tailieunhanh - Báo cáo y học: "α Tumour necrosis factor-α production in fibrosing alveolitis is macrophage subset specific"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: "α Tumour necrosis factor-α production in fibrosing alveolitis is macrophage subset specific. | Available online http content 2 6 365 Research article Tumour necrosis factor-a production in fibrosing alveolitis is macrophage subset specific Panos Pantelidis Deirdre S McGrath Anne Marie Southcott Carol M Black and Roland M du Bois Interstitial Lung Disease Unit Department of Occupational and Environmental Medicine Royal Brompton Hospital National Heart and Lung Institute London UK Department of Rheumatology Royal Free Hospital School of Medicine London UK Correspondence Professor RM du Bois Interstitial Lung Disease Unit Department of Occupational and Environmental Medicine Royal Brompton Hospital London England SW3 6LR. Tel 44 20 7351 8327 fax 44 20 7351 8336 e-mail Received 29 March 2001 Revisions requested 14 May 2001 Revisions received 6 July 2001 Accepted 8 August 2001 Published 8 October 2001 Respir Res 2001 2 365-372 2001 Pantelidis et al. licensee BioMed Central Ltd Print ISSN 1465-9921 Online ISSN 1465-993X Abstract Background Previous studies have revealed that tumour necrosis factor TNF -a is upregulated in fibrosing alveolitis FA in humans. The aim of this study was to compare the TNF-a secretory profile of alveolar macrophages AMs and peripheral blood monocytes Mos of patients with cryptogenic FA and systemic sclerosis SSc a rheumatological disorder in which lung fibrosis can occur. In particular we wished to assess whether TNF-a levels differ between SSc patients with FA FASSc and a nonfibrotic group. Methods The reverse haemolytic plaque assay was used to evaluate the secretion of cytokine at a single cell level while immunostaining allowed subtyping of AMs and Mos. Results This study demonstrated a difference in total TNF-a levels produced by AMs when the levels in subjects with FA cryptogenic FA and FASSc were compared to levels in either SSc patients without FA P or normal healthy controls P . In addition AMs from patients with FASSc secreted more TNF-a than those of patients .