High-affinity immunoglobulin E receptor expression is increased in large and small airways in fatal asthma.

BACKGROUND: IgE and its high-affinity receptor FcɛRI play an important role in allergy and asthma. The distribution of FcɛRI expression in the airways and within the airway wall, however, is largely unknown. OBJECTIVE: In this study, we aimed to map the distribution of FcɛRI in different layers of large airways (LA) and small airways (SA) in lung tissue from non-smoking and smoking patients who died of asthma [fatal asthma (FA)] and non-smoking controls (CTR). METHODS: Postmortem lung tissue from 24 cases of non-smoking FA, 13 smoking FA patients and from 19 subjects who died of non-pulmonary causes (CTR) was immunohistochemically stained for FcɛRI and AA1 (mast cell tryptase marker). The expression of these markers was analysed in inner, muscle, and outer layers of both LA and SA by image analysis. RESULTS: FcɛRI expression was higher in non-smoking and smoking FA compared with CTR in the inner and outer layer of SA. In the outer layer of LA, FcɛRI expression was higher in non-smoking FA compared with CTR. AA1 was higher in non-smoking FA compared with smoking FA and CTR in the outer layer of the SA, which was correlated with FcɛRI in this layer. CONCLUSION: Our results show that the expression of FcɛRI is higher in both LA and SA in FA compared with CTR. These differences are predominantly found in the outer layer where they can be attributed in part to the increased mast cell numbers. These results indicate an increased capacity to mount IgE-mediated reactions in FA, both in LA and SA.

Subchronic effects of nasally instilled diesel exhaust particulates on the nasal and airway epithelia in mice.

Diesel exhaust is the major source of ultrafine particles released during traffic-related pollution. Subjects with chronic respiratory diseases are at greater risk for exacerbations during exposure to air pollution. This study evaluated the effects of subchronic exposure to a low-dose of diesel exhaust particles (DEP). Sixty male BALB/c mice were divided into two groups: (a) Saline: nasal instillation of saline (n = 30); and (b) DEP: nasal instillation of 30 microg of DEP/10 microl of saline (n = 30). Nasal instillations were performed 5 days a week, over 30 and 60 days. Animals were anesthetized with pentobarbital sodium (50 mg/kg intraperitoneal [i.p.]) and sacrificed by exsanguination. Bronchoalveolar lavage (BAL) fluid was performed to evaluate the inflammatory cell count and the concentrations of the interleukin (IL)-4, IL-10, and IL-13 by enzyme-linked immunosorbent assay (ELISA). The gene expression of oligomeric mucus/gel-forming (Muc5ac) was evaluated by real-time polymerase chain reaction (PCR). Histological analysis in the nasal septum and bronchioles was used to evaluate the bronchial and nasal epithelium thickness as well as the acidic and neutral nasal mucus content. The saline group (30 and 60 days) did not show any changes in any of the parameters. However, the instillation of DEP over 60 days increased the expression of Muc5ac in the lungs and the acid mucus content in the nose compared with the 30-day treatment, and it increased the total leukocytes in the BAL and the nasal epithelium thickness compared with saline for 60 days. Cytokines concentrations in the BAL were detectable, with no differences among the groups. Our data suggest that a low-dose of DEP over 60 days induces respiratory tract inflammation.