Tumor Necrosis Factor-α Plays a Central Role in Interleukin-2-Induced Pulmonary Vascular Leak and Lymphocyte Accumulation

Dubinett, Steven M.; Huang, Min; Lichtenstein, Alan; McBride, William H.; Wang, Jianyi; Markovitz, Gerald H; Kelley, Diane G.; Grody, Wayne W.; Mintz, Leah E.; Dhanani, Shawkat

doi:10.1006/cimm.1994.1214

Cited by 46 publications

(14 citation statements)

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“…The significance of this is unknown since sTNF-Rs inhibit the infiltration of lymphocytes into the lungs [26], and lymphocyte numbers in the BALF from sarcoidosis patients were correlated significantly with the levels of type II sTNF-R in this study. Furthermore, TNF plays a central role in interleukin-2-induced pulmonary lymphocyte accumulation [10]. Soluble type II receptors may function as inhibitors for lymphocyte infiltration to the lungs in sarcoidosis.…”

Section: Discussionmentioning

confidence: 99%

Elevated Levels of Type II Soluble Tumor Necrosis Factor Receptors in the Bronchoalveolar Lavage Fluids of Patients with Sarcoidosis

Hino

Nakamura

Shibata

et al. 1997

Lung

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Since tumor necrosis factor (TNF) is known to be involved in granuloma formation in sarcoidosis, and soluble TNF receptors (sTNF-Rs) inhibit TNF action in vivo, we evaluated the levels of sTNF-Rs in the bronchoalveolar lavage fluids (BALF) of 31 subjects using an enzyme-linked immunosorbent assay. Our group consisted of 13 patients with sarcoidosis (7 sarcoidosis patients who received no treatment and 6 who received corticosteroid therapy) and 18 control subjects (11 healthy nonsmokers and 7 asymptomatic smokers). Type II (75-kDa), but not type I (55 kDa) sTNF-R in BALF was elevated significantly in patients with sarcoidosis compared with the healthy nonsmokers (type I: 126.7 +/- 17.6 pg/ml BALF vs 79.4 +/- 16.5 pg/ml BALF, p > 0.05; type II: 98.3 +/- 27.8 pg/ml BALF vs 26.7 +/- 4.9 pg/ml BALF, p < 0.05). Although levels of type I sTNF-R in BALF from sarcoidosis patients were not correlated with any cellular profiles of BALF, concentrations of type II correlated significantly with the numbers of lymphocytes in BALF. We concluded that sTNF-R is a normal constituent of the epithelial lining fluids and that levels of type II sTNF-R are elevated significantly in the BALF from individuals with sarcoidosis. This suggests that sTNF-Rs may influence the local bioactivity of TNF and may also contribute to the pathogenesis of sarcoidosis.

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Section: Discussionmentioning

confidence: 99%

Elevated Levels of Type II Soluble Tumor Necrosis Factor Receptors in the Bronchoalveolar Lavage Fluids of Patients with Sarcoidosis

Hino

Nakamura

Shibata

et al. 1997

Lung

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“…Initial preclinical studies suggested that microvasculature damage, causing a generalized increase of vascular permeability to albumin, was the basic mechanism of rIL-2-induced NCPE [25]. Subsequent studies went into more detail and associated the systemic administration of rIL-2 with lesions of venous and capillary endothelia, alveolar basement membrane, and type I epithelial cells in animals, while leukocyte or platelet activation, generation of free radicals, and activation of the complement system have also been suggested to be involved in its pathogenesis [92][93][94][95][96][97]. Despite a widening evidence of the involvement of various cytokines released by activated lymphoid cells in the pathogenesis of rIL-2-induced NCPE, the exact mechanism of the damaging events that drive this clinical syndrome remain unclear [23,33].…”

Section: Pathophysiologymentioning

confidence: 99%

Noncardiogenic Pulmonary Edema: An Unusual and Serious Complication of Anticancer Therapy

Briasoulis

Pavlidis

2001

The Oncologist

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Noncardiogenic pulmonary edema (NCPE) is a rare and less well-recognizable pulmonotoxic syndrome of anticancer therapy than pneumonitis/fibrosis. NCPE is a clinical syndrome characterized by simultaneous presence of severe hypoxemia, bilateral alveolar infiltrates on chest radiograph, and no evidence of left atrial hypertension/congestive heart failure. The diagnosis of drug-related NCPE relies upon documented exclusion of any infectious, metabolic, or cancer-related causes. The Oncologist 2001;6:153-161 www.TheOncologist.com Correspondence: Evangelos Briasoulis, M.D., Medical Oncology Department, Ioannina University, Ioannina, 45110, Greece. Telephone and Fax: 30-651-99394; e-mail: ebriasou@otenet.gr. Received August 15, 2000; accepted for publication November 30, 2000. ©AlphaMed Press 1083-7159/2001 INTRODUCTIONSeveral cancer therapeutic drugs are known to induce pulmonary damage, which may result in a variety of clinicopathologic syndromes with minor to severe clinical consequences [1]. Clinical syndromes associated with drug-induced pulmonary toxicity include pneumonitis/fibrosis, hypersensitivity lung disease, and noncardiogenic pulmonary edema (NCPE)/acute respiratory distress syndrome (ARDS). These syndromes share a similar symptomatology but differ in regard to the time-relation to cancer treatment, the radiographic findings, the duration of pulmonary damage, and the long-term outcome [2]. Non-specific symptomatology of cough, progressive dyspnea, and often a low-grade fever alert clinicians confronted with the diagnostic challenge to recognize subclinical syndromes and differentiate fully developed drug-induced pulmonary reactions from lung injuries caused by infectious, cardiac, and neoplastic causes.

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“…[5][6][7][8][9] Inflammatory cytokines appear to exert both beneficial and deleterious effects following ischemia. This dual effect may complicate the task of developing hypoxic-ischemic brain injury and capillary leakage against the inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Status epilepticus and capillary leak syndrome in a neonate related to perinatal hypoxic-ischemic encephalopathy

et al. 2010

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Tumor Necrosis Factor-α Plays a Central Role in Interleukin-2-Induced Pulmonary Vascular Leak and Lymphocyte Accumulation

Cited by 46 publications

References 0 publications

Elevated Levels of Type II Soluble Tumor Necrosis Factor Receptors in the Bronchoalveolar Lavage Fluids of Patients with Sarcoidosis

Elevated Levels of Type II Soluble Tumor Necrosis Factor Receptors in the Bronchoalveolar Lavage Fluids of Patients with Sarcoidosis

Noncardiogenic Pulmonary Edema: An Unusual and Serious Complication of Anticancer Therapy

Status epilepticus and capillary leak syndrome in a neonate related to perinatal hypoxic-ischemic encephalopathy

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