Activation of macrophage mediated host defense against Salmonella typhimurium by Morus alba L

The innate immune system plays a crucial role in the initiation and subsequent direction of adaptive immune responses, as well as in the removal of pathogens that have been targeted by an adaptive immune response. L. was reported to have immunostimulatory properties that might protect against infect...

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Bibliographic Details
Published in:Food & nutrition research 2018-02, Vol.62, p.1-10
Main Authors: Chang, BoYoon, Koo, BongSeong, Lee, HyeonCheol, Oh, Joa Sub, Kim, SungYeon
Format: Article
Language:English
Subjects:
Adaptive immunity
Antibiotics
Bacteria
Bacterial infections
Cell activation
Cytokines
Flavonoids
immune defense
Immune response
Immune system
Immunology
Immunostimulation
Infections
Infectious diseases
Innate immunity
Interferon
Interleukin 12
Lethal dose
Leukocytes (neutrophilic)
Life span
Lymphocytes T
macrophage
Macrophages
Mice
Monocytes
Morus alba
Morus alba L
Original
Penicillin
Peritoneum
Phagocytosis
Rodents
Salmonella
Salmonella Typhimurium
Signal transduction
Sublethal dosage
TLR4
TLR4 protein
Toll-like receptors
Tumor necrosis factor-TNF
Tumor necrosis factor-α
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Summary:The innate immune system plays a crucial role in the initiation and subsequent direction of adaptive immune responses, as well as in the removal of pathogens that have been targeted by an adaptive immune response. L. was reported to have immunostimulatory properties that might protect against infectious diseases. However, this possibility has not yet been explored. The present study investigated the protective and immune-enhancing ability of L. against infectious disease and the mechanisms involved. To investigate the immune-enhancing effects of L., we used a bacterial infection model. The lifespan of mice infected with a lethal dose of (1 × 10 colony forming units - CFU) was significantly extended when they were administered L. Furthermore, L. activated macrophages, monocytes, and neutrophils and induced Th1 cytokines (IL-12, IFN-γ, TNF-α) in mice infected with a sublethal dose (1 × 10 CFU) of . L. significantly stimulated the uptake of bacteria into peritoneal macrophages as indicated by increased phagocytosis. Peritoneal macrophages derived from C3H/HeJ mice significantly inhibited L. induced NO production and TNF-α secretion compared with peritoneal macrophages derived from C3H/HeN mice. These results suggest that the innate immune activity of L. against bacterial infection in mice occurs through activation of the TLR4 signaling pathway.
ISSN:1654-661X
1654-661X
DOI:10.29219/fnr.v62.1289