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

Fowler, Christopher J.; Sandberg, Monica; Tiger, Gunnar

doi:10.1007/s00011-003-1202-8

Cited by 18 publications

(13 citation statements)

References 31 publications

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“…However, an effect on gut motility was not assessed under these conditions [9]. Moreover, C48/80 has other non-specific effects amongst which inducing oxidative stress [31],vasodilatation [32], and it acts on other immune and non-immune cells including basophils [33], neurons [34], [35] and fibroblasts [36]. In line with these findings, the interpretation of the data acquired using the mast cell stabilizers such as ketotifen or doxantrazole should be used with caution, considering their broad anti-inflammatory effect mainly independent of mast cells [37]–[40].…”

Section: Discussionmentioning

confidence: 99%

Mast Cells Play No Role in the Pathogenesis of Postoperative Ileus Induced by Intestinal Manipulation

et al. 2014

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IntroductionIntestinal manipulation (IM) during abdominal surgery results in intestinal inflammation leading to hypomotility or ileus. Mast cell activation is thought to play a crucial role in the pathophysiology of postoperative ileus (POI). However, this conclusion was mainly drawn using mast cell-deficient mouse models with abnormal Kit signaling. These mice also lack interstitial cells of Cajal (ICC) resulting in aberrant gastrointestinal motility even prior to surgery, compromising their use as model to study POI. To avoid these experimental weaknesses we took advantage of a newly developed knock-in mouse model, Cpa3Cre/+, devoid of mast cells but with intact Kit signaling.DesignThe role of mast cells in the development of POI and intestinal inflammation was evaluated assessing gastrointestinal transit and muscularis externa inflammation after IM in two strains of mice lacking mast cells, i.e. KitW-sh/W-sh and Cpa3Cre/+ mice, and by use of the mast cell stabilizer cromolyn.Results KitW-sh/W-sh mice lack ICC networks and already revealed significantly delayed gastrointestinal transit even before surgery. IM did not further delay intestinal transit, but induced infiltration of myeloperoxidase positive cells, expression of inflammatory cytokines and recruitment of monocytes and neutrophils into the muscularis externa. On the contrary, Cpa3Cre/+ mice have a normal network of ICC and normal gastrointestinal. Surprisingly, IM in Cpa3Cre/+ mice caused delay in gut motility and intestinal inflammation as in wild type littermates mice (Cpa3+/+). Furthermore, treatment with the mast cell inhibitor cromolyn resulted in an inhibition of mast cells without preventing POI.ConclusionsHere, we confirm that IM induced mast cell degranulation. However, our data demonstrate that mast cells are not required for the pathogenesis of POI in mice. Although there might be species differences between mouse and human, our results argue against mast cell inhibitors as a therapeutic approach to shorten POI.

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Section: Discussionmentioning

confidence: 99%

Mast Cells Play No Role in the Pathogenesis of Postoperative Ileus Induced by Intestinal Manipulation

et al. 2014

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“…In order to confirm cell viability in CSE solution, an MTT assay was performed (Additional file 1, Figure S1). The CSE solution was used in the stimulation of BMMCs at final concentration of 0.1, 0.5, and 1.0% [36]. Optimal concentration and time of CSE solution for BMMCs stimulation were 1.0% and 6 h, respectively, in preliminary experiments.…”

Section: Methodsmentioning

confidence: 99%

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

et al. 2011

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BackgroundMany studies have found that smoking reduces lung function, but the relationship between cigarette smoke and allergic asthma has not been clearly elucidated, particularly the role of mast cells. This study aimed to investigate the effects of smoke exposure on allergic asthma and its association with mast cells.MethodsBALB/c mice were sensitized and challenged by OVA to induce asthma, and bone marrow-derived mast cells (BMMCs) were stimulated with antigen/antibody reaction. Mice or BMMCs were exposed to cigarette smoke or CSE solution for 1 mo or 6 h, respectively. The recruitment of inflammatory cells into BAL fluid or lung tissues was determined by Diff-Quik or H&E staining, collagen deposition by Sircol assay, penh values by a whole-body plethysmography, co-localization of tryptase and Smad3 by immunohistochemistry, IgE and TGF-β level by ELISA, expressions of Smads proteins, activities of signaling molecules, or TGF-β mRNA by immunoblotting and RT-PCR.ResultsCigarette smoke enhanced OVA-specific IgE levels, penh values, recruitment of inflammatory cells including mast cells, expressions of smad family, TGF-β mRNA and proteins, and cytokines, phosphorylations of Smad2 and 3, and MAP kinases, co-localization of tryptase and Smad3, and collagen deposition more than those of BAL cells and lung tissues of OVA-induced allergic mice. CSE solution pretreatment enhanced expressions of TGF-β, Smad3, activities of MAP kinases, NF-κB/AP-1 or PAI-1 more than those of activated-BMMCs.ConclusionsThe data suggest that smoke exposure enhances antigen-induced mast cell activation via TGF-β/Smad signaling pathways in mouse allergic asthma, and that it exacerbates airway inflammation and remodeling.

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“…Mast cell degranulation was detected by measuring the release of the granular enzyme b-hexosaminidase, as described previously [17]. …”

Section: B-hexosaminidase Assaymentioning

confidence: 99%

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

Zhang

Fang

et al. 2010

Inflamm. Res.

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

Abstract: 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.

Cited by 18 publications

References 31 publications

Mast Cells Play No Role in the Pathogenesis of Postoperative Ileus Induced by Intestinal Manipulation

Mast Cells Play No Role in the Pathogenesis of Postoperative Ileus Induced by Intestinal Manipulation

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

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

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