Asthma and rhinosinusitis.

Allergic rhinoconjunctivitis and asthma are becoming more common in industrialized societies, particularly in the second and third decades of life, when those affected are at a vital stage of their education and career. It is therefore of paramount importance that the treatment options available be effective, improve quality of life, and above all, they must be without any significant unwanted effects. National and international guidelines for the treatment of both allergic rhinitis and asthma have been released recently that put forward recommendations based on an extensive evidence-based review of the literature for the care of these diseases that would meet these goals of disease management.

Effect of ozone and nitrogen dioxide on the permeability of bronchial epithelial cell cultures of non-asthmatic and asthmatic subjects.

Background: Although epidemiological as well as in vivo exposure studies suggest that ozone (O3) and nitrogen dioxide (NO2) may play a role in airway diseases such as asthma, the underlying mechanisms are not clear.

Objective: Our aim was to investigate the effect of O3 and NO2 on the permeability of human bronchial epithelial cell (HBEC) cultures obtained from non-atopic non-asthmatic (non-asthmatics) and atopic mild asthmatic (asthmatics) individuals.

Methods: We cultured HBECs from bronchial biopsies of non-asthmatics and asthmatics, and exposed these for 6 h to air, 10 to 100 parts per billion (p.

Anaphylaxis and anaphylactoid reactions. A guide to prevention, recognition, and emergent treatment.

Anaphylaxis and anaphylactoid reactions are adverse immunologic responses that require early intervention to prevent life-threatening consequences. The initial symptoms, such as nasal congestion or pruritus, can quickly progress to cardiac collapse or asphyxiation. In this article, Drs Rusznak and Peebles discuss the mechanisms of these reactions, common causative agents, preventive strategies, recognition, and treatment.

Interaction of cigarette smoke and house dust mite allergens on inflammatory mediator release from primary cultures of human bronchial epithelial cells.

Several studies have shown that exposure to cigarette smoke and/or house dust mite (HDM) can lead to increased airway inflammation in susceptible individuals. The underlying mechanisms, however, are not defined. To investigate the interaction between cigarette smoke and HDM allergen on mediator release from primary cultures of human bronchial epithelial cells.

Cigarette smoke decreases the expression of secretory component in human bronchial epithelial cells, in vitro.

Epithelial secretory component (SC) is thought to be essential for immunologic protection of the respiratory tract from viral and bacterial infection, since it transports polymeric IgA from the basolateral to the luminal surface of epithelial cells. We have hypothesized that recurrent infection in airways of cigarette smokers is at least partly a consequence of cigarette smoke-induced downregulation of the expression and/or release of SC from airway epithelial cells, subsequently resulting in decreased transcytosis of secretory IgA to the airway lumen. To test this hypothesis, we have cultured human bronchial epithelial cells (HBEC) from surgical tissues and exposed these for 20 minutes to either air or cigarette smoke.