The role of atopy in grain dust-induced airway disease.

Abstract

To determine whether atopy influences the physiologic or inflammatory response to grain dust, we compared spirometric measures of airflow and bronchoalveolar lavage (BAL) measures of lower respiratory tract inflammation between demographically similar nonatopic (n = 10) and atopic (n = 10) study subjects after each of two inhalation exposures: Hanks' balanced salt solution (HBSS) and corn dust extract (CDE; 0.4 microgram of endotoxin/kg body weight). Subjects were healthy nonsmokers with similar baseline pulmonary function, without bronchial hyperreactivity, and had not participated in agriculture. Atopic subjects had two or more positive skin responses to 10 common environmental allergens. Both groups developed significant airflow obstruction and lower airway inflammation after CDE inhalation. Importantly, the magnitude of the post-CDE exposure airflow decrements, BAL cellularity, and BAL concentration of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), IL-6, and IL-8 did not significantly differ between atopics and nonatopics. The concentrations of histamine and eosinophils in the BAL fluid were unaffected by CDE inhalation and did not significantly differ between atopics and nonatopics. Atopic status does not appear to be a significant determinant of airflow obstruction or lower airway inflammation following CDE inhalation. Our findings suggest that atopy may play, at most, a minor role in the development of grain dust-induced airway disease.

Role of p38 MAP kinase in LPS‐induced airway inflammation in the rat

“…This response requires the upregulation of adhesion molecules on circulating leukocytes and the pulmonary vascular endothelium and the expression of endogenous chemotactic factors that draw the marginated leukocytes across the endothelial and epithelial barriers into the air spaces (Tang et al, 1995b;Ulich et al, 1991b;Strieter & Kunkel, 1994). Inhalation challenge studies have also shown that LPS causes neutrophilic in¯ammation in nonatopic subjects, non-asthmatic atopic subjects, and asthmatic subjects (Sandstrom et al, 1994;Blaski et al, 1996;Nightengale et al, 1998;Michel et al, 1997).…”

Region-related risk factors for respiratory symptoms in European and Californian farmers

“…For farmers exposed to livestock, the pathogenetic role of gases, dusts and aeroallergens from mammals, poultry, insects and mites has been well characterised [9]. For crop farmers, symptoms have been related to exposure to a variety of agents present in agricultural settings, among them pollens, grain dust, mites, moulds and endotoxin [10,11]. When farmers have been compared to nonfarming control populations from the same regions, an increased prevalence of respiratory symptoms has been commonly observed [12][13][14][15], but studies of the prevalence of respiratory symptoms in different farming regions have revealed great geographical variability [16][17][18].…”

Wheat flour exposure results in recruitment of inflammatory cells in the lungs of healthy individuals

“…In this and previous studies using the exposure chamber, we exposed healthy individuals to dust on a single occasion, while previous studies have concentrated on the effects of individuals with baker's asthma sensitized to wheat flour allergens [Górski et al, 2000]. Interestingly, one comparative study of non-atopic versus atopic subjects showed that atopy did not seem to play a major role in the development of grain-dust induced airway disease [Blaski et al, 1996a]. Since sensitization requires repeated exposures, our type of study would not reveal any allergic reactions to flour allergens.…”