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Laboratory and Animal Investigations |

Production of Soluble Tumor Necrosis Factor Receptors and Tumor Necrosis Factor-α by Alveolar Macrophages in Sarcoidosis and Extrinsic Allergic Alveolitis*

Huaping Dai, MD; Josune Guzman, MD; Baomin Chen, MD; Ulrich Costabel, MD, FCCP
Author and Funding Information

*From the Department of Pneumology and Allergy (Drs. Dai, Chen, and Costabel), Ruhrlandklinik, Medical Faculty, University of Essen, Essen, Germany; and General and Experimental Pathology (Dr. Guzman), Ruhr University, Bochum, Germany.

Correspondence to: Ulrich Costabel, MD, FCCP, Ruhrlandklinik, Tüschener Weg 40, D-45239 Essen, Germany; erj.costabel@t-online.de



Chest. 2005;127(1):251-256. doi:10.1378/chest.127.1.251
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Background: Alveolar macrophage (AM)-derived tumor necrosis factor (TNF)-α plays a pivotal role in the pathogenesis of sarcoidosis and extrinsic allergic alveolitis (EAA). The effects of TNF-α are mediated by membrane TNF receptor (mTNFR)-1 and mTNFR-2, and can be blocked by soluble TNF receptor (sTNFR)-1 and sTNFR-2.

Methods: We measured the production of the two sTNFRs and TNF-α in AM culture supernatants from 10 patients with active sarcoidosis, 12 patients with EAA, and 9 control subjects using an enzyme-linked immunosorbent assay method.

Results: Compared with control subjects, the spontaneous and lipopolysaccharide (LPS)-stimulated production of sTNFR-1, sTNFR-2, and TNF-α was significantly increased in patients with sarcoidosis and EAA. The concentrations of both sTNFRs, but especially of sTNFR-2, were closely related to those of TNF-α. The LPS-induced increase was 1.5-fold for sTNFR-1, at least fourfold for sTNFR-2, and at least 25-fold for TNF-α in all study populations.

Conclusion: These results indicate that AMs can release the two sTNFRs in relation to TNF-α. sTNFR-2 may be more liable to shedding than sTNFR-1. Both sTNFR-1 and sTNFR-2 may be involved in the pathogenesis of sarcoidosis and EAA, possibly as counterregulators of TNF-α.

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