Human Lung Mast Cells and Pulmonary Macrophages Produce Tumor Necrosis Factor-<i>α</i> in Sensitized Lung Tissue after IgE Receptor Triggering

Ohkawara, Yuichi; Yamauchi, Kohei; Tanno, Yasuo; Tamura, Gen; Ohtani, Haruo; Nishimura, Hiroshi; Ohkuda, Kazuhisa; Takishima, Tamotsu

doi:10.1165/ajrcmb/7.4.385

Cited by 142 publications

(69 citation statements)

References 19 publications

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“…TNF-α is a multifunctional proinflammatory TH 1 cytokine which has been suggested to play a critical role in the initiation, maintenance and progression of airway inflammation in asthma. TNF-α is stored in granules and is known to be released during allergic responses both from mast cells and macrophages via Ig-E dependant mechanisms 34 . Many other cell types that play a contributing role in the pathogenesis of asthma are also significant sources of TNF-α, including eosionphils 35 , epithelial cells 36 and T cells 37 .…”

Section: Discussionmentioning

confidence: 99%

Mechanistic Evaluation of Butea Monosperma Using in Vitro and in Vivo Murine Models of Bronchial Asthma

Shirole¹,

Sutariya²,

Saraf³

2013

Int. J. Res. Ayurveda Pharm.

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The present investigation aimed to elucidate the probable mechanism of antiasthmatic action of Butea monosperma. Bioactive fractionations of methanolic extract of B. monosperma (MBM) were carried out to get, ethyl acetate fraction (EBM) and butanolic fraction (BBM) of Butea monosperma. All fractions were evaluated mechanistically for its antiasthmatic actions in vitro using lipoxygenase assay. The lipoxygenase inhibitory effect of the extract followed the order BBM > MBM > EBM. Based on in vitro lipoxygenase assay BBM was selected for in vitro compound 48/80 induced mast cell degranulation assay and in vivo lipopolysaccharide induced inflammation in rats. BBM 50, 100 and 200μg/ml inhibited compound 48/80 induced mast cell degranulation. BBM exhibited dose dependent (50, 100 and 200mg/kg i.p.) inhibition of lipopolysaccharide-induced increased in total cell count, differential leukocyte count, nitrate-nitrite, total protein and albumin levels in bronchoalveolar fluid (BALF) and myeloperoxidase (MPO) levels in lungs homogenate.

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Section: Discussionmentioning

confidence: 99%

Mechanistic Evaluation of Butea Monosperma Using in Vitro and in Vivo Murine Models of Bronchial Asthma

Shirole¹,

Sutariya²,

Saraf³

2013

Int. J. Res. Ayurveda Pharm.

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“…Observations that TNF-α is released via the IgE-dependent activation of mast cells (Gordon et al, 1990) or in the sensitized human lung (Ohkawara et al, 1992) suggest that TNF-α contributes to the allergen-induced inflammatory response. Amrani et al (1995) showed that exposure of human airway smooth muscle cells to TNF-α for 24 hr potentiates the increase in cytosolic free calcium induced by contractile agonists such as carbachol and bradykinin.…”

Section: Discussionmentioning

confidence: 99%

TNF-.ALPHA. augments the expression of RhoA in the rat bronchus

Sakai

Otogoto

Chiba

et al. 2004

J. Smooth Muscle Res.

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While nonspecific airway hyperresponsiveness (AHR) is a central feature of allergic bronchial asthma, the mechanism underlying the developmont of AHR is not clearly understood. We have previously demonstrated in vitro hyperresponsiveness of bronchial smooth muscle to acetylcholine (ACh) in rats that were actively sensitized and repeatedly challenged with aerosolized antigen. It has also been demonstrated that the AChinduced, RhoA-mediated Ca 2+ sensitization is markedly augmented concomitantly with an increased expression and activation of RhoA protein in the bronchial smooth muscle of the antigen-treated rats. In the present study, we have investigated whether TNF-α, a proinflammatory cytokine which is involved in bronchial asthma, causes upregulation of RhoA mRNA and protein in the rat bronchus. Treatment of rat bronchial smooth muscle preparations with TNF-α (300 ng/ml for 24 hr) significantly shifted the concentrationresponse curve to ACh upwards, but did not alter the response to high K + , when compared to that of control tissues. Levels of RhoA mRNA and protein in the TNF-α-treated bronchus were significantly greater than those in the control group. In conclusion, it is suggested that the augmentation of the ACh-induced contractile response evoked by TNF-α might be mediated by an upregulation of RhoA in rat bronchial smooth muscle.

