The dysregulation of surfactant-associated proteins’ homeostasis in cavernous tuberculosis of lungs

Despite the progress and development of socially important scientific areas in medicine, tuberculosis remains one of the global problems. The surfactant system is one of the key mechanisms in the formation of immune response expression. In this regard, the aim of our study was investigation of surfactant apoproteins’ state both in the foci of specific destruction and in the surrounding intact lung tissue to assess its functional activity, the degree of respiratory failure and possible dissemination of tuberculosis inflammation. The materials for the study were fragments of human lungs taken from patients died or operated about of cavernous pulmonary tuberculosis (n=163) with an active bacterial discharge (n=89) and with clinical abacillation (n=74). A complex morphological study revealed the stereotypical dynamic depression of the surfactant-associated proteins A, B and C in all the samples both in cavernous areas of destruction and pericavitic areas, and in intact lung tissue. The maximum intensity of immunohistochemical expression
was recorded in alveolar macrophages, which indicated intensive recycling and utilization of surfactant components. At the same time, the synthetic activity of type II alveolocytes was activated mainly to the SP-A and to SP-B in the lower extent. The most sensitive was SP-C, the amount of which was significantly reduced in intact lung tissue. At that, this collectin totally disappeared both in the area of cavernous destruction and in pericavitic area. Minimizing of surfactant components’ production and its active utilization in intact lung tissue leads to disorganization of the monolayer on the inner surface of the alveoli with their subsequent collapse and progressive respiratory failure.