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

Hino, Toshihiko; Nakamura, Hidenori; Shibata, Yoko; Abe, Shuichi; Kato, Shigeaki; Tomoike, Hitonobu

doi:10.1007/pl00007566

Cited by 28 publications

(21 citation statements)

References 29 publications

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“…Increased levels of TNF-Rs have been seen in the plasma and BAL fluid of patients with sarcoidosis. 11 Armstrong et al 12 showed that TNFα bioactivity in the lungs of subjects with sarcoidosis may be inhibited by increased levels of soluble TNF-R. This inhibition may be greater in stage I disease than in stage II/III, indicating a homeostatic mechanism which protects the lung from excessive TNFα production.…”

Section: -5mentioning

confidence: 99%

Increased interleukin-13 expression in patients with sarcoidosis

Hauber

Gholami²,

Meyer³

et al. 2003

Thorax

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Section: -5mentioning

confidence: 99%

Increased interleukin-13 expression in patients with sarcoidosis

Hauber

Gholami²,

Meyer³

et al. 2003

Thorax

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“…Serum TNF-␣ and plasma sTNF-R55 and sTNF-R75 concentrations were measured in duplicate with enzyme-linked immunosorbent assay (ELISA) kits (Quantikine; R&D Systems, Minneapolis, MN) (23,24). Briefly, a microtiter plate was coated with a murine monoclonal antibody specific for TNF-␣ , sTNF-R55, or sTNF-R75.…”

Section: Determination Of Serum Tnf-␣ and Plasma Stnf-r Levelsmentioning

confidence: 99%

The Relationship between Chronic Hypoxemia and Activation of the Tumor Necrosis Factor- α System in Patients with Chronic Obstructive Pulmonary Disease

Takabatake

Nakamura

Abe

et al. 2000

Am J Respir Crit Care Med

292

164

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Although circulating tumor necrosis factor (TNF)-alpha levels have been found to be increased in weight-losing patients with chronic obstructive pulmonary disease (COPD), the main causes for this phenomenon remain to be elucidated. Since hypoxia itself can enhance the production of the TNF-alpha in vitro, we studied the relationship between hypoxemia and activities of the TNF-alpha system, including circulating TNF-alpha and soluble TNF-receptors (sTNF-R; sTNF-R55 and -R75) levels, in 27 COPD patients and 15 age-matched healthy controls. The COPD patients showed a significant weight loss (body mass index = 18.1 +/- 2.8 versus 22.8 +/- 2.2 [mean +/- SD] kg/m(2); p < 0.0001. % fat = 16.3 +/- 5.9 versus 24.3 +/- 4.9 %; p < 0.001), and hypoxemia (Pa(O2 )= 62.2 +/- 9.5 versus 88.6 +/- 5.9 mm Hg; p < 0.0001) as compared with the healthy controls. Serum TNF-alpha (6.15 +/- 1.08 versus 5.41 +/- 1.60 pg/ml; p < 0.05) and plasma sTNF-R55 (1.15 +/- 0.49 versus 0.67 +/- 0.13 ng/ml; p < 0.0001) and sTNF-R75 (3.54 +/- 1.16 versus 2.25 +/- 0.43; p < 0.0001) levels were significantly higher in the COPD patients than in the healthy controls. There were inverse correlations between Pa(O(2)) and circulating TNF-alpha and sTNF-R levels in patients with COPD (TNF-alpha; r = -0.426, p = 0.0297; sTNF-R55: r = -0.587, p = 0.0027; sTNF-R75: r = -0.573, p = 0.0035). In addition, we found inverse correlations between sTNF-R levels and % fat in COPD patients (sTNF-R55: r = -0.442, p = 0.0272; sTNF-R75: r = -0. 484, p = 0.0155). TNF-alpha levels correlated well with sTNF-R levels (sTNF-R55: r = 0.488, p = 0.0127; sTNF-R75: r = 0.609, p = 0. 0019). These relationships were not observed in the healthy controls. These data suggest that systemic hypoxemia noted in patients with COPD is associated with activation of the TNF-alpha system in vivo, which may be a factor contributing to the weight loss in patients with the disease.

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“…Serum TNF-␣ and plasma sTNF-R55 and sTNF-R75 concentrations were measured in duplicate with enzyme-linked immunosorbent assay (ELISA) kits (Quantikine; R&D Systems, Minneapolis, MN) (31). Briefly, a microtiter plate was coated with a murine monoclonal antibody specific for TNF-␣ , sTNF-R55, or sTNF-R75.…”

Section: Determination Of Serum Leptin and Tnf Levelsmentioning

confidence: 99%

Circulating Leptin in Patients with Chronic Obstructive Pulmonary Disease

Takabatake

Nakamura

Abe

et al. 1999

Am J Respir Crit Care Med

179

100

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Unexplained weight loss is common in patients with chronic obstructive pulmonary disease (COPD). Since leptin, an obesity gene product, is known to play important roles in the control of body weight and energy expenditure, we investigated serum leptin levels, along with circulating tumor necrosis factor-alpha (TNF-alpha) and soluble TNF receptor (sTNF-R55 and -R75) levels, in 31 patients with COPD and 15 age-matched healthy controls. The body mass index (BMI) and percent body fat (%fat) were significantly lower in the COPD patients than in the healthy controls (BMI = 18.1 +/- 2.7 kg/m2 versus 22.8 +/- 2.2 kg/m2 [mean +/- SD]; p < 0.0001; %fat = 16.9 +/- 5.8% versus 24.3 +/- 4.9%; p < 0.001). Serum leptin levels were significantly lower in the COPD patients than in the healthy controls (1.14 +/- 1.17 ng/ml versus 2.47 +/- 2.01 ng/ml; p < 0.05). In contrast, serum TNF-alpha levels (6.59 +/- 1.92 pg/ml versus 5.41 +/- 1.60 pg/ml; p < 0.05), plasma sTNF-R55 (1.16 +/- 0.47 ng/ml versus 0.67 +/- 0.13 ng/ml; p < 0.0001) and sTNF-R75 (3.65 +/- 1.29 ng/ml versus 2.25 +/- 0.43 ng/ml; p < 0.0001) levels were significantly higher in the COPD patients than in the healthy controls. Importantly, circulating leptin levels (log transformed) did correlate well with BMI and %fat, but not with TNF-alpha or with sTNF-R levels in the COPD patients. These data suggest that circulating leptin is independent of the TNF-alpha system and is regulated physiologically even in the presence of cachexia in patients with COPD.

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

Cited by 28 publications

References 29 publications

Increased interleukin-13 expression in patients with sarcoidosis

Increased interleukin-13 expression in patients with sarcoidosis

The Relationship between Chronic Hypoxemia and Activation of the Tumor Necrosis Factor- α System in Patients with Chronic Obstructive Pulmonary Disease

Circulating Leptin in Patients with Chronic Obstructive Pulmonary Disease

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