR6 (Th17 cells) than mothers without mastitis. Milk from mothers with previous infections in the past 1–4 months had higher gene expression of CD4, CD8A, CD44, and CD62L, and lower CCR7 and CCR6 (Th17 cells) than mothers without infection. Mastitis or influenza did not affect the concentrations of cytokine-related T cells in human milk, indicating the return to their regular composition of immune regulatory mediators. These findings suggest that mothers with previous influenza infections may transfer high human milk-activated/memory T cells to their infants. Whether this transfer of antigen-experienced T cells enhances infants’ protection against infection remains to be investigated. The authors (VDM, CD, and ED) disclosed receipt of the financial support from Medolac Laboratories for the conduct of the study.