Transmissible gastroenteritis of swine: Virus-intestinal cell interactions I. Immunofluorescence, histopathology and virus production in the small intestine through the course of infection

1970 ◽  
Vol 31 (3-4) ◽  
pp. 321-334 ◽  
Author(s):  
M. Pensaert ◽  
E. O. Haelterman ◽  
T. Burnstein
Keyword(s):  
Small Intestine ◽  
Virus Production ◽  
Cell Interactions ◽  
Intestinal Cell ◽  
Swine Virus ◽  
Transmissible Gastroenteritis

Is polyamine synthesis involved in the proliferative response of the intestinal epithelium to urogastrone-epidermal growth factor?

1989 ◽  
Vol 76 (6) ◽  
pp. 595-598 ◽  
Author(s):  
R. A. Goodlad ◽  
H. Gregory ◽  
N. A. Wright
Keyword(s):  
Cell Proliferation ◽  
Small Intestine ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Proliferative Response ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Polyamine Synthesis ◽  
Proliferative Effect ◽  
Epidermal Growth

1. Intestinal epithelial cell proliferation was measured in rats maintained on total parenteral nutriton (TPN), in TPN rats given 300 μg of recombinant human epidermal growth factor (urogastrone-epidermal growth factor, URO-EGF) day−1 kg−1, and in further groups given URO-EGF and difluoromethylornithine (DFMO), an inhibitor of the enzyme ornithine decarboxylase (ODC). 2. URO-EGF significantly increased intestinal cell proliferation throughout the gastrointestinal tract. The proliferative response of the colon was particularly pronounced. 3. DFMO reduced the proliferative effect of urogastrone in the stomach and small intestine. DFMO also reduced URO-EGF-stimulated intestinal cell proliferation in the colon, but to a lesser extent. 4. It is concluded that ODC is essential for effecting the proliferative response of the stomach and small intestine to URO-EGF, but this role may be less important in the colon.

Absence of a cAMP-mediated antiabsorptive effect in an undifferentiated jejunal epithelium

1987 ◽  
Vol 252 (6) ◽  
pp. G776-G782
Author(s):  
R. J. MacLeod ◽  
J. R. Hamilton
Keyword(s):  
Small Intestine ◽  
Thymidine Kinase ◽  
Jejunal Mucosa ◽  
Ussing Chambers ◽  
Luminal Membrane ◽  
Viral Enteritis ◽  
Transmissible Gastroenteritis ◽  
Camp Levels ◽  
Nacl Cotransport

In the relatively undifferentiated jejunal mucosa occurring in piglet viral enteritis, we measured the response of transepithelial Na+ and Cl- fluxes in vitro to raised intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels. At the acute 40-h stage of transmissible gastroenteritis (TGE), luminal membrane markers, sucrase and lactase, and a basolateral jejunal epithelial membrane marker Na+-K+-ATPase, were significantly decreased in activity, while a proliferative marker, thymidine kinase, was significantly enriched; these enzyme characteristics are typical of enterocytes isolated from crypts of other species. As expected, control piglet jejunum in short-circuited Ussing chambers after theophylline (10 mM) developed significant net secretory Na and Cl fluxes primarily due to significant antiabsorptive effects (delta JNa m----s = 3.48 +/- 0.52, delta JCl m----s = 2.59 +/- 0.28). Furosemide (10(-4) M), an inhibitor of electroneutral NaCl cotransport, produced antiabsorptive effects (delta JNa m----s = 2.53 +/- 0.31, delta JCl m----s = 2.58 +/- 0.28) in control jejunum that were not significantly different from those seen in response to theophylline. TGE jejunum, however, responded to theophylline not by an antiabsorptive effect but by significant electrogenic Cl- secretion (delta JCl s----m = 1.59 +/- 0.48); furosemide had no effect on ion fluxes in TGE tissue. Control and TGE jejunal mucosal homogenates did not differ in their basal or theophylline-stimulated levels of cAMP. We conclude that the relatively undifferentiated small intestine occurring in acute TGE does not generate either a cAMP-mediated antiabsorptive effect or a furosemide-mediated antiabsorptive effect.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Rotavirus Reprograms Multiple Interferon Receptors and Restricts Their Intestinal Antiviral and Inflammatory Functions

