PubMed1997
Comprehensive clinical, X-ray, cytochemical, morphological, biochemical, and immunological studies of 14 patients with caseous pneumonia have provided evidence that significant structural, metabolic, and functional disorders of mononuclear phagocytes (MNP) play a leading role in the pathogenesis of acute tuberculosis. Structural and metabolic disorders of macrophages and monocytes in patients with caseous pneumonia result from impaired mitochondrial oxidation and glycolysis, aggregation and latinization of the membranes of lysosomes, release of their contents into the cytosol with damages to intracellular structures and the cellular membrane itself. This is also suggested by a drastic rise in the production of prostaglandins E2 and F2 alpha, prostaglandins E2 in particular, in the supernatants of cultured monocytes (100 nM). This is determined as the membrane-damaging effect of MNP due to the toxic action of rapidly multiplying mycobacterial population not only in the lung, but even in blood. MNP structural and metabolic disturbances are an equivalent to their lowered functional activity, as evidenced by a considerable deficiency of synthesis of intracellular and secretory pools of interleukin I and by a fall in their migrational and adhesive activities, two thirds of macrophages having signs of dystrophy and cytolysis. On entering the specific inflammatory area of the lung, these cells abundantly disintegrate. Their destruction leads to the elaboration of enzymes, prostaglandins, and other biologically active agents, which promotes the occurrence of extensive caseously destructive changes and creates conditions for rapid multiplication of mycobacteria.