Please use this identifier to cite or link to this item: https://doi.org/10.1128/IAI.02279-14
Title: Differential regulation of proinflammatory cytokine expression by mitogen-activated protein kinases in macrophages in response to intestinal parasite infection
Authors: Lim, M.X 
Png, C.W 
Tay, C.Y.B
Teo, J.D.W
Jiao, H 
Lehming, N 
Tan, K.S.W 
Zhang, Y 
Keywords: interleukin 1beta
interleukin 6
Janus kinase
mitogen activated protein kinase
mitogen activated protein kinase p38
tumor necrosis factor alpha
cytokine
mitogen activated protein kinase kinase
animal cell
animal experiment
animal model
Article
blastocystosis
cell viability
controlled study
cytokine response
enzyme activation
enzyme inhibition
enzyme phosphorylation
host pathogen interaction
intestine cell
intestine epithelium
macrophage
male
mouse
nonhuman
pathogenesis
protein expression
protein function
regulatory mechanism
signal transduction
upregulation
animal
antagonists and inhibitors
Blastocystis
blastocystosis
cell line
gene expression regulation
genetics
immunology
macrophage
metabolism
tissue culture technique
Animals
Blastocystis
Blastocystis Infections
Cell Line
Cytokines
Gene Expression Regulation
Macrophages
Mice
Mitogen-Activated Protein Kinase Kinases
Tissue Culture Techniques
Issue Date: 2014
Publisher: American Society for Microbiology
Citation: Lim, M.X, Png, C.W, Tay, C.Y.B, Teo, J.D.W, Jiao, H, Lehming, N, Tan, K.S.W, Zhang, Y (2014). Differential regulation of proinflammatory cytokine expression by mitogen-activated protein kinases in macrophages in response to intestinal parasite infection. Infection and Immunity 82 (11) : 4789-4801. ScholarBank@NUS Repository. https://doi.org/10.1128/IAI.02279-14
Abstract: Blastocystis is a common enteric protistan parasite that can cause acute, as well as chronic, infection and is associated with irritable bowel syndrome (IBS). However, the pathogenic status of Blastocystis infection remains unclear. In this study, we found that Blastocystis antigens induced abundant expression of proinflammatory cytokines, including interleukin 1? (IL-1?), IL-6, and tumor necrosis factor alpha (TNF-?), in mouse intestinal explants, in mouse colitis colon, and in macrophages. Further investigation utilizing RAW264.7 murine macrophages showed that Blastocystis treatment in RAW264.7 macrophages induced the activation of ERK, JNK, and p38, the three major groups of mammalian mitogen-activated protein (MAP) kinases that play essential roles in the expression of proinflammatory cytokines. ERK inhibition in macrophages significantly suppressed both mRNA and protein expression of IL-6 and TNF-? and mRNA expression of IL-1?. On the other hand, JNK inhibition resulted in reductions in both c-Jun and ERK activation and significant suppression of all three proinflammatory cytokines at both the mRNA and protein levels. Inhibition of p38 suppressed only IL-6 protein expression with no effect on the expression of IL-1? and TNF-?. Furthermore, we found that serine proteases produced by Blastocystis play an important role in the induction of ERK activation and proinflammatory cytokine expression by macrophages. Our study thus demonstrated for the first time that Blastocystis could induce the expression of various proinflammatory cytokines via the activation of MAP kinases and that infection with Blastocystis may contribute to the pathogenesis of inflammatory intestinal diseases through the activation of inflammatory pathways in host immune cells, such as macrophages. © 2014, American Society for Microbiology.
Source Title: Infection and Immunity
URI: https://scholarbank.nus.edu.sg/handle/10635/175313
ISSN: 0019-9567
DOI: 10.1128/IAI.02279-14
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