Allergen-induced impairment of bronchoprotective nitric oxide synthesis in asthma

Ricciardolo, Fabio Luigi Massimo; Timmersa, Mieke C.; Geppetti, Pierangelo; Schadewijkd, Annemarie van; Brahim, Joey J.; Sont, Jacob K.; Gouw, H. W. F. M. De; Hiemstra, Pieter S.; Krieken, J. Han J.M. van; Sterk, Peter J.

doi:10.1067/mai.2001.116572

Cited by 84 publications

(87 citation statements)

References 41 publications

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“…A deficiency of cNOS activity and endogenous bronchodilating NO contributing to AHR was also demonstrated after repeated allergen challenge of sensitised guinea pigs [98,99]. Importantly, it was demonstrated that a reduction in cNOS-derived NO may also contribute to AHR in patients with severe asthma [100], and may similarly be induced by allergen exposure [101]. Interestingly, decreased cNOS (presumably iNANC)-derived NO could also contribute to reduced bronchoprotection by means of deep inspiration in asthmatic patients, which has been recognised as an important factor contributing to AHR [102][103][104][105].…”

Section: Acute Modulation Of Ahrmentioning

confidence: 89%

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Airway hyperresponsiveness in asthma: lessons fromin vitromodel systems and animal models: Fig. 1—

Gosens¹,

Zaagsma²

2008

Eur Respir J

107

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Airway hyperresponsiveness (AHR) is a hallmark clinical symptom of asthma. At least two components of AHR have been identified: 1) baseline AHR, which is persistent and presumably caused by airway remodelling due to chronic recurrent airway inflammation; and 2) acute and variable AHR, which is associated with an episodic increase in airway inflammation due to environmental factors such as allergen exposure.Despite intensive research, the mechanisms underlying acute and chronic AHR are poorly understood. Owing to the complex variety of interactive processes that may be involved, in vitro model systems and animal models are indispensable to the unravelling of these mechanisms at the cellular and molecular level.The present paper focuses on a number of translational studies addressing the emerging central role of the airway smooth muscle cell, as a multicompetent cell involved in acute airway constriction as well as structural changes in the airways, in the pathophysiology of airway hyperresponsiveness.

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Section: Acute Modulation Of Ahrmentioning

confidence: 89%

“…Reduced expression of eNOS or nNOS has been observed after repeated allergen challenge in guinea pigs and mild asthmatic patients, respectively [101,106]. In addition, it has been demonstrated that reduced bioavailability of Larginine, the substrate for NOS, may underlie the deficiency in NO and subsequent AHR [96,107].…”

Section: Acute Modulation Of Ahrmentioning

confidence: 99%

Airway hyperresponsiveness in asthma: lessons fromin vitromodel systems and animal models: Fig. 1—

Gosens¹,

Zaagsma²

2008

Eur Respir J

107

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“…We previously demonstrated in a larger asthma clinical trial that allergen exposure is able to raise FeNO during LAR (8) and to worsen AHR to bradykinin (11). We postulated that allergen-induced increase in FeNO could be related to heightened mucosal eosinophils and AHR to bradykinin in atopic asthma.…”

mentioning

confidence: 99%

“…We postulated that allergen-induced increase in FeNO could be related to heightened mucosal eosinophils and AHR to bradykinin in atopic asthma. For this purpose we performed new immunohistochemical analysis on bronchial biopsy specimens, obtained from the same large project (11) in order to assess the number of mucosal eosinophils and other inflammatory cells 48 hours after diluent and allergen (house dust mite) exposures. Furthermore, inflammatory cell counts were related to the previously published data (FeNO and AHR to bradykinin).…”

mentioning

confidence: 99%

Exhaled Nitric Oxide is Related to Bronchial Eosinophilia and Airway Hyperresponsiveness to Bradykinin in Allergen-Induced Asthma Exacerbation

Ricciardolo

Stefano

Silvestri

et al. 2012

Int J Immunopathol Pharmacol

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Exhaled nitric oxide (FeNO) has been associated with bronchial eosinophilia and with airway hyperresponsiveness (AHR) in mild stable asthma. We previously demonstrated in a large project that allergen exposure is able to raise FeNO and to worsen AHR to bradykinin. We postulated that allergen-induced increase in FeNO could be related to heightened mucosal eosinophils and AHR to bradykinin in atopic asthma. We performed a new immunohistochemical analysis on bronchial biopsy specimens, previously obtained from the same large project, in order to assess the number of mucosal eosinophils (EG-r cell) and other inflammatory cells at 48 hours after diluent and allergen exposures. Inflammatory cell counts were related to FeNO and AHR to BK (expressed as logPD 2o bradykinin). In 10 atopic mild asthmatics, we found that the numbers of EG-r and CD4+ cells in bronchial submucosa were significantly increased after allergen compared to the respective counts after diluent (p < 0.01). EG-r cells in the bronchial submucosa were negatively correlated with logPD 2o bradykinin only after allergen challenge (rho = -0.709, I? = 0.027). We also found a positive strong correlation between EG-r cells and FeNO values in atopic asthmatics at 48 hours after both diluent (rho = 0.746, P = 0.017) and allergen (rho = 0.644, P = 0.049) challenge. FeNO values negatively correlated with responsiveness to bradykinin only after allergen challenge (rho = -0.675, P = 0.039). This study indicates that after allergen exposure heightened level of exhaled NO may reflect augmented airway eosinophilic inflammation and airway responsiveness to bradykinin indicating loss of asthma control.A plethora of studies, by using bronchial mucosal biopsies, have demonstrated that bronchial asthma is a chronic inflammatory disease of the airways characterized by the presence of an array of activated inflammatory cells and mediators. Biopsy specimens from proximal bronchi obtained through a fiberoptic bronchoscope are the most direct method of measuring airway inflammation and are considered the "gold standard" for assessment of airway inflammation in asthma against which other

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“…Η βρογχοπροστατευτική επίδραση του ΝΟ στο άσθμα περιλαμβάνει χάλαση και αναστολή του πολλαπλασιασμού των ΛΜΙ. Η αυξημένη υπεραντιδραστικότητα των αεραγωγών μπορεί να οφείλεται σε ελιπή παραγωγή ΝΟ, το οποίο προέρχεται από ενεργοποίηση της cNOS, σε τοπικό επίπεδο [135] . Από την άλλη το άσθμα συνδέεται με τοπική αύξηση της παραγωγής του ΝΟ το οποίο προέρχεται από ενεργοποίηση της iNOS, και η οποία μακροπρόθεσμα έχει βλαπτική επίδραση στους αεραγωγούς.…”

Section: Nounclassified

Παράγοντες Που Επηρεάζουν Την Απελευθέρωση Του Μονοξειδίου Του Αζώτου (NO) Στους Αεραγωγούς

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Allergen-induced impairment of bronchoprotective nitric oxide synthesis in asthma

Cited by 84 publications

References 41 publications

Airway hyperresponsiveness in asthma: lessons fromin vitromodel systems and animal models: Fig. 1—

Airway hyperresponsiveness in asthma: lessons fromin vitromodel systems and animal models: Fig. 1—

Exhaled Nitric Oxide is Related to Bronchial Eosinophilia and Airway Hyperresponsiveness to Bradykinin in Allergen-Induced Asthma Exacerbation

Παράγοντες Που Επηρεάζουν Την Απελευθέρωση Του Μονοξειδίου Του Αζώτου (NO) Στους Αεραγωγούς

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