PubMed · 3751540
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M Bussi, M E Amasio. [Changes in nasal function after rhinoplastic intervention].. https://pubmed.ncbi.nlm.nih.gov/3751540/
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The present consensus on the diagnosis and treatment of asthma relies on symptoms and lung function measurements for the monitoring of disease severity. Even though this probably remains the cornerstone of asthma management, the rapidly increasing insight into the pathogenesis and pathophysiology of the disease is presently leading to the development of more direct measurements of airway inflammation, which may provide potentially relevant information on its clinical course and prognosis. However, at present none of these has sufficiently been validated for current use in monitoring patients with asthma. First, there are new ways of looking at symptoms and lung function. Careful measurements of symptoms by visual analogue scale (VAS) are suggesting that inflammatory activity within the airways can be subjectively perceived, a sensitivity which may be blunted in patients with brittle asthma. In addition, modern physiological parameters, such as the degree of bronchodilatation following a deep breath (M/P-ratio), are strongly associated with airway inflammation. Second, there are multiple cellular and/or soluble markers of inflammation in peripheral blood (using PCR, in situ hybridization, flow cytometry, or circulating mediators and cytokines) and in urine (LTE4, EPX). Recently this has been extended by similar measurements in hypertonic saline-induced sputum (cell differentials and specific stainings on cytospins, flow cytometry, and levels of e.g. ECP, IL-5, IL-8). Finally, mediators and cytokines in the condensate of exhaled air (H2O2, leukotrienes, IL-5?) as well as exhaled NO are currently under evaluation. Adding such markers of airway inflammation as guides in asthma therapy is potentially useful. As a first step towards such a new approach we have recently shown that adding the reduction of airway hyperresponsiveness to the aims of asthma therapy leads to a better clinical as well as histological outcome after two years of treatment. In conclusion, there are new and exciting perspectives in the monitoring of disease severity in asthma in the future. Longitudinal studies presently ongoing will elucidate which parameter is potentially most useful in guiding asthma management.
Mast cells are the main effector cells of immediate hypersensitivity and anaphylaxis. Their role in the development of allergen-induced airway hyperresponsiveness (AHR) is controversial and based on indirect evidence. To address these issues, mast cell-deficient mice (W/W v) and their congenic littermates were sensitized to ovalbumin (OVA) by intraperitoneal injection and subsequently challenged with OVA via the airways. Comparison of OVA-specific immunoglobulin E (IgE) levels in the serum and numbers of eosinophils in bronchoalveolar lavage fluid or lung digests showed no differences between the two groups of mice. Further, measurements of airway resistance and dynamic compliance at baseline and after inhalation of methacholine were similar. These data indicate that mast cells or IgE-mast cell activation is not required for the development of eosinophilic inflammation and AHR in mice sensitized to allergen via the intraperitoneal route and challenged via the airways.
Asthma is a chronic inflammatory disorder of the airways in which many cells participate. This inflammation causes recurrent episodes and symptoms that are associated with widespread but variable airflow limitation that is at least partly reversible either spontaneously or with treatment. Therefore, an investigation of useful remedies for the treatment of bronchial asthma is proposed. In this study, we determined whether both forms of pituitary adenylate cyclase activating polypeptide (PACAP 38 and PACAP 27) belonging to the vasoactive intestinal peptide (VIP) family of peptides could inhibit the effects of histamine-induced respiratory resistance (Rr) in anesthetized guinea pigs, when compared with VIP. The order for 50% suppression (ED50) of Rr induced by peptides was VIP > PACAP 27 > PACAP 38. The inhibitory effects induced by PACAP 38 on histamine-induced Rr in guinea pigs were more prolonged than with the other two peptides. Moreover, adding the endopeptidase inhibitor phosphoramidon prolonged the inhibitory effects of PACAPs. These results suggested that the exogenous peptides of the inhibitory nonadrenergic noncholinergic nervous (i-NANC) peptides could become a useful remedy for treatment of bronchial asthma, because these belong to an important intrinsic hormone.