Category Archives: Panbronchiolitis

Erythromycin Inhibits Neutrophil Chemotaxis in Bronchoalveoli of Diffuse Panbronchiolitis: Comment

Erythromycin Inhibits Neutrophil Chemotaxis in Bronchoalveoli of Diffuse Panbronchiolitis: CommentThe mobilization of neutrophils from the intravascular compartment into the respiratory tract is crucial for effective host defense. In other clinical settings, however, such as adult respiratory distress syndrome and chronic lower respiratory tract infection, neutrophils are injurious to the host in terms of generating oxygen radicals and in terms of the action of elastase Thus, excessive inflammation contributes to tissue damage asthma inhalers.

Several researchers have described the inhibitory effect of EM on chemotaxis in vitro and on neutrophil migration into the murine lung in response to Proteus mirabilus in vivo.sl In our present study, we found that treatment with EM significantly reduced the number of intra-pulmonary neutrophils, indicating that, in DPB, EM might act first by reducing neutrophil migration and then by inhibiting inappropriate and excessive inflammation in the lower respiratory tract.

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Erythromycin Inhibits Neutrophil Chemotaxis in Bronchoalveoli of Diffuse Panbronchiolitis: Conclusion

Other antibiotics, including doxycycline, lymecy-cline, and rifampin, have also been found to inhibit chemotaxis of human neutrophils and to suppress phytohemagglutinin-induced lymphocyte transformation in vitro. Recently, FK506, a macrolide antibiotic, has been shown to inhibit T-cell activation by a mechanism that appears similar to that of cyclosporin A.

Various studies have reported the influence of EM on the host defense mechanisms of patients with DPB, in terms of the changes in lymphocyte subsets increased natural killer cell activity, suppression of oxygen radical products, and suppression of elastase activity. We have previously reported that the BAL fluid supernatant obtained from patients with DPB enhanced superoxide production by neutrophils isolated from healthy volunteers, and that this enhancing effect was reduced to near normal after EM treatment flovent inhalers.

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Erythromycin Inhibits Neutrophil Chemotaxis in Bronchoalveoli of Diffuse Panbronchiolitis: Discussion

Erythromycin Inhibits Neutrophil Chemotaxis in Bronchoalveoli of Diffuse Panbronchiolitis: DiscussionDiffuse panbronchiolitis is a chronic inflammatory disease that is manifested in a diffuse fashion in both lungs in the region of the respiratory bronchioles. Typical features of the lesions are thickening of the walls of the bronchioles, with infiltration of lymphocytes, plasma cells, and histiocytes; proliferation of lymphfollicles; accumulation of foamy cells within the wall and neighboring area; and extension of these inflammatory changes toward the peribronchiolar tissues review.

The treatment for this disease used to involve steroid administration and oxygen inhalation in the first stage, and antibiotics, expectorants, and bronchodi-lators in the advanced stage. Prognosis was poor, however, especially when there was super infect ion with P aeruginosa. In 1984, Kudoh et al reported that low dose long-term EM therapy was effective in chronic lower respiratory tract disease, including DPB, and that great improvements were shown in clinical symptoms. Since that time, this has been the preferred therapy for DPB. Its mechanism of action, however, remains obscure.

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Erythromycin Inhibits Neutrophil Chemotaxis in Bronchoalveoli of Diffuse Panbronchiolitis: BAL Fluid

Additionally, there were no significant correlations between the recovery rate and NCA either in initial BAL fluid samples (r=0.017, p>0.6) or in repeated samples (r= —0.316, p>0.6). Albumin concentration and NCA did not correlate in either the initial or the repeated samples of BAL fluid (initial samples: r=0.102, p>0.6; repeated samples: r=0.254, p>0.6). Thus, we regarded NCA as being unaffected by recovery rate or by albumin concentration, and we, therefore, expressed without correction. Although BAL fluid samples from DPB patients may contain more bacterial endotoxin than samples from healthy subjects, we believe it to be that the endotoxin would not have affected the chemotaxis findings, both in the light of report by Issekutz and Bhimji that endotoxin did not induce neutrophil chemotaxis in the in vitro assay and in the light of our observation here that neither of the two endotoxin preparations (P aeruginosa serotype 10 and Salmonella typhosa; Sigma) tested induced neutrophil chemotaxis in the in vitro assay at concentrations 10 to 100 times higher than those inducing leukocyte infiltration in vivo (data not shown) Here.

