scholarly journals Anti-Inflammatory Effect ofLactobacillus caseionShigella-Infected Human Intestinal Epithelial Cells

2006 ◽  
Vol 176 (2) ◽  
pp. 1228-1237 ◽  
Author(s):  
Meng-Tsung Tien ◽  
Stephen E. Girardin ◽  
Béatrice Regnault ◽  
Lionel Le Bourhis ◽  
Marie-Agnès Dillies ◽  
...  

2019 ◽  
Vol 13 (2) ◽  
pp. 95 ◽  
Author(s):  
So-Rok Lee ◽  
Hye-Jeong Hwang ◽  
Ju-Gyeong Yoon ◽  
Eun Young Bae ◽  
Kyo-Suk Goo ◽  
...  


2006 ◽  
Vol 176 (6) ◽  
pp. 3841.3-3841 ◽  
Author(s):  
M.-T. Tien ◽  
S. E. Girardin ◽  
B. Regnault ◽  
L. Le Bourhis ◽  
M.-A. Dillies ◽  
...  




2017 ◽  
Vol 4 (1) ◽  
pp. 46-52 ◽  
Author(s):  
Aadra P. Bhatt ◽  
Dulan B. Gunasekara ◽  
Jennifer Speer ◽  
Mark I. Reed ◽  
Alexis N. Peña ◽  
...  




2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Alex I. Chernyavsky ◽  
Valentin Galitovskiy ◽  
Igor B. Shchepotin ◽  
Sergei A. Grando

A search for novel and more efficient therapeutic modalities of inflammatory bowel disease (IBD) is one of the most important tasks of contemporary medicine. The anti-inflammatory action of nicotine in IBD might be therapeutic, but its toxicity due to off-target and nonreceptor effects limited its use and prompted a search for nontoxic nicotinergic drugs. We tested the hypothesis that SLURP-1 and -2—the physiological nicotinergic substances produced by the human intestinal epithelial cells (IEC) and immunocytes—can mimic the anti-inflammatory effects of nicotine. We used human CCL-241 enterocytes, CCL-248 colonocytes, CCRF-CEM T-cells, and U937 macrophages. SLURP-1 diminished the TLR9-dependent secretion of IL-8 by CCL-241, and IFNγ-induced upregulation of ICAM-1 in both IEC types. rSLURP-2 inhibited IL-1β-induced secretion of IL-6 and TLR4- and TLR9-dependent induction of CXCL10 and IL-8, respectively, in CCL-241. rSLURP-1 decreased production of TNFαby T-cells, downregulated IL-1βand IL-6 secretion by macrophages, and moderately upregulated IL-10 production by both types of immunocytes. SLURP-2 downregulated TNFαand IFNγR in T-cells and reduced IL-6 production by macrophages. Combining both SLURPs amplified their anti-inflammatory effects. Learning the pharmacology of SLURP-1 and -2 actions on enterocytes, colonocytes, T cells, and macrophages may help develop novel effective treatments of IBD.





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