Toll-Like Receptor 2 and<i>Muc2</i>Expression on Human Intestinal Epithelial Cells by Gymnophalloides seoi Adult Antigen

Lee, Ki-Doek; Guk, Sang-Mee; Chai, Jong-Yil

doi:10.1645/ge-2195.1

Cited by 28 publications

(20 citation statements)

References 33 publications

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“…The increase in the expression level of TLR2 and TLR4 has been observed in human cholangiocytes stimulated with Cryptosporidium parvum (Chen et al, 2005). In addition, the expression of TLR2 and TLR4 in human intestinal epithelial cells has been induced by intestinal trematode Gymnophalloides seoi (Lee et al, 2010) and in dendritic cells and macrophages by soluble extracts from Schistosoma mansoni eggs (Kane et al, 2008). In murine neurocysticercosis, all TLRs (TLR1-TLR13) have been shown to be up-regulated and differentially expressed among the various central nervous system cell types and infiltrating leukocytes (Mishra et al, 2008(Mishra et al, , 2006.…”

Section: Discussionmentioning

confidence: 99%

Hymenolepis diminuta: Analysis of the expression of Toll-like receptor genes (TLR2 and TLR4) in the small and large intestines of rats. Part II

Kosik-Bogacka

Wojtkowiak-Giera

Kolasa

et al. 2013

Experimental Parasitology

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Section: Discussionmentioning

confidence: 99%

Hymenolepis diminuta: Analysis of the expression of Toll-like receptor genes (TLR2 and TLR4) in the small and large intestines of rats. Part II

Kosik-Bogacka

Wojtkowiak-Giera

Kolasa

et al. 2013

Experimental Parasitology

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“…GC mucins are also an important component of innate defense against T. muris infection, because mucin gene deficient mice have impaired host resistance against parasite infection [30]. In human intestinal epithelial cells cultured in vitro, MUC2 gene expression is upregulated upon stimulation with G. seoi antigen [26]. In the present study, GC hyperplasia was closely associated with expulsion of G. seoi worms regardless of the mouse strain, which was consistent with our previous reports [23,24].…”

Section: Discussionmentioning

confidence: 99%

“…CD4 + T-cells were important in regulating the GC responses in G. seoi -infected C57BL/6 mice [24]. Toll-like receptor 2 and MUC2 gene are highly expressed on intestinal epithelial cells stimulated with G. seoi antigen suggesting their roles in host defense mechanisms [26]. However, no studies have been performed on intestinal epithelial cell turnover and intestinal smooth muscle contraction in G. seoi -infected mice.…”

Section: Introductionmentioning

confidence: 99%

Increased Intestinal Epithelial Cell Turnover and Intestinal Motility in Gymnophalloides seoi-Infected C57BL/6 Mice

et al. 2014

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The changing patterns of goblet cell hyperplasia, intestinal epithelial cell turnover, and intestinal motility were studied in ICR and C57BL/6 mice infected with Gymnophalloides seoi (Digenea: Gymnophallidae). Whereas ICR mice retained G. seoi worms until day 7 post-infection (PI), C57BL/6 mice showed a rapid worm expulsion within day 3 PI. Immunosuppression with Depo-Medrol significantly delayed the worm expulsion in C57BL/6 mice. Goblet cell counts were increased in both strains of mice, peaking at day 1 PI in C57BL/6 mice and slowly increasing until day 7 PI in ICR mice. In C57BL/6 mice infected with G. seoi, newly proliferating intestinal epithelial cells were remarkably increased in the crypt, and the increase was the highest at day 1 PI. However, in ICR mice, newly proliferating intestinal epithelial cells increased slowly from day 1 to day 7 PI. Intestinal motility was increased in G. seoi-infected mice, and its chronological pattern was highly correlated with the worm load in both strains of mice. Meanwhile, immunosuppression of C57BL/6 mice abrogated the goblet cell proliferation, reduced the epithelial cell proliferation, and suppressed the intestinal motility. Goblet cell hyperplasia, increased intestinal epithelial cell turnover, and increased intestinal motility should be important mucosal defense mechanisms in G. seoi-infected C57BL/6 mice.

