Respiratory Reovirus 1/L Induction of Diffuse Alveolar Damage: A Model of Acute Respiratory Distress Syndrome

London, Lucille; Majeski, Elizabeth I.; Paintlia, Manjeet K.; Harley, Russell A.; London, Steven D.

doi:10.1006/exmp.2001.2414

Cited by 28 publications

(42 citation statements)

References 23 publications

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“…27 However, in reovirus 1/L-induced ARDS, the fibrotic component was not inhibited and IFN-␥ expression levels remained high in either corticosteroid-treated or nTx animals. [25][26][27] Further, treatment of reovirus 1/Linduced BOOP with an anti-IFN-␥ neutralizing monoclonal antibody inhibited fibrotic lesion development on both days 14 and 21 postinfection, further supporting our hypothesis that IFN-␥ plays a significant role in fibrotic lesion development. Our data also demonstrate an increased expression of MCP-1 in reovirus-1/L induced BOOP that was modified after corticosteroid treatment or within CD4-or CD8-depleted mice.…”

Section: Discussionsupporting

confidence: 78%

“…We believe that our data supports a role for IFN-␥ in the fibrotic process and that it acts as a profibrotic agent in the spectrum of fibrosis induced in reovirus 1/L-infected mice. 22,[25][26][27] Our data demonstrate that when the inflammatory and fibrotic process in BOOP is inhibited either by corticosteroid treatment or CD4 or CD8 depletion, the concentration of IFN-␥ in the BAL fluid decreases. Both a decrease in IFN-␥ expression and limited fibrotic lesion development was also demonstrated in T-cell-deficient nTx mice that were infected with reovirus 1/L-induced BOOP.…”

Section: Discussionmentioning

confidence: 63%

“…19 -21 We have described a spectrum of inflammatory lung diseases after respiratory infection with reovirus serotype 1, strain Lang (reovirus 1/L), which is dependent on the strain of mice used. [22][23][24][25][26][27] In this spectrum CBA/J mice infected with 1 ϫ 10 6 PFU reovirus 1/L develop a histologically severe inflammation characterized by an infiltration of lymphocytes organized adjacent to the pulmonary vasculature of the lung. 23 This pattern of mononuclear cell organization without the involvement of intraluminal fibrosis results in lesions histopathologically consistent with the non-fibrotic human syndrome termed follicular bronchiolitis (FB).…”

Section: Bronchiolitis Obliterans Organizing Pneumonia (Boop) Ismentioning

confidence: 99%

“…25,26,33 Mice were sacrificed at various intervals after infection with reovirus 1/L and the lungs were removed, lyophilized, and weighed. Differences between groups were examined for statistical significance using two-tailed Student's t-test.…”

Section: Hydroxyproline (Hp) Assaymentioning

confidence: 99%

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Respiratory Reovirus 1/L Induction of Intraluminal Fibrosis, a Model of Bronchiolitis Obliterans Organizing Pneumonia, Is Dependent on T Lymphocytes

Majeski

Paintlia

Lopez

et al. 2003

The American Journal of Pathology

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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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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 63%

Section: Bronchiolitis Obliterans Organizing Pneumonia (Boop) Ismentioning

confidence: 99%

Section: Hydroxyproline (Hp) Assaymentioning

confidence: 99%

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Respiratory Reovirus 1/L Induction of Intraluminal Fibrosis, a Model of Bronchiolitis Obliterans Organizing Pneumonia, Is Dependent on T Lymphocytes

Majeski

Paintlia

Lopez

et al. 2003

The American Journal of Pathology

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“…Interestingly, these lesions develop in CBA/J, but not in other strains of mice, suggesting that genetic host factors are critical in the development of intra-alveolar fibrosis. A model of diffuse alveolar damage with typical hyaline membranes and high mortality has been obtained with the same animal model but using a higher titre (10 7 pfu) of reovirus 1 [38,39]. Thus, the degree of severity of the initial injury seems to be a critical determinant in the progression towards either organising pneumonia or diffuse alveolar damage [38].…”

Section: Pathogenesismentioning

confidence: 98%

Cryptogenic organising pneumonia

Jf¹

2006

European Respiratory Journal

477

466

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Organising pneumonia is defined histopathologically by intra-alveolar buds of granulation tissue, consisting of intermixed myofibroblasts and connective tissue. Although nonspecific, this histopathological pattern, together with characteristic clinical and imaging features, defines cryptogenic organising pneumonia when no cause or peculiar underlying context is found. Rapid clinical and imaging improvement is obtained with corticosteroid treatment, but relapses are common after stopping treatment.

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Respiratory Reovirus 1/L Induction of Diffuse Alveolar Damage: Pulmonary Fibrosis Is Not Modulated by Corticosteroids in Acute Respiratory Distress Syndrome in Mice

London

Majeski

Altman-Hamamdzic

et al. 2002

Clinical Immunology

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Respiratory Reovirus 1/L Induction of Diffuse Alveolar Damage: A Model of Acute Respiratory Distress Syndrome

Cited by 28 publications

References 23 publications

Respiratory Reovirus 1/L Induction of Intraluminal Fibrosis, a Model of Bronchiolitis Obliterans Organizing Pneumonia, Is Dependent on T Lymphocytes

Respiratory Reovirus 1/L Induction of Intraluminal Fibrosis, a Model of Bronchiolitis Obliterans Organizing Pneumonia, Is Dependent on T Lymphocytes

Cryptogenic organising pneumonia

Respiratory Reovirus 1/L Induction of Diffuse Alveolar Damage: Pulmonary Fibrosis Is Not Modulated by Corticosteroids in Acute Respiratory Distress Syndrome in Mice

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