Hydrogen peroxide release by alveolar macrophages from sarcoid patients and by alveolar macrophages from normals after exposure to recombinant interferons alpha A, beta, and gamma and 1,25-dihydroxyvitamin D3.

Fels, Anna; Nathan, Carl; Cohn, Z. A.

doi:10.1172/jci113083

Cited by 78 publications

(37 citation statements)

References 28 publications

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“…The increased H202 production was demonstrated for both stimulated and unstimulated cells. These results are similar to the data reported in adult inflammatory lung diseases such as sarcoidosis (26) and in children with interstitial lung diseases (2 1). The mechanisms by which these species may play a role in lung injury have been intensively investigated and many possibilities have been proposed.…”

Section: Discussionsupporting

confidence: 91%

Alveolar Macrophage Status in Bronchopulmonary Dysplasia

et al. 1988

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ABSTRACT. The predominant inflammatory cell type within the alveolar structure in bronchopulmonary dysplasia (BPD) is the alveolar macrophage (AM). AM ability to release hydrogen peroxide, a way to evaluate the cell status, was studied in nine infants who developed clinical and radiological evidence of BPD, and was compared to those from infants without lung parenchymal disorders (n = 6). AM were collected by bronchoalveolar lavage which was done after the mechanical ventilation stage in the BPD group. The experiments were performed on unstimulated AM and on AM stimulated by phorbol myristate acetate. Results revealed that the amount of hydrogen peroxide accumulated in the culture medium was significantly enhanced in the BPD group, in both experimental conditions (p < 0.01 and ~0.001, respectively). Furthermore, improvement of patients treated with glucocorticoids was closely related to a reduction of the alveolitis with a decrease of AM ability to generate hydrogen peroxide. These data indicate that AM activation is a central component of alveolitis in BPD and that extracellular production of oxidants by stimulated AM may play a critical role in the pathogenesis of the disease. According to numerous studies on the pathology of BPD, diffuse alveolar damage appears to be an early event in the development of this chronic lung disease, and histological descriptions have revealed a chronological progression from an

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Section: Discussionsupporting

confidence: 91%

Alveolar Macrophage Status in Bronchopulmonary Dysplasia

et al. 1988

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“…Several investigators have demonstrated that alveolar macrophages isolated from the BAL of sarcoidosis patients possess an enhanced capacity to metabolize oxygen and to produce hydrogen peroxide and superoxide anions, especially under the influence of activating substances [6,[13][14][15][16]. In accordance to these in vitro observed phenomena, the EBC of sarcoidosis patients has elevated levels of 8-isoprostane [8,9], whereas in the present study a systemic redox imbalance was also observed.…”

Section: Discussionsupporting

confidence: 86%

Systemic oxidative stress in patients with pulmonary sarcoidosis

Koutsokera

Papaioannou

Malli

et al. 2009

Pulmonary Pharmacology & Therapeutics

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Background: A local redox imbalance has been reported in pulmonary sarcoidosis.However, so far no study has described a systemic redox imbalance in this context.The aim of the present study was to evaluate the systemic oxidative stress in patients with sarcoidosis and determine its relationship to treatment and indices of disease severity.Methods: 35 patients with histologically proven pulmonary sarcoidosis and 13 healthy volunteers were included in the study. All patients were studied during a stable phase of their disease. Systemic oxidative stress was quantified in serum with the use of a commercially available spectrophotometric method (D-ROM test) which determines overall oxidative stress, by measuring total hydroperoxides. Oxidative stress was expressed in conventional units, i.e. Carratelli Units (UCarr), where 1UCarr corresponds to 0.8mg/L H 2 O 2 .Results: Serum oxidative stress levels were significantly higher in patients with sarcoidosis compared to those of normal subjects (390±25 vs 300±18) UCarr respectively, p=0.04). Patients not receiving systemic corticosteroids had higher levels of oxidative stress compared to steroid-treated patients (461.5±38 vs 315±20, p<0.01) and compared to controls (461.5±38 vs 300±18 UCarr, p<0.01). Oxidative stress did not correlate with diffusion lung capacity (DLCO), partial arterial oxygen tension (PaO 2 ), MRC dyspnoea scale or chest X-ray stage. Conclusions:Systemic oxidative stress is increased in patients with stable pulmonary sarcoidosis who do not receive systemic corticosteroids. This finding suggests a sustained oxidative burden even when clinical, functional and radiological criteria indicate disease stability.

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“…The generation of ROS has been previously observed in the chronic inflammatory environment of granulomatous lung diseases, such as sarcoidosis (12,13). Increased levels of glutathione and glutathione peroxidase have been measured in the epithelial lining fluid of patients with CBD, suggesting a role for the glutathione antioxidant system in granulomatous lung disease (14).…”

Section: Discussionmentioning

confidence: 86%

Modulation of Lymphocyte Proliferation by Antioxidants in Chronic Beryllium Disease

Dobis

Sawyer²,

Gillespie³

et al. 2008

Am J Respir Crit Care Med

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Rationale: Occupational exposure to beryllium (Be) can result in chronic granulomatous inflammation characterized by the presence of Be-specific CD4 1 T cells. Studies show that oxidative stress plays a role in the pathogenesis of chronic inflammatory disorders. Objectives: We hypothesized that Be-induced oxidative stress modulates the proliferation of Be-specific CD4 1 T cells. Methods: Thirty-three subjects with chronic beryllium disease (CBD), 15 subjects with beryllium sensitization, and 28 healthy normal control subjects were consecutively enrolled from the Occupational and Environmental Health Clinic of the National Jewish Medical and Research Center. Measurements and Main Results: All studies were performed with Ficoll-Hypaque-isolated peripheral blood mononuclear cells from subsets of the study subjects. Decreased intracellular levels of the thiol antioxidants, glutathione and cysteine, were observed in peripheral blood mononuclear cells from subjects with beryllium sensitization and CBD, as compared with healthy control subjects. Beryllium stimulation decreased intracellular thiol antioxidants by more than 40%, accompanied by increased reactive oxygen species levels and the proliferation of Be-specific blood CD4 1 T cells from subjects with CBD. Be-induced T-cell proliferation was inhibited by treatment with the thiol antioxidant N-acetylcysteine or the catalytic antioxidant manganese(III) 5,10,15,20-tetrakis(4-benzoic acid)porphyrin (MnTBAP). MnTBAP treatment also inhibited T-cell proliferation in response to the unrelated, MHC class II-restricted antigen tetanus toxoid. Treatment of CBD blood lymphocytes, but not antigen-presenting cells, with MnTBAP decreased Be-induced T-cell proliferation by more than 40%. Conclusions: Beryllium can mediate a thiol imbalance leading to oxidative stress that may modulate the proliferation and clonal expansion of Be-specific blood CD4 1 T cells. These data suggest that Be-induced oxidative stress plays a role in the pathogenesis of granulomatous inflammation in CBD.

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Hydrogen peroxide release by alveolar macrophages from sarcoid patients and by alveolar macrophages from normals after exposure to recombinant interferons alpha A, beta, and gamma and 1,25-dihydroxyvitamin D3.

Cited by 78 publications

References 28 publications

Alveolar Macrophage Status in Bronchopulmonary Dysplasia

Alveolar Macrophage Status in Bronchopulmonary Dysplasia

Systemic oxidative stress in patients with pulmonary sarcoidosis

Modulation of Lymphocyte Proliferation by Antioxidants in Chronic Beryllium Disease

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