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“…Lee, et al [282] studied the effects of Gymnophalloides seoi antigen on the host's intestinal epithelial cells, to determine expression of Toll-like receptors (TLRs) and mucinrelated (MUC) genes on a human intestinal epithelial cell line (HT29 cells) induced by Gymnophalloides (G) seoi. They reported that TLR2 and MUC2 expression on human intestinal epithelial cells were up regulated by G. seoi antigen.…”

Section: Intestine Inflammatory Bowel Disease (Ibd)mentioning

confidence: 99%

“…Regulation of microflora composition (e.g., by probiotics and prebiotics) offers the possibility to influence the development of mucosal and systemic immunity but it can play a role also in prevention and treatment of some diseases. Disruption of this negative feedback pathway, perhaps by variants in MUC1, might contribute to inflammatory bowel disease in patients [286,281,282] Jostins et al [287] expanded on the knowledge of relevant pathways by undertaking a meta-analysis of Crohn's disease and ulcerative colitis genome-wide association scans and observed considerable overlap between susceptibility loci for IBD and mycobacterial infection. Gene co-expression network analysis emphasized this relationship, with pathways shared between host responses to mycobacteria and those predisposing to IBD.…”

Section: Intestine Inflammatory Bowel Disease (Ibd)mentioning

confidence: 99%

Exploring the role and diversity of mucins in health and disease with special insight into non-communicable diseases

et al. 2015

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Mucins are major glycoprotein components of the mucus that coats the surfaces of cells lining the respiratory, digestive, gastrointestinal and urogenital tracts. They function to protect epithelial cells from infection, dehydration and physical or chemical injury, as well as to aid the passage of materials through a tract i.e., lubrication. They are also implicated in the pathogenesis of benign and malignant diseases of secretory epithelial cells. In Human there are two types of mucins, membrane-bound and secreted that are originated from mucous producing goblet cells localized in the epithelial cell layer or in mucous producing glands and encoded by MUC gene. Mucins belong to a heterogeneous family of high molecular weight proteins composed of a long peptidic chain with a large number of tandem repeats that form the so-called mucin domain. The molecular weight is generally high, ranging between 0.2 and 10 million Dalton and all mucins contain one or more domains which are highly glycosylated. The size and number of repeats vary between mucins and the genetic polymorphism represents number of repeats (VNTR polymorphisms), which means the size of individual mucins can differ substantially between individuals which can be used as markers. In human it is only MUC1 and MUC7 that have mucin domains with less than 40% serine and threonine which in turn could reduce number of PTS domains. Mucins can be considered as powerful two-edged sword, as its normal function protects from unwanted substances and organisms at an arm's length while, malfunction of mucus may be an important factor in human diseases. In this review we have unearthed the current status of different mucin proteins in understanding its role and function in various non-communicable diseases in human with special reference to its organ specific locations. The findings described in this review may be of direct relevance to the major research area in biomedicine with reference to mucin and mucin associated diseases.

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Toll-Like Receptor 2 andMuc2Expression on Human Intestinal Epithelial Cells by Gymnophalloides seoi Adult Antigen

Cited by 28 publications

References 33 publications

Hymenolepis diminuta: Analysis of the expression of Toll-like receptor genes (TLR2 and TLR4) in the small and large intestines of rats. Part II

Hymenolepis diminuta: Analysis of the expression of Toll-like receptor genes (TLR2 and TLR4) in the small and large intestines of rats. Part II

Increased Intestinal Epithelial Cell Turnover and Intestinal Motility in Gymnophalloides seoi-Infected C57BL/6 Mice

Exploring the role and diversity of mucins in health and disease with special insight into non-communicable diseases

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