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M9650249.TXT
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1996-03-09
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Document 0249
DOCN M9650249
TI Increased release of interleukin-1 beta, interleukin-6, and tumor
necrosis factor-alpha by bronchoalveolar cells lavaged from involved
sites in pulmonary tuberculosis.
DT 9605
AU Law K; Weiden M; Harkin T; Tchou-Wong K; Chi C; Rom WN; Department of
Medicine, New York University Medical Center, New; York 10016, USA.
SO Am J Respir Crit Care Med. 1996 Feb;153(2):799-804. Unique Identifier :
AIDSLINE MED/96160601
AB Mycobacterium tuberculosis and its components have been shown to
stimulate mononuclear phagocytes in vitro to release interleukin-1 beta
(IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6
(IL-6). Animal models of tuberculosis (TB) also demonstrate the presence
of cytokines in granulomas. We hypothesized that bronchoalveolar lavage
(BAL) cells from patients with pulmonary TB would have increased
spontaneous release of IL-1 beta, IL-6, and TNF-alpha and would have a
concomitant alveolitis. We performed BAL on 26 patients with active TB
and on six normal volunteers. BAL fluid from radiographically involved
and uninvolved sites was evaluated separately for cell types and the
spontaneous release of cytokines. The alveolar inflammation in involved
sites was characterized by an increase in lymphocytes (miliary TB, 38
+/- 10%; involved sites, 22 +/- 4%; uninvolved sites, 13 +/- 2%; normal,
5 +/- 2%) and neutrophils (involved sites, 21 +/- 7%; uninvolved sites,
3 +/- 2%). There was a significant increase in the spontaneous release
of IL-1 beta (501 +/- 280 pg/ml), TNF-alpha (782 +/- 165 pg/ml), and
IL-6 (473 +/- 157 pg/ml) from involved sites of TB patients that was 5-
to 20-fold greater than uninvolved sites, normal controls, or miliary
TB. Northern analysis revealed increased gene expression of IL-1 beta,
TNF-alpha, and IL-6 from the involved sites from two patients with TB
compared with two negative controls. We conclude that BAL cells,
especially alveolar macrophages, are activated in the alveolar
inflammation of active TB and spontaneously release increased quantities
of IL-1 beta, IL-6, and TNF-alpha, and that these cytokines are likely
to be involved in directing granuloma formation and control of M.
tuberculosis infection.
DE Adult AIDS-Related Opportunistic Infections/METABOLISM Blotting,
Northern Bronchoalveolar Lavage Fluid/*CYTOLOGY Cell Count Cells,
Cultured Enzyme-Linked Immunosorbent Assay Female Human
Interleukin-1/GENETICS/*METABOLISM Interleukin-6/GENETICS/*METABOLISM
Lymphocytes/PATHOLOGY Macrophages/PATHOLOGY Male
Neutrophils/PATHOLOGY RNA, Messenger/ANALYSIS Support, Non-U.S. Gov't
Support, U.S. Gov't, P.H.S. Tuberculosis,
Pulmonary/*METABOLISM/PATHOLOGY Tumor Necrosis
Factor/GENETICS/*METABOLISM JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).