Diffuse 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.
Antibiotics generally act directly on infecting micro-organisms. For example, the tetracyclines inhibit bacterial protein synthesis by binding to the 30S subunits of bacterial ribosomes. Chloramphenicol acts on the 50S ribosomal subunit and suppresses peptidyl transferase. Erythromycin, a broad-spec-trum macrolide antibiotic commonly used in patients with lower respiratory infections, also interferes with bacterial protein synthesis by binding to the ribosomal subunit.
On the other hand, many investigators have found that some commonly used antibiotics exert their effects by influencing host defense mechanisms, eg, by acting on neutrophil chemotaxis, lymphocyte transformation, delayed hypersensitivity, and so on. In 1950, Munoz and Geister showed that chlortetracycline inhibited normal human leukocyte phagocytosis, and they addressed the question of antibiotic modulation of the immune system.