Literature DB >> 14652680

Effects of water-soluble cigarette smoke extracts upon the release of beta-hexosaminidase from RBL-2H3 basophilic leukaemia cells in response to substance P, compound 48/80, concanavalin A and antigen stimulation.

C J Fowler1, M Sandberg, G Tiger.   

Abstract

OBJECTIVE AND
DESIGN: To determine whether water-soluble constituents of cigarette smoke affect mast cell function using an in vitro model, RBL-2H3 basophilic leukaemia cells.
MATERIALS AND METHODS: RBL-2H3 cells were induced to degranulate in response to compound 48/80 and substance P, as assessed by monitoring the release of the granular enzyme beta-hexosaminidase, by treatment for 7 days with 20 microM quercetin. Responses to concanavalin A and antigen were determined by measuring the beta-hexosaminidase release from cells cultured on fibronectin-coated plates.
RESULTS: The beta-hexosaminidase release response to compound 48/80 induced by quercetin treatment was accompanied by a release of lactate dehydrogenase, suggesting that degranulation is not the only process triggered by compound 48/80 under these conditions. Quercetin treatment reduced the beta-hexosaminidase release response to concanavalin A. Precoating of the culture wells with rat fibronectin enhanced the beta-hexosaminidase response to calcimycin, but not to concanavalin A. Under these conditions, concanavalin A did not induce a release of lactate dehydrogenase. The responses to c48/80, substance P, calcimycin, concanavalin A and antigen (after IgE pretreatment) were reduced by treatment with cigarette smoke solution obtained from standard and low-tar cigarettes (IR3 and IR5F). The effect of cigarette smoke solution from IR5F cigarettes upon the beta-hexosaminidase release elicited by compound 48/80 (in quercetin-treated cells) and by concanavalin A (in cells cultured on fibronectin-coated wells) could be prevented by N-acetyl-L-cysteine, but not with either hemoglobin, alpha-tocopherol, catalase or palmitoylethanolamide. N-acetyl-L-cysteine also reduced the effect of cigarette smoke solution upon the degranulation response to antigen.
CONCLUSIONS: Under the conditions used, oxidants present in cigarette smoke solution from IR5F cigarettes reduce the ability of RBL-2H3 cells to degranulate in response to both immunological and non-immunological stimuli.

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Year:  2003        PMID: 14652680     DOI: 10.1007/s00011-003-1202-8

Source DB:  PubMed          Journal:  Inflamm Res        ISSN: 1023-3830            Impact factor:   4.575


  5 in total

1.  Effects of endogenous substance P expression on degranulation in RBL-2H3 cells.

Authors:  Hua Hu; Ruxin Zhang; Xiaoyun Fang; Min Yu; Shaoqing Yu; Jie Zhang; Hong Wang
Journal:  Inflamm Res       Date:  2010-12-29       Impact factor: 4.575

2.  Cigarette smoke exacerbates mouse allergic asthma through Smad proteins expressed in mast cells.

Authors:  Dae Yong Kim; Eun Young Kwon; Gwan Ui Hong; Yun Song Lee; Seung-Hyo Lee; Jai Youl Ro
Journal:  Respir Res       Date:  2011-04-18

3.  Mast cells play no role in the pathogenesis of postoperative ileus induced by intestinal manipulation.

Authors:  Pedro J Gomez-Pinilla; Giovanna Farro; Martina Di Giovangiulio; Nathalie Stakenborg; Andrea Némethova; Annick de Vries; Adrian Liston; Thorsten B Feyerabend; Hans-Reimer Rodewald; Hans-Reimwer Rodewald; Guy E Boeckxstaens; Gianluca Matteoli
Journal:  PLoS One       Date:  2014-01-09       Impact factor: 3.240

4.  The antinociception of oxytocin on colonic hypersensitivity in rats was mediated by inhibition of mast cell degranulation via Ca(2+)-NOS pathway.

Authors:  Liping Gong; Jing Li; Yan Tang; Ting Han; Chuanfei Wei; Xiao Yu; Jingxin Li; Rong Wang; Xuelian Ma; Kejing Liu; Lingyun Geng; Shaozhuang Liu; Bing Yan; Chuanyong Liu
Journal:  Sci Rep       Date:  2016-08-19       Impact factor: 4.379

Review 5.  The Basal Pharmacology of Palmitoylethanolamide.

Authors:  Linda Rankin; Christopher J Fowler
Journal:  Int J Mol Sci       Date:  2020-10-26       Impact factor: 5.923

  5 in total

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