Disease relevance of Bronchial Hyperreactivity

• Airway eosinophilia, Th2 cytokine induction, IgE production, and bronchial hyperreactivity were prevented by coadministration of CpG ODN with the Ag [1].
• Requirements for electrolytes are minimally increased, and the need for additional iron is unclear in light of "sports anemia." There is no evidence to support the use of vitamins C and E as ergogenic aids; however, the findings relating vitamin C to bronchospasm and bronchial hyperreactivity are interesting [2].
• A double-blind, randomized study of sodium cromoglycate versus placebo in patients with cystic fibrosis and bronchial hyperreactivity [3].
• Relationships among allergen-induced early and late phase airway obstructions, bronchial hyperreactivity, and inflammation in conscious, unrestrained guinea pigs [4].
• This suggests that, although reduced airway calibre may be a factor underlying bronchial hyperreactivity in bronchiectasis, it is not the only mechanism [5].

High impact information on Bronchial Hyperreactivity

• Allergen intranasal challenge in OVA-sensitized mice induced LTB4 and LTC4 release into the airspace, widespread mucus occlusion of the airways, leukocytic infiltration of the airway tissue and broncho-alveolar lavage fluid that was predominantly eosinophils, and bronchial hyperreactivity to methacholine [6].
• This report examines the effect of an anti-VLA-4 monoclonal antibody (mAb) HP1/2 on antigen-induced bronchial hyperreactivity to methacholine, and on eosinophil and T lymphocyte infiltration in the airways of guinea pigs sensitized and challenged by aerosolized ovalbumin and used 24 h thereafter [7].
• Antigen-challenged animals exhibited bronchial hyperreactivity to inhale acetylcholine at 72 h, but not at 6 or 24 h [8].
• Neutralization of endogenously secreted MBP by a specific antiserum prevented antigen-induced bronchial hyperreactivity, suggesting that eosinophil degranulation plays an important role in the alterations of bronchopulmonary function in the guinea pig [8].
• Airway epithelial cell expression of interleukin-6 in transgenic mice. Uncoupling of airway inflammation and bronchial hyperreactivity [9].

Chemical compound and disease context of Bronchial Hyperreactivity

• Reduction of bronchial hyperreactivity during prolonged allergen avoidance [10].
• Saturation with histamine abrogated the inhibitory effect of EV131 on bronchial hyperreactivity [11].
• Angiotensin-converting enzyme inhibitors increase bronchial hyperreactivity in patients who develop cough during treatment and may, in certain cases, worsen or even induce asthma, probably by opposing inactivation by hydrolysis of tachykinins and of bradykinins [12].
• The proportion of patients with an optimal therapeutic index, in terms of a good airway response (fourfold decrease in bronchial hyperreactivity) and minimal systemic response (overnight urinary cortisol greater than 20 nmol), was similar at low-dose (46%) and at high-dose (52%) budesonide [13].
• Modification of bronchial hyperreactivity after treatment with sodium cromoglycate during pollen season [14].

Biological context of Bronchial Hyperreactivity

• To evaluate the influence of aging on bronchial hyperreactivity (BHR) during the childhood period, age-related changes in bronchial reactivity to methacholine (BRm) in children from 2 to 13 yr of age were studied using the same method, employing a methacholine inhalation challenge with transcutaneous oxygen pressure (tcPO2) monitoring [15].
• We speculated that histamine tachyphylaxis might be related to the degree of bronchial hyperreactivity (BHR) to histamine [16].
• A validated dietary questionnaire was used to measure food intake of cases, defined, firstly, as people with seasonal allergic-type symptoms and, secondly, those with bronchial hyperreactivity confirmed by methacholine challenge, and of controls without allergic symptoms or bronchial reactivity [17].
• Immunohistochemical studies of mucosal biopsies from the bronchi of aspirin-intolerant asthmatics show that LTC4S is overrepresented in individuals with this phenotype, and this finding correlates with overproduction of cysteinyl leukotrienes and lysine-aspirin bronchial hyperreactivity [18].
• Our data support that LPS-induced bronchial hyperreactivity to capsaicin is related closely to the upregulation of tachykinin gene expression, but not the upregulation of NEP [19].

Anatomical context of Bronchial Hyperreactivity

• We conclude that, in contrast to inhaled terbutaline, inhaled budesonide improved lung function and bronchial hyperreactivity in adult subjects with asthma treated for 3 months and that this corticosteroid was more effective in ameliorating abnormalities of the bronchial epithelium and decreasing inflammation in the airways [20].
• CONCLUSIONS: Our data demonstrate for the first time that nasal and bronchial hyperreactivity to airborne latex allergens are associated with an increase of eosinophils and mediators (e.g. ECP, NO derivatives, IL-5, tryptase) in nasal mucosa [21].
• We suggest that the increased PMA-induced whole blood chemiluminescence in bronchial hyperreactivity is due mainly to an activation of neutrophils, and that the assay might be useful as a systemic inflammatory marker in patients with pulmonary inflammatory processes resulting in bronchial hyperreactivity [22].
• A [3H]leukotriene D4 radioreceptor binding assay has been established in rat lung and has been used to fully characterize the leukotriene D4 receptor in lung membranes from an inbred strain of rats displaying non-specific bronchial hyperreactivity [23].
• These data suggest that tachykinins released from C-fibers upon acute or repeated exposures to high or low concentrations of TDI, respectively, play an essential role in the observed bronchial hyperreactivity, and that the inhibition of NEP by TDI cannot completely account for the observed airway hyperreactivity [24].

Gene context of Bronchial Hyperreactivity

• The TNF system may play a key role in the pathomechanism of bronchial hyperreactivity [25].
• Relationship between the tumor necrosis factor system and the serum interleukin-4, interleukin-5, interleukin-8, eosinophil cationic protein, and immunoglobulin E levels in the bronchial hyperreactivity of adults and their children [25].
• These results show that IL-5 and eosinophilic inflammation play a substantial role in the pathophysiology of allergic airway disease and, moreover, that aeroallergen-induced bronchial hyperreactivity is not exclusively regulated by IL-4 [26].
• Eosinophil-derived agents such as PAF, LTC4, MBP and ECP might be responsible for submucosal oedema and non-specific bronchial hyperreactivity which are characteristic features of late-phase reactions [27].
• The potential for therapeutic intervention with ADAM 33 is extremely attractive and further work will not only focus on the specific domains of ADAM 33, but also the mechanisms by which they lead to bronchial hyperreactivity [28].

Analytical, diagnostic and therapeutic context of Bronchial Hyperreactivity

• We performed a double-blind crossover study to compare the effects of long-term treatment of inhaled budesonide and terbutaline on bronchial hyperreactivity in 17 patients with allergic asthma [29].
• Intravenous magnesium sulfate for bronchial hyperreactivity: a randomized, controlled, double-blind study [30].
• Subjects completed a detailed respiratory questionnaire, a validated semiquantitative food-frequency questionnaire, skin-prick testing, and lung function tests, including a methacholine challenge test for bronchial hyperreactivity (BHR) [31].
• The effects of H2 receptor blockade with cimetidine on bronchial hyperreactivity to histamine were studied in 10 asthmatic volunteers by whole body plethysmography [32].
• Lung function, bronchial hyperreactivity to histamine, duration of local anesthesia, and lidocaine and ropivacaine plasma concentrations were measured [33].

References