Effect of human breast milk on innate immune response: Up-regulation of bacterial pattern recognition receptors and innate cytokines in THP-1 monocytic cells
- Abstract
- Human breast milk (HBM) contains many bioactive components that protect infants from various microorganisms. Pattern recognition receptors on phagocytic cells recognize microbial pathogens and promote the innate immune system. This study aimed to evaluate the effect of HBM on the expression of pattern recognition receptors and innate cytokines in the monocytic cell line THP-1 and the phagocytic activity of RAW264.7 macrophages. Expression levels of specific mRNAs in THP-1 cells were quantitated using reverse transcription-polymerase chain reaction. Phagocytic activity was measured by fluorescence microscopy to detect the uptake of fluorescent dye-labeled carboxylate-modified polystyrene latex beads in RAW264.7 macrophages. HBM stimulated the phagocytic activity of RAW264.7 macrophages. HBM increased mRNA expression of pattern recognition receptors, including the cluster of differentiation 14 and toll-like receptor 2 and 4, and various innate cytokines, including tumor necrosis factor alpha, interleukin-1 beta, C-X-C motif chemokine 8, and C-C motif chemokine ligand 2, in THP-1 monocytic cells. Furthermore, milk oligosaccharides in HBM, such as lacto-N-fucopentaose I, enhanced the expression of pattern recognition receptors and various innate cytokines. HBM is able to modulate the innate immune response by upregulating the expression of pattern recognition receptors and various innate cytokines in monocytes/macrophages.
- All Author(s)
- W. H. Hahn
; S. Y. Shin
; J. H. Song
; N. M. Kang
- Issued Date
- 2021
- Type
- Article
- Keyword
- cluster of differentiation 14; human breast milk; human milk oligosaccharides; innate immunity; pattern recognition receptor; toll-like receptor
- ISSN
- 1721-727X
- Citation Title
- European Journal of Inflammation
- Citation Volume
- 19
- Citation Start Page
- 1
- Citation End Page
- 12
- Language(ISO)
- eng
- DOI
- 10.1177/20587392211026107
- URI
- http://schca-ir.schmc.ac.kr/handle/2022.oak/2653
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