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Bronchiolitis obliterans organizing pneumonia (BOOP) isBronchiolitis obliterans organizing pneumonia (BOOP), first described in 1985, is a pattern of injury characterized histologically as "patchy plugs of fibrous tissue (Masson bodies) filling bronchiolar lumens (bronchiolitis obliterans) and alveolar ducts and spaces (organizing pneumonis)." [1][2][3] This patchy fibrosis may begin as focal lesions within the alveoli and the terminal bronchioles of the lung and progress bilaterally over time. 1 Other histological features include clusters of mononuclear inflammatory cells, chronic inflammation in the walls of the surrounding alveoli with reactive type II cells, increased numbers of foamy macrophages in the alveoli, and preserved lung architecture. 2,4 The development of BOOP is often of unknown etiology (idiopathic BOOP) but BOOP has also been associated as a consequence of lung injury due to environmental toxins, bacterial infections, viral infections, and lung or bone marrow transplantation. 3,5 BOOP is responsive to corticosteroids and treatment with prednisone continues to be the primary treatment for patients with symptomatic and progressive disease. [2][3][4] Since infiltrating lymphocytes are associated with the initiation of BOOP lesions, 6,7 it is possible that these cells play an active role in the progression of inflammatory foci into lesions that are progressively dominated by fibroblasts. In patients with BOOP, there is an increase of activated bronchoalveolar lavage (BAL) lymphocytes with up to 80% to 95% of this cellular infiltrate being comprised of cytotoxic/ suppressor CD8 ϩ T cells. 6 -9 These cells may be involved in the inflammation and subsequent fibrosis occurring in BOOP patients. 2,5,7,10 -12 Several studies have shown that the infiltration of T lymphocytes may be important in the development of other forms of pulmonary fibrosis, although the data from both animal models and patients has been equivocal. [13][14][15][16][17][18] Although these existing models of experimental pulmonary fibrosis have been useful for histopathological and functional investigations of other types of fibrotic events in the lung, the process of fibrotic lesion development in these models may be distinct from BOOP lesion development. Thus, differences in the phenotype of the inflammatory cell infiltrate, expression of soluble mediators, and response to various treatments may be different and,

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Bronchiolitis obliterans organizing pneumonia (BOOP) and Acute Respiratory Distress Syndrome (ARDS) are two pulmonary diseases with fibrotic components. BOOP is characterized by perivascular/peribronchiolar leukocyte infiltration leading to the development of intra-alveolar fibrosis. ARDS is a biphasic disease that includes an acute phase, consisting of severe leukocyte infiltration, edema, hemorrhage, and the formation of hyaline membranes, and a chronic phase, which is characterized by persistent intra-alveolar and interstitial fibrosis. CBA/J mice infected with 1 x 10(6) plaque-forming units (pfu) reovirus 1/L develop follicular bronchiolitis and intra-alveolar fibrosis similar to BOOP. In contrast, CBA/J mice infected with 1 x 10(7) pfu reovirus 1/L develop histologic characteristics of ARDS including diffuse alveolar damage, hyaline membranes, and intra-alveolar fibrosis. In this report, we demonstrate a differential role for T lymphocytes in the development of fibrosis associated with BOOP versus ARDS. Neonatally thymectomized CBA/J mice infected with 1 x 10(7) pfu (ARDS) reovirus 1/L still develop the hallmark characteristics of ARDS, including a severe viral pneumonia with cellular infiltrates comprised mainly of macrophages and neutrophils, hyaline membrane formation, and hemorrhage during the acute phase of the disease and persistent intra-alveolar fibrosis during the chronic phase of the disease. In contrast, neonatally thymectomized CBA/J mice infected with 1 x 10(6) pfu (BOOP) reovirus 1/L do not develop intra-alveolar fibrosis associated with BOOP. Therefore, while T cells are necessary for the development of intraluminal fibrosis associated with BOOP, they are not necessary for the development of intraluminal fibrosis associated with ARDS. Furthermore, we suggest that interferon-gamma plays a key role in the fibrotic process and that elevated levels of interferon-gamma are associated with a continuum from least to more severe fibrosis.