[Current views of tuberculosis inflammation]

The value of histological and histochemical studies in the diagnosis of a phase of tuberculosis progression or healing is shown. Electron microscopic study of tuberculous inflammation in different phases of its evolution evaluated the functional status of cellular elements of the lung and granuloma. The body's antituberculous resistance due to molecular genetic mechanisms is realized through intercellular interactions and macrophageal functions. Immune macrophages are characterized by a higher metabolic activity, they suppress the intracellular multiplication of Mycobacterium tuberculosis (MBT) and are more protected from their toxic action. The pathogenetic mechanisms responsible for caseous pneumonia were studied. Three stages of evolution of the process: Stage 1 is the breakdown of defense and adaptive mechanisms: disorganization of connective tissue and alveolar parenchyma; enhanced permeability of blood and lymphatic microvascular walls with developed interstitial and intraalveolar edema, plasma and fibrin exudation, fibrinoid swelling of collagenous fibers, and their lysis; occurrence of lung parenchymal microinfarcts and infarction-pneumonia; type 2 alveolocytic dysfunction with surfactant destruction; Stage 2 is the breakdown of local immunity; exudative and alterative tuberculous inflammation with involvement of immunocompetent organs; suppressed T-cellular immunity, a shift of a T helper/T suppressor ratio to the latter, lymphopenia; impaired intercellular interactions, cellular apoptosis in blood and inflammation areas, and suppressed granulomatous reaction; inhibited L transformation of Mycobacteria tuberculosis, intensive MBT multiplication in the foci of tuberculous inflammation, particularly those which are resistant to many antibiotic drugs, a larger number of associations of the nonspecific microflora and fungi. Stage 3 is caseous pneumonia and generalization of a tuberculous process: a predominance of an alterative reaction of inflammation; the presence of allergic and caseous and necrotic vasculitis, bronchiolitis, and endo-panbronchitis; depressed granulomatous reaction; the development of acute alterative sequestrating pneumoniogenic caverns. Histological, histochemical, and electron microscopic studies of tuberculous inflammation may specify the mechanisms of the pathogenesis of tuberculosis and may serve as the basis for early diagnosis of the disease and for timely correction of performed treatment in order to enhance its efficiency.