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.

scholarly journals Medium- and Long-Chain Fatty Acids Differentially Modulate Interleukin-8 Secretion in Human Fetal Intestinal Epithelial Cells

2000 ◽  
Vol 130 (11) ◽  
pp. 2636-2640 ◽  
Author(s):  
Akira Andoh ◽  
Hiroki Takaya ◽  
Yoshio Araki ◽  
Tomoyuki Tsujikawa ◽  
Yoshihide Fujiyama ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Interleukin 8 ◽  
Long Chain Fatty Acids ◽  
Intestinal Epithelial ◽  
Long Chain ◽  
Chain Fatty Acids

scholarly journals Anti-Inflammatory Properties of Streptococcus salivarius, a Commensal Bacterium of the Oral Cavity and Digestive Tract

2013 ◽  
Vol 80 (3) ◽  
pp. 928-934 ◽  
Author(s):  
Ghalia Kaci ◽  
Denise Goudercourt ◽  
Véronique Dennin ◽  
Bruno Pot ◽  
Joël Doré ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Oral Cavity ◽  
Mononuclear Cells ◽  
Inflammatory Responses ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Streptococcus Salivarius ◽  
Content Type ◽  
Anti Inflammatory

ABSTRACTStreptococcus salivariusis one of the first colonizers of the human oral cavity and gut after birth and therefore may contribute to the establishment of immune homeostasis and regulation of host inflammatory responses. The anti-inflammatory potential ofS. salivariuswas first evaluatedin vitroon human intestinal epithelial cells and human peripheral blood mononuclear cells. We show that liveS. salivariusstrains inhibitedin vitrothe activation of the NF-κB pathway on intestinal epithelial cells. We also demonstrate that the liveS. salivariusJIM8772 strain significantly inhibited inflammation in severe and moderate colitis mouse models. Thesein vitroandin vivoanti-inflammatory properties were not found with heat-killedS. salivarius, suggesting a protective response exclusively with metabolically active bacteria.

The recognition of long chain fatty acids on the intestinal epithelial cells

1994 ◽  
Vol 1 ◽  
pp. 195
Author(s):  
N. Takahashi ◽  
T. Shitani ◽  
K. Murota ◽  
T. Kawada ◽  
N.A. Abumrad ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Long Chain Fatty Acids ◽  
Intestinal Epithelial ◽  
Long Chain ◽  
Chain Fatty Acids

scholarly journals Host Cell Tropism Underlies Species Restriction of Human and Bovine Cryptosporidium parvum Genotypes

2004 ◽  
Vol 72 (10) ◽  
pp. 6125-6131 ◽  
Author(s):  
Amna Hashim ◽  
Marguerite Clyne ◽  
Grace Mulcahy ◽  
Donna Akiyoshi ◽  
Rachel Chalmers ◽  
...  
Keyword(s):  
Small Bowel ◽  
Epithelial Cells ◽  
Cryptosporidium Parvum ◽  
Intestinal Epithelial Cells ◽  
Specific Cell ◽  
Cell Tropism ◽  
Intestinal Epithelial ◽  
Genotype I ◽  
Genotype Ii

ABSTRACT It has been recognized recently that human cryptosporidiosis is usually caused by Cryptosporidium parvum genotype I (“human” C. parvum), which is not found in animals. Compared to C. parvum genotype II, little is known of the biology of invasion of the human-restricted C. parvum genotype I. The aims of the present study were (i) to explore and compare with genotype II the pathogenesis of C. parvum genotype I infection by using an established in vitro model of infection and (ii) to examine the possibility that host-specific cell tropism determines species restriction among C. parvum genotypes by using a novel ex vivo small intestinal primary cell model of infection. Oocysts of C. parvum genotypes I and II were used to infect HCT-8 cells and primary intestinal epithelial cells in vitro. Primary cells were harvested from human endoscopic small-bowel biopsies and from bovine duodenum postmortem. C. parvum genotype I infected HCT-8 cells with lower efficiency than C. parvum genotype II. Actin colocalization at the host parasite interface and reduction in levels of invasion after treatment with microfilament inhibitors (cytochalasin B and cytochalasin D) were observed for both genotypes. C. parvum genotype II invaded primary intestinal epithelial cells, regardless of the species of origin. In contrast, C. parvum genotype I invaded only human small-bowel cells. The pathogenesis of C. parvum genotype I differs from C. parvum genotype II. C parvum genotype I does not enter primary bovine intestinal cells, suggesting that the species restriction of this genotype is due to host tissue tropism of the infecting isolate.

scholarly journals Gut metabolites influence susceptibility of neonatal mice to cryptosporidiosis

2020 ◽  
Author(s):  
Kelli L. VanDussen ◽  
Lisa J. Funkhouser-Jones ◽  
Marianna E. Akey ◽  
Deborah A. Schaefer ◽  
Kevin Ackman ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Unsaturated Fatty Acids ◽  
Diarrheal Disease ◽  
De Novo ◽  
Saturated Fatty Acids ◽  
Intestinal Lumen ◽  
Apical Surface ◽  
Neonatal Mice ◽  
Long Chain

AbstractThe protozoan parasite Cryptosporidium is a leading cause of diarrheal disease in those with compromised or under-developed immune systems, particularly infants and toddlers in resource-poor localities. As an enteric pathogen, Cryptosporidium 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. Our findings demonstrate that medium or long-chain saturated fatty acids inhibit C. parvum growth, while long-chain unsaturated fatty acids enhance C. parvum invasion. The influence of these two classes of metabolites on C. parvum infection likely reflects the streamlined metabolism in C. parvum, which is unable to synthesize fatty acids. Hence, gut metabolites, either from diet or produced by the microbiota, play an important role in the early susceptibility to cryptosporidiosis seen in young animals.ImportanceCryptosporidium 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 growth of C. parvum in vitro and may increase susceptibility to infection in young mice. Interestingly, metabolites that significantly altered parasite growth were fatty acids, a class of molecules that Cryptosporidium is unable to synthesize de novo. The enhancing effects of polyunsaturated fatty acids and the inhibitory effects of saturated fatty acids provide further insight into reliance on fatty acid salvage and metabolism of this enteric parasite.

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