2020 ◽  
Vol 94 (6) ◽  
Author(s):  
Adrish Sen ◽  
Nima D. Namsa ◽  
Ningguo Feng ◽  
Harry B. Greenberg
Keyword(s):  
Small Intestine ◽  
Small Bowel ◽  
Inflammatory Cytokines ◽  
Host Species ◽  
Intestinal Cell ◽  
Intestinal Damage ◽  
Range Restriction ◽  
Severe Diarrhea ◽  
Stat1 Signaling ◽  
Bystander Cells

ABSTRACT Rotaviruses (RV) cause acute severe diarrhea in the absence of substantial intestinal inflammation. They are also highly infectious in their homologous host species. The replication capacity of RV in the small bowel is substantially due to its ability to inhibit different types of interferons (IFNs). Here, we found that during RV infection in vitro, both virus-infected and uninfected bystander cells resist STAT1 phosphorylation and interferon regulatory factor 7 (IRF7) induction in response to exogenous interferon (IFN). Functionally, cellular transcription in response to stimulation with IFN, but not intracellular double-stranded RNA (dsRNA), was inhibited by RV. Further, IFNAR1 stimulation during RV infection significantly repressed a set of virus-induced transcripts. Regulation of IFN signaling in vivo was studied in suckling mice using the highly infectious murine EW RV strain. Kinetic studies indicated that sustained EW RV replication and IFN induction in the small intestine are accompanied by significant decreases in IFN-stimulated transcripts. Lipopolysaccharide (LPS)-mediated intestinal damage, driven by STAT1-induced inflammation, was also prevented in EW RV-infected mice. Remarkably, by ectopically stimulating either IFNAR1 or IFNGR1 in EW RV-infected mice, we could eliminate several intestinal antiviral and inflammatory transcriptional responses to RV. In contrast to infection with homologous RV, infection with a STAT1-sensitive heterologous RV strain induced IFN-stimulated transcripts, inflammatory cytokines, and intestinal expression of STAT1-pY701. Finally, RV strain-specific STAT1 regulation also likely determines the intestinal activation of multiple caspases. The simian RRV strain, but not murine EW RV, uniquely triggers the cleavage of both extrinsic and intrinsic caspases (caspases 8, 9, and 3) in a STAT1-mediated manner. Collectively, our findings reveal efficient reprograming of multiple IFN receptors toward a negative-feedback mode of signaling, accompanied by suppression of IFN-mediated antiviral, apoptotic, and inflammatory functions, during natural RV intestinal infection. IMPORTANCE Rotavirus is a highly infectious pathogen that causes severe diarrhea. Replication of RV in the small intestine is restricted to homologous host species, and host range restriction is substantially determined by the interferon response. In this study, we demonstrate that during infection, RV bystander cells resist exogenous IFN-mediated STAT1 signaling and transcription. In a suckling mouse model, ectopically stimulating different intestinal interferon receptors during RV infection eliminates several innate and inflammatory antiviral responses. Different intestinal inflammatory cytokines were also suppressed by homologous RV, as was intestinal damage in response to endotoxin. The ability of RV to suppress IFN-mediated receptors likely impacts intestinal cell homeostasis, as the cleavage of multiple intestinal caspases during RV infection is mediated by the IFN-STAT1 signaling pathway. Together, our results provide a mechanism underlying both the remarkable interferon resistance of homologous RV and its ability to prevent substantial inflammatory damage to the small bowel.

Global proteomic analysis of transporter proteins in the human small intestine and established intestinal cell lines

2018 ◽  
Vol 33 (1) ◽  
pp. S56-S57 ◽  
Author(s):  
Janett Müller ◽  
Elke Hammer ◽  
Manuela Gesell Salazar ◽  
Anja Fritz ◽  
Lars Ivo Partecke ◽  
...  
Keyword(s):  
Small Intestine ◽  
Cell Lines ◽  
Proteomic Analysis ◽  
Intestinal Cell ◽  
Transporter Proteins ◽  
Human Small Intestine ◽  
Intestinal Cell Lines

Targeted disruption of the homeobox transcription factor Nkx2-3 in mice results in postnatal lethality and abnormal development of small intestine and spleen

