Abstract:
: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 IFN γ-induced upregulation of ICAM-1 in both IEC types. rSLURP-2 inhibited IL-1 β-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 TNFα by T-cells, downregulated IL-1 β and IL-6 secretion by macrophages, and moderately upregulated IL-10 production by both types of immunocytes. SLURP-2 downregulated TNFα and IFNγ R 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.
journal_name
Biomed Res Intjournal_title
BioMed research internationalauthors
Chernyavsky AI,Galitovskiy V,Shchepotin IB,Grando SAdoi
10.1155/2014/609086subject
Has Abstractpub_date
2014-01-01 00:00:00pages
609086eissn
2314-6133issn
2314-6141journal_volume
2014pub_type
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journal_title:BioMed research international
pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章,评审
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pub_type: 杂志文章,meta分析
doi:10.1155/2019/2139834
更新日期:2019-11-26 00:00:00
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doi:10.1155/2013/909860
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pub_type: 杂志文章,已发布勘误
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pub_type: 临床试验,杂志文章
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pub_type: 杂志文章,meta分析,评审
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