No abstract

These findings suggest that inhaled corticosteroid treatment of asthma reduced airway wall vascularity during airway remodelling.

Stromal cell-derived factor-1 (SDF-1) acts as a chemoattractant for leukocytes and can induce neovascularisation. To examine the role of SDF-1 in the development of angiogenesis, immunohistochemical studies were performed on bronchial biopsy specimens from asthmatic and control subjects.Bronchial biopsy specimens were obtained from 13 asthmatic and eight control subjects. The number of vessels and the percentage area they occupied were estimated after staining for type-IV collagen. In addition the number of SDF-1-positive cells was determined.There was a significant increase in the number of vessels and the percentage vascularity in the submucosa of asthmatic subjects compared with control subjects. Asthmatic subjects exhibited a greater number of SDF-1-positive cells in the airway mucosa than control subjects. The degree of vascularity was associated with the number of SDF-1-positive cells. Furthermore, the number of SDF-1-positive cells was inversely correlated with airway calibre and airway hyperresponsiveness. Colocalisation studies revealed that endothelial cells, macrophages and T-lymphocytes were the major sources of SDF-1.These findings suggest that increased vascularity of bronchial mucosa in asthmatic subjects is closely related to the expression of stromal cell-derived factor-1 positive cells, which may play a role in remodelling of airways via angiogenesis. Eur Respir J 2003; 21: 804-809.

bInfection from fluoroquinolone-resistant Enterobacteriaceae is an increasing health problem worldwide. In the present study, we developed a pyrosequencing-based high-throughput method for analyzing the nucleotide sequence of the quinolone resistance-determining regions (QRDRs) of gyrA and parC. By using this method, we successfully determined the QRDR sequences of 139 out of 140 clinical Escherichia coli isolates, 28% of which were nonsusceptible to ciprofloxacin. Sequence results obtained by the pyrosequencing method were in complete agreement with those obtained by the Sanger method. All fluoroquinolone-resistant isolates (n ‫؍‬ 35; 25%) contained mutations leading to three or four amino acid substitutions in the QRDRs. In contrast, all isolates lacking a mutation in the QRDR (n ‫؍‬ 81; 57%) were susceptible to ciprofloxacin, levofloxacin, and nalidixic acid. The qnr determinants, namely, the qnrA, qnrB, and qnrS genes, were not detected in the isolates, and the aac(6=)-Ib-cr gene was detected in 2 (1.4%) of the isolates. Multilocus sequence typing of 34 randomly selected isolates revealed that sequence type 131 (ST131) (n ‫؍‬ 7; 20%) is the most prevalent lineage and is significantly resistant to quinolones (P < 0.01). The genetic background of quinolone-susceptible isolates seemed more diverse, and interestingly, neighboring STs of ST131 in the phylogenetic tree were all susceptible to ciprofloxacin. In conclusion, our investigation reveals the relationship between fluoroquinolone resistance caused by mutations of QRDRs and the population structure of clinical extraintestinal E. coli isolates. This highthroughput method for analyzing QRDR mutations by pyrosequencing is a powerful tool for epidemiological studies of fluoroquinolone resistance in bacteria.

A 47-year-old woman was admitted to hospital with severe Legionella pneumonia. The respiratory symptoms improved dramatically and the X-rays revealed a decrease in the diffuse chest infiltrates after treatment with erythromycin and rifampicin. However, chest CT scans showed that the reticulonodular opacities persisted for several weeks after the onset of pneumonia. Two months after admission, the chest X-rays showed the progression of small nodules in both lungs and there was increasing respiratory distress. A diagnosis of miliary tuberculosis was confirmed. The present case should alert physicians to this potentially confusing combination of respiratory pathogens.