Correction of immunologic disorders in patients with burns

Addition of immunomodulating therapy with Thymalin, a thymus agent, to the multimodality therapy of burnt patients contributes to a rapid normalization of immunological parameters. The most marked immune response was observed 7-10 days after a therapy course initiated in the early periods of burn disease in patients with severely depressed T-system immunity and a high sensitivity to the drug. Inclusion of a donor blood leukomass transfusion course activates the cellular link of the immune system just after the treatment course, but fails to favour a stable normalization of thymus-dependent lymphocyte ratios.     

Experimental study of the role of the local infectious focus in development ofPseudomonas aeruginosa septicemia

Department of Pathological Anatomy, Clinical-Biological Laboratory, and Laboratory of Immunology, Bacteriology, and Clinical Pharmacology, A. V. Vishnevskii Institute of Surgery, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR D. S. Sarkisov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 111, No. 3, pp. 285–287, March, 1991.     

Early bronchoscopic and morphological diagnostics and prognosis in thermal inhalation trauma

Thermal injury is diagnosed by fibrobronchoscopy within the first 5 days after inhalation burn trauma in 73 patients (34% of the total number of patients hospitalized during the last 2 years). Pathological changes of the mucosa with predominant multiple ulceration at different levels of the tracheobronchial tree are detected in 44% patients and in more than 70% patients with acute respiratory deficiency. These changes determine variation and severity of thermal inhalation injury in the patients, and, together with morphofunctional characteristics, provide objective basis for the early diagnostics and prognosis. Translated fromByullelen' Eksperimental'noi Biologii i Meditsiny, Vol. 124, No. 8, pp. 221–225, August, 1997     

Two pathways of exocytosis of cytoplasmic granule contents and target cell killing by cytokine-induced CD3+ CD56+ killer cells

Cytokine-induced killer (CIK) cells are non-major histocompatibility complex-restricted cytotoxic cells generated by incubation of peripheral blood lymphocytes with anti-CD3 monoclonal antibody (MoAb), interleukin-2 (IL-2), IL-1, and interferon-gamma. Cells with the greatest effector function in CIK cultures coexpress CD3 and CD56 surface molecules. CIK cell cytotoxicity can be blocked by MoAbs directed against the cell surface protein leukocyte function associated antigen-1 but not by anti-CD3 MoAbs. CIK cells undergo release of cytoplasmic cytotoxic granule contents to the extracellular space upon stimulation with anti-CD3 MoAbs or susceptible target cells. Maximal granule release was observed from the CD3+ CD56+ subset of effector cells. The cytoplasmic granule contents are lytic to target cells. Treatment of the effector cells with a cell-permeable analog of cyclic adenosine monophosphate (cAMP) inhibited anti-CD3 MoAb and target cell- induced degranulation and cytotoxicity of CIK cells. The immunosuppressive drugs cyclosporin (CsA) and FK506 inhibited anti-CD3- mediated degranulation, but did not affect cytotoxicity of CIK cells against tumor target cells. In addition, degranulation induced by target cells was unaffected by CsA and FK506. Our results indicate that two mechanisms of cytoplasmic granule release are operative in the CD3+ CD56+ killer cells; however, cytotoxicity proceeds through a cAMP- sensitive, CsA- and FK506-insensitive pathway triggered by yet-to-be- identified target cell surface molecules.