SUMMARYT cell lymphopenia in the peripheral blood lymphocytes (PBL) of patients with AT is mainly caused by a decrease of naive CD45RA /CD4 cells followed by a predominance of memory CD45RO lymphocytes. To relate these ®ndings to the regulation of programmed cell death, we investigated the activation state and apoptotic level of PBL in 12 patients and healthy controls by¯ow cytometry. In accordance with previous investigations, the number of naive CD4 /CD45RA cells was signi®cantly decreased in patients compared with healthy controls. This disturbed balance of CD45RA and CD45RO was also re¯ected in higher amounts of activated HLA-DR and CD95 expressing cells, with a concomitant decrease of Bcl-2 protected lymphocytes in the T cell population. With regard to its role in preventing oxidative-induced cell death, we analysed Bcl-2 expression and apoptosis in the presence of oxidative stress. In culture, cells of patients are more susceptible to spontaneous programmed cell death. However, in our stress-inducing system (hypoxanthine/xanthine oxidase system) the number of cells undergoing apoptosis was lower in patients' cell populations compared with controls. In addition, preliminary results suggest that Bcl-2 expression and level of spontaneous apoptosis in patients can be modi®ed by IL-2 and interferon-gamma.
Chronic obstructive bronchitis with inadequate response to inhaled steroid and bronchodilator therapy is a rather rare disorder in children. Persistence of an adenoviral infection has been described as a possible cause of unremitting airway obstruction. We studied a group of 11 children with the clinical feature of chronic bronchial obstruction. A high-resolution computed tomography (HR-CT) scan was performed and typically showed hyperinflation and ground-glass-like opacities. All children underwent either bronchoscopic transbronchial or open lung biopsy. Biopsy specimens were stained with monoclonal antibodies detecting adenoviral antigen and analyzed by light-microscopy. Bronchoalveolar lavage (BAL) fluid was cultured for adenovirus, and antigen detection tests were performed. While some children had a history of proven adenoviral infection at the onset of their disease, in none of the cases could a persistence of adenovirus be shown. We conclude that adenoviral infection might act as a starter of chronic obstructive bronchitis in children, but that pathogenetic mechanisms other than persistent infection must be responsible for the chronicity of the disease.
Adenovirus can cause severe bronchiolitis in previously healthy children. Diagnosis may be difficult to achieve. The role of antiviral therapy in the treatment of adenoviral infections remains to be cleared.
ABSTRACT. Severe adenoviral infections such as the necrotizing adenovirus bronchiolitis occur sporadically in infants. Ascertaining the etiologic role of adenovirus in cases of lung disease can pose a diagnostic problem. We present two cases of severe bronchiolitis in previously healthy children in which adenovirus could be shown to be the causing agent. Both children received immunosuppressive therapy with steroids and Cyclosporin for 3 mo and a course of intravenous Ribavirin for 10 d. The results were conflicting: despite therapy Patient 1 died due to respiratory failure, Patient 2 improved notably. Conclusions: Adenovirus can cause severe bronchiolitis in previously healthy children. Diagnosis may be difficult to achieve. The role of antiviral therapy in the treatment of adenoviral infections remains to be cleared. □Adenovirus, bronchiolitis
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