Tumour Necrosis Factor (TNF)-a, a pro-inflammatory
cytokine has a dual role in host immunity and
immunopathology of tuberculosis and is considered to
be pivotal for determining the clinical course of the
disease, either beneficial or detrimental. The assessment
of TNF-a in pleural tuberculosis will help us to
understand its role in host defence mechanism against
Mycobacterium tuberculosis (MTB) infection. In this
study, TNF-a and IFN-g levels were measured in plasma
and pleural fluid of both tuberculosis (TB) and non-
TB patients and in the supernatants of blood and
pleural fluid mononuclear cells (PBMCs and PFMCs)
stimulated in vitro with PPD, culture filtrate and heatkilled
(MTB). In addition, apoptosis induced by PPD
and MTB was also studied. TNF-a and IFN-g were
significantly elevated in pleural fluid than in plasma
of pleural tuberculosis patients, suggesting the compartmentalization
of Th1 cytokine-secreting cells at
the site of disease. In vitro stimulation of PFMCs with
PPD and MTB showed a significant increase in these
cytokine levels and also enhanced apoptosis of these
cells. This increase in TNF-a levels may contribute to
the containment of infection by synergizing with IFN-
g to activate infected macrophages or by the regulation
of T-cell apoptosis