In 50 of 94 patients with bronchiolitis obliterans we found no apparent cause or associated disease, and the bronchiolitis obliterans occurred with patchy organizing pneumonia. Histologic characteristics included polypoid masses of granulation tissue in lumens of small airways, alveolar ducts, and some alveoli. The fibrosis was uniform in age, suggesting that all repair had begun at the same time. The distribution was patchy, with preservation of background architecture. Clinically, there was cough or flu-like illness for 4 to 10 weeks, and crackles were heard in the lungs of 68 per cent of the patients. Radiographs showed an unusual pattern of patchy densities with a "ground glass" appearance in 81 per cent. Physiologically, there was restriction in 72 per cent of the patients, and 86 per cent had impaired diffusing capacity. Obstruction was limited to smokers. The mean follow-up period was four years. With corticosteroids, there was complete clinical and physiologic recovery in 65 per cent of the subjects; two died from progressive disease. This disorder differs from bronchiolitis obliterans with irreversible obstruction. It was confused most often with idiopathic pulmonary fibrosis. In view of the benign course and therapeutic response, a histologic distinction is important.

Bronchiolitis obliterans organizing pneumonia.

Of all the arachidonic acid metabolites, only prostaglandin E (PGE) has been shown to have a clear role in the regulation of cellular and humoral immune responses. In cellular immune responses such as T cell proliferation, lymphokine production, and cytotoxicity, PGE usually acts as a feedback inhibor of the response. This is also true of macrophage and natural killer cytotoxicity. In some instances PGE is responsible for cellular activation rather than inhibition. This is clearest in the control of humoral immunity, where PGE production is a necessary component in the generation of some type of T suppressor cells. Disturbances in immune function found in several human conditions and diseases have been linked to changes in PGE mediated immunoregulation. Either increased production of PGE or increased sensitivity to PGE results in depressed cellular immunity. Conversely drugs which inhibit PGE production act as stimulants of cellular immune functionin vitro andin vivo.

Regulation of the immune response by prostaglandins

Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high level irritant exposures.

MACROPHAGES play a central and essential part in the immune response by presenting antigen to lymphocytes during the development of specific immunity and by serving as supportive, "accessory" cells...

Current concepts: immunology. Monocytes and macrophages.

The histopathologic and ultrastructural features of intraluminal organizing and fibrotic changes were studied in open lung biopsies and autopsy specimens from 373 patients with interstitial lung disorders, including hypersensitivity pneumonitis (n = 44), idiopathic pulmonary fibrosis (n = 92), collagen-vascular diseases (n = 20), chronic eosinophilic pneumonia (n = 10), pulmonary histiocytosis X (n-90), pulmonary sarcoidosis (n = 62), pneumoconioses (n = 25), Legionnaire's disease (n = 5), drug- and toxin-induced pneumonitis (n = 4), radiation-induced pneumonitis (n = 2), lymphangioleiomyomatosis (n = 11), and chronic organizing pneumonia of unknown cause (n = 8) Three patterns of intraluminal organization and fibrosis were recognized: 1) intraluminal buds, which partially filled the alveoli, alveolar ducts and/or distal bronchioles; 2) obliterative changes, in which loose connective tissue masses obliterated the lumens of alveoli, alveolar ducts or distal bronchioles, and 3) mural incorporation of previously intraluminal connective tissue masses, which fused with alveolar, alveolar ductal, or bronchiolar structures and frequently became reepithelialized All three patterns had common morphologic features, suggesting that, regardless of their severity, they resulted from a common pathogenetic mechanism, ie, the migration of activated connective tissue cells, through defects in the epithelial lining and its basement membrane, from the interstitial into the intraluminal compartment Intraluminal buds were observed most frequently in hypersensitivity pneumonitis, chronic eosinophilic pneumonia, and organizing pneumonia of unknown cause Mural incorporation and, to a lesser extent, obliterative changes were observed in most interstitial disorders and were very prominent in idiopathic pulmonary fibrosis Mural incorporation and obliterative changes play an important role in pulmonary remodeling, especially when several adjacent alveoli and/or other air spaces are involved Under these circumstances, intraluminal organization can mediate the fusion of adjacent alveolar structures by intraluminal connective tissue

Intraluminal fibrosis in interstitial lung disorders.

Bronchiolitis Obliterans: Report of Three Cases with Detailed Physiologic Studies

Report of Three Cases with Detailed Physiologic Studies

Indomethacin-responsive mononuclear cell dysfunction in “atypical” mycobacteriosis

Although chemotherapy of tuberculosis has resulted in a dramatic decrease in the number of new and active cases in the United States, relatively little improvement has been made in the treatment of diseases caused by nontuberculous mycobacteria. Depending on the type of hospital and population served by the hospital, the incidence of “atypical” mycobacteria may be as high as 30% of all mycobacterial infections (1). Aside from the clinical importance and economic consequences of these infections, these chronically ill patients provide a valuable source of new information concerning cellular defense mechanisms and resistance to chronic infectious diseases. Unlike patients with chronic fungal infections who commonly develop disease during early childhood, patients with “atypical” mycobacterial diseases are usually well during early childhood and adolescence (2). Thus, to explain the predisposition of individuals to infections with these organisms, one would predict an abnormality of immunoregulatory mechanisms rather than a failure to develop immunocompetent lymphoid cells.

Ulysses G. Mason

Papers

Bronchiolitis Obliterans: Report of Three Cases with Detailed Physiologic Studies

Report of Three Cases with Detailed Physiologic Studies

Indomethacin-responsive mononuclear cell dysfunction in “atypical” mycobacteriosis

Improvement of Abnormal Lymphocyte Responses in “Atypical” Mycobacteriosis with Indomethacin