An inflammation of the airway of patients with diffuse panbronchiolitis (DPB), is characterized by dense neutrophil infiltration. Resolution of the inflammation can be achieved by the removal of apoptotic neutrophils by human alveolar macrophages (AM) without liberating neutrophil proteases in the airway. To understand clinical efficacy for the treatment of DPB by 14-or 15-member macrolides, their effects on the phagocytosis of apoptotic neutrophils by AM were examined. Treatment of AM with erythromycin (ERY) or clarithromycin at clinically achievable levels significantly increased the levels of phagocytosis of apoptotic neutrophils. A serum factor was not essential for the enhancement by these 14-member macrolides. Of the antibiotics tested, these effects were specific for the 14-member macrolides and a 15-member macrolide, azithromycin, but not for the 16-member macrolides, clindamycin or ␤-lactam antibiotics. The enhanced phagocytosis of apoptotic neutrophils by ERY had no effect on the levels of interleukin-8 or tumor necrosis factor alpha production by lipopolysaccharide-stimulated AM after phagocytosis of the apoptotic neutrophils. The increased phagocytosis of apoptotic neutrophils by ERY was also found to be phosphatidylserine receptor-dependent for AM. These data indicate a novel anti-inflammatory action of 14-member and 15-member macrolides, and suggest that such antibiotics achieve clinical efficacy for patients with DPB, in part, through enhancing the nonphlogistic phagocytosis of apoptotic neutrophils by AM.

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Moraxella (Branhamella) catarrhalis is an aerobic gram-negative, oxidase positive diplococcus, and was once considered a nonpathogenic commensal of the upper respiratory tract. However it has been regarded as a potential pathogen since the mid-1980s (6). In many countries, M. catarrhalis has become the third most common cause of bacterial lower respiratory tract infection after Haemophilus influenzae and Streptococcus pneumoniae (3). In general, M. catarrhalis is also recognized as a major cause of community-acquired respiratory infections (18,26), otitis media, and sinusitis (4), and a cause of nosocomial respiratory infections (1,5,8,15,19,20). While nosocomial outbreaks of M. catarrhalis were suspected in previous studies, confirmation was hampered by the lack of an established typing system. In fact, several epidemiological typing methods have been used to characterize strains of M. catarrhalis such as phenotypic characterization, electrophoretic mobility of esterases, outer membrane proteins, whole-cell proteins, plasmid profiles, isoelectric focusing of β-lactamase A and B). Of the three patterns, two patterns (A and B) were found in both inpatients and outpatients. More interestingly, two subtypes of pattern B (B1 and B4) were simultaneously found in both inpatients and outpatients. Our results indicated that PFGE with SmaI chromosomal digestion is a suitable technique to establish the inter-strain genetic relatedness of M. catarrhalis, and suggested that the outbreak of M. catarrhalis occasionally included miscellaneous PFGE patterns. The results also showed that PFGE patterns of M. catarrhalis isolates were similar between hospitaland community-acquired respiratory infections. Analysis of the subtypes suggested that there might be some association between hospital-and community-acquired respiratory infections caused by M. catarrhalis.

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A 60-year-old woman seen at the National Hospital Organization Nagasaki Medical Center of Neurology with a cough and abnormal chest radiography was found in CT to have interstitial shadows in the bilateral lower lung fields. She was diagnosed with interstitial pneumonia and treated with steroids. Treatment was effective, and the predonisolone dosage was gradually tapered. When dosage was 17.5 mg/day, her chest Xray showed exacerbation. Cyclophosphamide at 50mg/day was added, and chest radiography improved. Two months later, her chest radiography showed infiltration with cavities in the left lung field. Although several antibiotics (sulbactam/cefoperazone, levofloxacin) were administered, no improvement was seen. Sputa on hospital day 60 showed the presence of gram-positive branched rods, identified as Nocardia beijingensis. We administered sulfamethoxazole/trimethoprim, meropenem and levofloxacin together, and shadows improved. With recurrent aggravation of interstitial pneumonia, however, new cavity shadows occurred in the bilateral lung due to Aspergillus fumigatus. Shadows worsened and she died of respiratory failure. Testing for pulmonary nocardiosis should be added to differential diagnosis procedures as an opportunistic infection in immune-compromised hosts.