Development ◽  
1999 ◽  
Vol 126 (10) ◽  
pp. 2215-2225 ◽  
Author(s):  
O. Pabst ◽  
R. Zweigerdt ◽  
H.H. Arnold
Keyword(s):  
Transcription Factor ◽  
Small Intestine ◽  
Cell Lineage ◽  
Cell Types ◽  
Abnormal Development ◽  
Intestinal Cell ◽  
White Pulp ◽  
Morphological Alterations ◽  
Signalling Molecules ◽  
Adult Mice

The homeodomain transcription factor Nkx2-3 is expressed in gut mesenchyme and spleen of embryonic and adult mice. Targeted inactivation of the Nkx2-3 gene results in severe morphological alterations of both organs and early postnatal lethality in the majority of homozygous mutants. Villus formation in the small intestine appears considerably delayed in Nkx2-3(−)/- foetuses due to reduced proliferation of the epithelium, while massively increased growth of crypt cells ensues in surviving adult mutants. Interestingly, differentiated cell types of the intestinal epithelium are present in homozygous mutants, suggesting that Nkx2-3 is not required for their cell lineage allocation or migration-dependent differentiation. Hyperproliferation of the gut epithelium in adult mutants is associated with markedly reduced expression of BMP-2 and BMP-4, suggesting that these signalling molecules may be involved in mediating non-cell-autonomous control of intestinal cell growth. Spleens of Nkx2-3 mutants are generally smaller and contain drastically reduced numbers of lymphatic cells. The white pulp appears anatomically disorganized, possibly owing to a homing defect in the spleen parenchyme. Moreover, some of the Nkx2-3 mutants exhibit asplenia. Taken together these observations indicate that Nkx2-3 is essential for normal development and functions of the small intestine and spleen.

scholarly journals The response of the small intestine to vitamin D. Correlation between calcium-binding-protein production and increased calcium absorption

1974 ◽  
Vol 144 (2) ◽  
pp. 339-346 ◽  
Author(s):  
J S Emtage ◽  
D E M Lawson ◽  
E Kodicek
Keyword(s):  
Vitamin D ◽  
Protein Synthesis ◽  
Small Intestine ◽  
Calcium Binding ◽  
Protein Production ◽  
Calcium Absorption ◽  
Binding Protein ◽  
Calcium Binding Protein ◽  
Intestinal Cell ◽  
Stimulation Of

1. The synthesis of calcium-binding protein, a protein produced in the small intestine in response to vitamin D, was investigated with a view to determining whether calcium-binding-protein production could be correlated with the stimulation of calcium absorption by vitamin D. 2. A radioimmunological assay, which can quantitatively estimate calcium-binding-protein concentrations as low as 1μg/g wet wt., was used to detect the synthesis of soluble calcium-binding protein. 3. When used on intestinal supernatants from chicks dosed with vitamin D, calcium-binding protein was not detectable at 8h but was present after 12h at a concentration of 8.6μg/g wet wt.; in agreement with this an increase in calcium absorption due to vitamin D was detected at 12h but not at 8h. 4. The synthesis of calcium-binding protein was also monitored directly by making use of the ability of the iodinated antiserum to bind specifically to nascent calcium-binding protein chains on intestinal polyribosomes; in this way calcium-binding-protein synthesis could be detected 8h after dosage with vitamin D. Further, the binding reaction indicated a near linear increase in the calcium-binding-protein-synthesizing capacity over a 16h period. 5. From the amount of calcium-binding protein present 12 and 24h after vitamin D administration it is calculated that calcium-binding-protein mRNA is produced at approx. 1mol/min per intestinal cell. 6. It is concluded that the high correlation between the initiation of calcium-binding-protein synthesis and the stimulation of calcium absorption by vitamin D strengthens the proposal that calcium-binding protein plays an important role in calcium transport.

Subepithelial fmroblasts in rat small intestine: Mediators of nerve — Epithelial cell interactions?

2000 ◽  
Vol 118 (4) ◽  
pp. A632
Author(s):  
Hermann Salmhofer ◽  
Winfried L. Neuhuber ◽  
Andrea Huber ◽  
Peter Ruth ◽  
Doris Koesling ◽  
...  
Keyword(s):  
Small Intestine ◽  
Epithelial Cell ◽  
Cell Interactions ◽  
Rat Small Intestine
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