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Erythromycin Inhibits Neutrophil Chemotaxis in Bronchoalveoli of Diffuse Panbronchiolitis: Changes in RAL Findings

Erythromycin Inhibits Neutrophil Chemotaxis in Bronchoalveoli of Diffuse Panbronchiolitis: Changes in RAL FindingsErythromycin was administered to the patients for 9.3 ±0.8 months. After the treatment, H influenzae was eradicated in three patients but replaced by P aeruginosa in one case. In all 3 patients originally exhibiting P aeruginosa in cultures, the organism was eradicated. In the one patient (case 1) with S aureus, this organism was eradicated, but replaced by H influenzae. In one of the patients with normal flora, these were replaced by H influenzae; in the other such patient, these flora were replaced by P aeruginosa. The bacteria eradication rate was 75.0 percent (6/8).

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Erythromycin Inhibits Neutrophil Chemotaxis in Bronchoalveoli of Diffuse Panbronchiolitis: Gel-filtration

The neutrophils (50 aliquots) were placed in the upper wells, at a concentration of 3X106 cells/ml, in Hank’s solution with 0.1 percent BSA. Chambers were incubated for 30 min at 37°С in a humidified atmosphere of 95 percent air: 5 percent CO2; the filters were removed, fixed in absolute methanol, and stained with eosin-azur (Diff-Quik, Harleco; Gibbstown, NJ). The cells that migrated through the filter to the other side were counted. The NCA was measured as the mean number of cells per 10 high power fields (1,000X). The results were expressed as the percentage of the chemotactic response to FMLP 10-7 M. In each experiment, a negative control was assessed, using Hank’s solution for the BAL fluid and the fraction fluid further.

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Erythromycin Inhibits Neutrophil Chemotaxis in Bronchoalveoli of Diffuse Panbronchiolitis: Erythromycin Treatment

Erythromycin Inhibits Neutrophil Chemotaxis in Bronchoalveoli of Diffuse Panbronchiolitis: Erythromycin TreatmentAll patients received 200 mg of erythromycin stearate orally 3 times per day for more than 6 months until BAL was repeated. The patients were instructed at each outpatient attendance to take one tablet every 8 hours, at home, and they were given a 4-week supply. They were instructed to bring back any remaining tablets at each visit to that the numbers of remaining tablets could be checked. None of the patients received corticosteroids or antibiotics other than EM for the duration of this study read only.

The patients were premedicated intramuscularly with atropine (0.5 mg) and local anesthesia was produced with 2 percent lidocaine; airway examination was then carried out with a flexible fiberoptic bronchoscope (Olympas BF-P20 type; Olympus Corp, New Hyde Park, NY).

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Erythromycin Inhibits Neutrophil Chemotaxis in Bronchoalveoli of Diffuse Panbronchiolitis: Patient Population

Diffuse panbronchiolitis progresses insidiously and the prognosis, especially after Pseudomonas aeruginosa superinfection, is generally poor. Recently, low dose long-term erythromycin (EM) treatment has become the preferred therapy for chronic lower respiratory tract disease, including DPB. That erythromycin may act as an anti-inflammatory agent is indicated by recent reports that it raises natural killer cell activity and has potent capacity to suppress the polymorphonuclear leukocyte (PMN) chemilumi-nescence induced by N-formyl-methionyl-leucyl-phenylalanine (FMLP), opsonized zymosan, and the calcium ionophore, A23187.

The mechanism responsible for the therapeutic action of EM, however, is still unclear. Our recent finding indicated marked neutrophil accumulation in the lung of patients with DPB. Accordingly, in an attempt to elucidate this mechanism, we investigated the effect of EM on neutrophil migration, and we attempted to characterize the neutrophil chemotactic factors in the bronchoalveolar lavage (BAL) fluid of patients with DPB online antibiotics.

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Erythromycin Inhibits Neutrophil Chemotaxis in Bronchoalveoli of Diffuse Panbronchiolitis

Erythromycin Inhibits Neutrophil Chemotaxis in Bronchoalveoli of Diffuse PanbronchiolitisDyffuse panbronchiolitis (DPB), an important pulmonary disease entity, was first reported in 1969 in Japan as an entity distinct from bronchial asthma, chronic bronchitis, chronic pulmonary emphysema, bronchiectasis, and alveolitis. This disease is characterized by chronic inflammation localized predominantly in the region of the respiratory bronchioles with inflammatory cell infiltration; its pathogenesis remains unknown. Although not uncommon in Japan, the disease is rare elsewhere.

There have been recent reports, however, documented of two cases in white North American patients and of the first case in an Italian patient. The chief signs of this disease are chronic cough, pyomucous sputum, shortness of breath, wheezing, and hypoxemia. About three-quarters of these patients have associated chronic parasinusitis. Chest roentgenograms show bilateral fine nodular densities, together with hyperinflation of both lungs. Pulmonary function tests show a mixed ventilatory impairment consisting of slight restrictive and marked obstructive disturbance. The HLA-Bw54, found specifically in Japanese and Chinese people, is found more frequently in DPB cases than in healthy persons. Associated diseases include ulcerative colitis, allergic angitis and granulomatosis, and T cell leukemia review.

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