INCREASED RELEASE OF INTERLEUKIN-1-BETA, INTERLEUKIN-6, AND TUMOR-NECROSIS-FACTOR-ALPHA BY BRONCHOALVEOLAR CELLS LAVAGED FROM INVOLVED SITES IN PULMONARY TUBERCULOSIS
K. Law et al., INCREASED RELEASE OF INTERLEUKIN-1-BETA, INTERLEUKIN-6, AND TUMOR-NECROSIS-FACTOR-ALPHA BY BRONCHOALVEOLAR CELLS LAVAGED FROM INVOLVED SITES IN PULMONARY TUBERCULOSIS, American journal of respiratory and critical care medicine, 153(2), 1996, pp. 799-804
Citations number
40
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
Mycobacterium tuberculosis and its components have been shown to stimu
late 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 presenc
e of cytokines in granulomas. We hypothesized that bronchoalveolar rav
age (BAL) cells from patients with pulmonary TB would have increased s
pontaneous 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 involve
d and uninvolved sites was evaluated separately for cell types and the
spontaneous release of cytokines. The alveolar inflammation in involv
ed sites was characterized by an increase in lymphocytes (miliary TB,
38 +/- 10%; involved sites, 22 +/- 4%; uninvolved sites, 13 +/- 2%; no
rmal, 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/m
l), and IL-6 (473 +/- 157 pg/ml) from involved sites of TB patients th
at was 5- to 20-fold greater than uninvolved sites, normal controls, o
r miliary TB. Northern analysis revealed increased gene expression of
IL-1 beta, TNF-alpha, and IL-6 from the involved sites from two patien
ts with TB compared with two negative controls. We conclude that BAL c
ells, especially alveolar macrophages, are activated in the alveolar i
nflammation of active TB and spontaneously release increased quantitie
s of IL-1 beta, IL-6, and TNF-alpha, and that these cytokines are like
ly to be involved in directing granuloma formation and control of M. t
uberculosis infection.