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“…Much higher levels of exhaled CO and NO during the late asthmatic reaction may also be due to HO-1 activation by inflammatory cytokines such as interleukin (IL)-1, IL-6, tumour necrosis factor (TNF-a) [32,33] and iNOS activation by IL-1 and TNF-a [34,35] which are abundant in BAL at the time of the late asthmatic reaction [36,37]. Increased production of oxidants by incoming inflammatory cells and tissue cells may contribute to HO-1 activation [38], explaining higher CO levels in dual responders than in single responders.…”

Section: Discussionmentioning

confidence: 99%

Changes in exhaled carbon monoxide and nitric oxide levels following allergen challenge in patients with asthma

et al. 1999

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Carbon monoxide is a product of haem degradation by haem oxygenase (HO), activated by inflammatory cytokines and oxidants. This study examined whether allergen challenge can increase exhaled CO levels, as a reflection of HO activation.Exhaled CO and nitric oxide, an expired gas also thought to reflect cytokine-induced airway inflammation, were measured in 15 atopic steroid-naive nonsmoking patients with asthma (13 males, aged 3062 yrs) before and for up to 20 h after allergen challenge.Baseline CO (4.40.3 parts per million (ppm)) and NO (20.661.2 parts per billion (ppb)) levels were elevated in asthmatic as compared with nonsmoking normal volunteers (n=37, 2.10.2 ppm and 7.00.1 ppb, respectively, p<0.05). In 10 patients with a dual response in the forced expiratory volume in one second (FEV1) there was a maximal increase in exhaled CO at 1 h (34.37.1%) and at 6 h (6912%, p<0.01), followed by a maximal fall in FEV1 (289%, p<0.05) at 9 h, whereas the maximal NO increase was observed at 10 h (50.211.8%). The maximal increase in exhaled CO in single response patients (n=5) was 302% during the early asthmatic reaction and 46.3 9.2% between 4 and 10 h, followed by a fall in FEV1 (93%, p>0.05) at 9 h, whereas exhaled NO was not significantly changed. In five patients exhaled CO was not attenuated by inhalation of increasing concentrations of histamine causing a 20% fall in FEV1 (PC20) or its subsequent relief by b 2 -agonists.In conclusion, exhaled carbon monoxide is increased during the early and late asthmatic reactions independently of the change in airway calibre, while exhaled nitric oxide is increased only during the late reaction and follows the increase in carbon monoxide and fall in the forced expiratory volume in one second in time. Eur Respir J 1999; 13: 48±52. There is considerable evidence for airway inflammation and oxidative stress in patients with asthma, even when the disease is mild [1,2]. Bronchoalveolar lavage (BAL) and bronchial biopsy studies have demonstrated the infiltration of activated inflammatory cells in the airway mucosa and there is a broad relationship between the intensity of inflammation and the clinical severity of asthma. Inhalation of allergen provides a model of asthmatic inflammation, as it provokes an early fall in forced expiratory volume in one second (FEV1) owing to the release of bronchoconstrictor mediators, such as histamine, leukotrienes and prostaglandins [3], and a late asthmatic response which is associated with a prolonged bronchoconstriction, influx of inflammatory cells [4] and mediators [5±7] and an increase in the oxidative stress in the airway.It is becoming clear that some oxidant-induced mediators and enzymes, such as haem oxygenase (HO), may also play a vital role in the airway protective response to oxidative stress. Two isoforms of HO have been described: the constitutive HO-2, which is highly expressed in the brain and testes, and the inducible HO-1, which is ubiquitously distributed. The latter is activated by a variety of pro-inflammatory cytoki...

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Human Lung Mast Cells and Pulmonary Macrophages Produce Tumor Necrosis Factor-α in Sensitized Lung Tissue after IgE Receptor Triggering

Cited by 142 publications

References 19 publications

Mechanistic Evaluation of Butea Monosperma Using in Vitro and in Vivo Murine Models of Bronchial Asthma

Mechanistic Evaluation of Butea Monosperma Using in Vitro and in Vivo Murine Models of Bronchial Asthma

TNF-.ALPHA. augments the expression of RhoA in the rat bronchus

Changes in exhaled carbon monoxide and nitric oxide levels following allergen challenge in patients with asthma

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