Bovine TLR2 and TLR4 mediate Cryptosporidium parvum recognition in bovine intestinal epithelial cells

2015 ◽  
Vol 85 ◽  
pp. 29-34 ◽  
Author(s):  
Zhengtao Yang ◽  
Yunhe Fu ◽  
Pengtao Gong ◽  
Jingtong Zheng ◽  
Li Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cryptosporidium Parvum ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Bovine Intestinal Epithelial Cells

scholarly journals Decreased SLC26A3 expression and function in intestinal epithelial cells in response to Cryptosporidium parvum infection

2019 ◽  
Vol 317 (6) ◽  
pp. C1205-C1212 ◽  
Author(s):  
Anoop Kumar ◽  
Dulari Jayawardena ◽  
Arivarasu N. Anbazhagan ◽  
Ishita Chatterjee ◽  
Shubha Priyamvada ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cryptosporidium Parvum ◽  
Diarrheal Disease ◽  
Intestinal Epithelial Cells ◽  
Ex Vivo ◽  
Jejunal Mucosa ◽  
Intestinal Epithelial ◽  
Chloride Absorption ◽  
And Function

The protozoan parasite Cryptosporidium parvum (CP) causes cryptosporidiosis, a diarrheal disease worldwide. Infection in immunocompetent hosts typically results in acute, self-limiting, or recurrent diarrhea. However, in immunocompromised individuals infection can cause fulminant diarrhea, extraintestinal manifestations, and death. To date, the mechanisms underlying CP-induced diarrheal pathogenesis are poorly understood. Diarrheal diseases most commonly involve increased secretion and/or decreased absorption of fluid and electrolytes. We and others have previously shown impaired chloride absorption in infectious diarrhea due to dysregulation of SLC26A3 [downregulated in adenoma (DRA)], the human intestinal apical membrane Cl−/[Formula: see text] exchanger protein. However, there are no studies on the effects of CP infection on DRA activity. Therefore, we examined the expression and function of DRA in intestinal epithelial cells in response to CP infection in vitro and in vivo. CP infection (0.5 × 106 oocysts/well in 24-well plates, 24 h) of Caco-2 cell monolayers significantly decreased Cl−/[Formula: see text] exchange activity (measured as DIDS-sensitive 125I uptake) as well as DRA mRNA and protein levels. Substantial downregulation of DRA mRNA and protein was also observed following CP infection ex vivo in mouse enteroid-derived monolayers and in vivo in the ileal and jejunal mucosa of C57BL/6 mice for 24 h. However, at 48 h after infection in vivo, the effects on DRA mRNA and protein were attenuated and at 5 days after infection DRA returned to normal levels. Our results suggest that impaired chloride absorption due to downregulation of DRA could be one of the contributing factors to CP-induced acute, self-limiting diarrhea in immunocompetent hosts.

Sa1776 Decreased SLC26A3 Expression and Function in Intestinal Epithelial Cells in Response to Cryptosporidium parvum Infection

2015 ◽  
Vol 148 (4) ◽  
pp. S-329
Author(s):  
Anoop Kumar ◽  
Ishita Chatterjee ◽  
Waddah A. Alrefai ◽  
Pradeep K. Dudeja ◽  
Alip Borthakur
Keyword(s):  
Epithelial Cells ◽  
Cryptosporidium Parvum ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
And Function

Su1942 – Cryptosporidium Parvum Infection Induces Autophagy in Intestinal Epithelial Cells

2019 ◽  
Vol 156 (6) ◽  
pp. S-668
Author(s):  
Shubha Priyamvada ◽  
Anoop Kumar ◽  
Arivarasu Natarajan Anbazhagan ◽  
Dulari Jayawardena ◽  
Waddah A. Alrefai ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cryptosporidium Parvum ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

scholarly journals SHP-2 Mediates Cryptosporidium parvum Infectivity in Human Intestinal Epithelial Cells

PLoS ONE ◽  
2015 ◽  
Vol 10 (11) ◽  
pp. e0142219 ◽  
Author(s):  
Eunice A. Varughese ◽  
Susan Kasper ◽  
Emily M. Anneken ◽  
Jagjit S. Yadav
Keyword(s):  
Epithelial Cells ◽  
Cryptosporidium Parvum ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cells

scholarly journals Neonatal Mouse Gut Metabolites Influence Cryptosporidium parvum Infection in Intestinal Epithelial Cells

mBio ◽  
2020 ◽  
Vol 11 (6) ◽  
pp. e02582-20
Author(s):  
Kelli L. VanDussen ◽  
Lisa J. Funkhouser-Jones ◽  
Marianna E. Akey ◽  
Deborah A. Schaefer ◽  
Kevin Ackman ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Epithelial Cells ◽  
Cryptosporidium Parvum ◽  
Intestinal Epithelial Cells ◽  
Saturated Fatty Acids ◽  
Intestinal Lumen ◽  
Intestinal Epithelial ◽  
Content Type ◽  
Long Chain

ABSTRACTThe protozoan parasite Cryptosporidium sp. is a leading cause of diarrheal disease in those with compromised or underdeveloped immune systems, particularly infants and toddlers in resource-poor localities. As an enteric pathogen, Cryptosporidium sp. invades the apical surface of intestinal epithelial cells, where it resides in close proximity to metabolites in the intestinal lumen. However, the effect of gut metabolites on susceptibility to Cryptosporidium infection remains largely unstudied. Here, we first identified which gut metabolites are prevalent in neonatal mice when they are most susceptible to Cryptosporidium parvum infection and then tested the isolated effects of these metabolites on C. parvum invasion and growth in intestinal epithelial cells. Our findings demonstrate that medium or long-chain saturated fatty acids inhibit C. parvum growth, perhaps by negatively affecting the streamlined metabolism in C. parvum, which is unable to synthesize fatty acids. Conversely, long-chain unsaturated fatty acids enhanced C. parvum invasion, possibly by modulating membrane fluidity. Hence, gut metabolites, either from diet or produced by the microbiota, influence C. parvum growth in vitro and may also contribute to the early susceptibility to cryptosporidiosis seen in young animals.IMPORTANCECryptosporidium sp. occupies a unique intracellular niche that exposes the parasite to both host cell contents and the intestinal lumen, including metabolites from the diet and produced by the microbiota. Both dietary and microbial products change over the course of early development and could contribute to the changes seen in susceptibility to cryptosporidiosis in humans and mice. Consistent with this model, we show that the immature gut metabolome influenced the growth of Cryptosporidium parvumin vitro. Interestingly, metabolites that significantly altered parasite growth were fatty acids, a class of molecules that Cryptosporidium sp. is unable to synthesize de novo. The enhancing effects of polyunsaturated fatty acids and the inhibitory effects of saturated fatty acids presented in this study may provide a framework for future studies into this enteric parasite’s interactions with exogenous fatty acids during the initial stages of infection.

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