scholarly journals Effect of human breast milk on innate immune response: Up-regulation of bacterial pattern recognition receptors and innate cytokines in THP-1 monocytic cells

2021 ◽  
Vol 19 ◽  
pp. 205873922110261
Author(s):  
Won-Ho Hahn ◽  
Soon Young Shin ◽  
Jun Hwan Song ◽  
Nam Mi Kang

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 α, interleukin-1β, 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.

2018 ◽  
Vol 148 (11) ◽  
pp. 1860-1870 ◽  
Author(s):  
John J Miklavcic ◽  
Thomas M Badger ◽  
Anne K Bowlin ◽  
Katelin S Matazel ◽  
Mario A Cleves ◽  
...  

Viruses ◽  
2011 ◽  
Vol 3 (6) ◽  
pp. 920-940 ◽  
Author(s):  
Mikayla R. Thompson ◽  
John J. Kaminski ◽  
Evelyn A. Kurt-Jones ◽  
Katherine A. Fitzgerald

2014 ◽  
Vol 41 (2) ◽  
pp. 423-435 ◽  
Author(s):  
Brett M. Jakaitis ◽  
Patricia W. Denning

2001 ◽  
Vol 59 (5) ◽  
pp. 330-334 ◽  
Author(s):  
Karine Vidal ◽  
Mario O. Labéta ◽  
Eduardo J. Schiffrin ◽  
Anne Donnet-Hughes

2021 ◽  
Vol 22 (17) ◽  
pp. 9259
Author(s):  
Pradip Devhare ◽  
Mridula Madiyal ◽  
Chiranjay Mukhopadhyay ◽  
Shiran Shetty ◽  
Shamee Shastry

Hepatitis E virus (HEV) usually causes self-limiting acute hepatitis, but the disease can become chronic in immunocompromised individuals. HEV infection in pregnant women is reported to cause up to 30% mortality, especially in the third trimester. Additionally, extrahepatic manifestations like neuronal and renal diseases and pancreatitis are also reported during the course of HEV infection. The mechanism of HEV pathogenesis remains poorly understood. Innate immunity is the first line of defense triggered within minutes to hours after the first pathogenic insult. Growing evidence based on reverse genetics systems, in vitro cell culture models, and representative studies in animal models including non-human primates, has implicated the role of the host’s innate immune response during HEV infection. HEV persists in presence of interferons (IFNs) plausibly by evading cellular antiviral defense. This review summarizes our current understanding of recognizing HEV-associated molecular patterns by host cell Pattern Recognition Receptors (PRRs) in eliciting innate immune response during HEV infection as well as mechanisms of virus-mediated immune evasion.


Sign in / Sign up

Export Citation Format

Share Document