Background: Asthma is an inflammatory airway disease associated with infiltration of T cells and eosinophils, increased levels of pro-inflammatory cytokines, and shedding of bronchial epithelial cells (EC). We have recently shown that T cells and eosinophils cooperate in inducing bronchial EC apoptosis in asthma through secretion of IFN-γ and TNF-α. Since EC shedding is a histologic hallmark of asthma, the intercellular junction of EC may be a target of pro-inflammatory cytokines. Methods: Bronchial EC, cultured and exposed to IFN-γ and TNF-α, were studied for the expression of adhesion molecules and apoptosis. In addition, the epithelial layer of bronchial biopsies from asthma patients was evaluated for apoptosis, shedding, and expression of adhesion molecules. Results: We demonstrate that the induction of EC apoptosis is accompanied by loss of E-cadherin. In situ examination of E-cadherin in asthma revealed a reduction in its expression on EC membranes. In contrast, the in vitro and in vivo expression of β1-integrins and intercellular adhesion molecule-1 (ICAM-1) increased on EC during asthmatic airway inflammation. Conclusions: Loss of cadherin-mediated intercellular adhesion and apoptosis could account for fragility and shedding of EC in asthma, especially since this occurs between columnar and basal EC.
Recently, an increasing number of patients were presented to our clinics with febrile and respiratory symptoms associated with exposure to a new type of domestic ultrasonic humidifier. We report on 11 patients who developed recurrent episodes of fever, cough and dyspnea after repeated exposure to ultrasonic misting fountains at home. A diagnosis of extrinsic allergic alveolitis (EAA) or toxic alveolitis was made on the basis of the history and the clinical, radiological, laboratory and immunological findings. Eight patients were subjected to inhalative challenge tests with their own ultrasonic misting fountains, and all of them exhibited positive reactions. Nine patients were diagnosed with an EAA (humidifier lung) and two patients with a toxic alveolitis (humidifier fever). This study demonstrates the potential for ultrasonic misting fountains to cause illness in the home. In view of the increasing popularity of these devices, humidifier lung and humidifier fever should be considered in the differential diagnosis of patients with unexplained pulmonary or flu-like illnesses with fever.
Among farmers, the prevalence of chronic bronchitis and asthma is higher than in the general population [1][2][3]. This phenomenon is due to the influence of immunological and nonimmunological components of organic dusts [4,5]. Particular importance is attached to the endotoxins [6][7][8]. Reduced exposure to organic dusts is an important preventive measure [9,10]. The utilization of a personal respiratory device (RD) is a common method of cleaning contaminated air [11]. Farmers suffering from respiratory symptoms tend to wear RDs more frequently than farmers without these symptoms [12]. However, it has been shown that even the use of RDs with P2 and P3 filters did not protect patients with farmer's lung; they developed systemic and pulmonary reactions after a challenge [13,14]. It has also been demonstrated that flour-dust asthmatics [15], pig farmers [16,17], grain workers [18,19], subjects suffering from laboratory animal allergy [20], and patients with a cedar allergy [21] cannot receive complete protection using RDs. This failure has been blamed on filter-and face-seal leaks. LACEY et al. [22] demonstrated that filters allow penetration of 0.1-3.1% of actinomycete spores, depending on design. MANNINEN et al. [23] demonstrated face-seal leakages of 2.4-3.4% in RDs.The present study examined whether RDs have a protective effect on farmers with occupational asthma. MethodsTwenty-six farmers from southern Bavaria with suspected occupational asthma were examined. The sample comprised eight females and 18 males with an age of 38.6± 11.8 yrs (mean±SD). Four of the females and six of the males were smokers. All 26 subjects were involved in dairy farming and/or bull breeding either using conventional straw bedding and mucking out by hand or working with manure. They all came in contact with grain dust, hay and straw daily and had been exposed to these conditions for a mean duration of 34±14.9 yrs. Health problems had been present for a mean of 9.1±6.8 yrs. The average daily duration of exposure to agricultural dust lasted up to 4 h. After the farmers had been exposed to hay, straw or grain dust, all of them suffered from coughing, dyspnoea and wheezing breath. Six of them had a history of atopy. A physical examination revealed no deviation from what is considered to be normal. The mean total serum immunoglobulin (Ig)E level was 325±403 IU·mL -1 . The mean serum levels of IgG, IgM, IgA and α 1 -antitrypsin were within normal limits. Table 1 shows the results of the lung-function tests of the 26 farmers at the time of their admission as inpatients. The patients were taking no antiinflammatory or bronchodilatory medicine at the time of the investigations.In all patients, nonspecific bronchial reactivity was tested. A test was rated positive if the specific airway resistance (sRaw) rose to at least twice the baseline value and the absolute value became Š2.0 kPa·s -1 . None of the patients showed a significant rise in sRaw following the inhalation of physiological saline and lactose powder. Eleven of the farmers experi...
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