PubMed · 1673502
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1991-05-04. Hepatitis G?. https://pubmed.ncbi.nlm.nih.gov/1673502/
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Multinucleated giant cells (MGC) are characteristic cells in granulomatous disorders such as sarcoidosis and also formed in vitro from peripheral blood mononuclear cells by stimulation with cytokines, including interferon-gamma (IFN-gamma), interleukin-3 (IL-3), IL-4, IL-13, and granulocyte-macrophage-colony stimulating factor. In addition to such inflammatory mediators, a factor derived from the pathogens of granulomatous disorders may be necessary for MGC formation. Muramyl dipeptide (MDP), a peptidoglycan portion of bacterial cell walls present in sarcoidal lesions, is one of the candidates and can preferentially induce Langhans-type cells (LGC) in in vitro MGC formation system. Although the exact mechanisms of in vitro MGC formation remains unknown, receptors such as P2X(7), integrins, CD98, and macrophage fusion protein are considered to be involved in cell-to-cell adhesion and subsequent fusion process. Monocytes from sarcoidosis patients expressed higher levels of P2X(7) and had a higher ability to induce MGC than those from healthy controls. Attributable cells for the formation were CD14(++)CD16(-) monocytes. Therefore, CD14(++)CD16(-) monocytes may infiltrate into sarcoidal lesions and be fused to form LGC by inflammatory mediators and MDP derived from the pathogens of the disorder. Effective agents for sarcoidosis such as tranilast, allopurinol, and captopril inhibited in vitro MGC formation through inhibiting the expression of adhesion molecule and purinergic receptor. Thus, an in vitro MGC formation model would be a useful tool to understand the relevance of MGC in granulomatous disorders.
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.
Immunohistochemical study of inflammatory infiltrate was carried out in five cases of subcutaneous phaeohyphomycosis before and after therapy. The infections were due to the genus Alternaria in four cases and genus Cladosporium in one. In four cases, infiltrating T cells with helper memory phenotype were slightly more abundant after therapy (70-80% versus 75-90% of T lymphocytes) and those with suppressor cytotoxic phenotype were slightly less abundant (20-25% versus 10-15%). In one case, CD8+, Tia-1+ lymphocytes constituted 50% of the T-cell infiltrate before and after therapy. In all cases, the infiltrate contained many CD79 a+ plasma cells, which increased slightly after therapy, and a high CD1a positivity of dendritic cells (presumably Langerhans cells) before and after therapy. The CD1a+ cells were detected in the epidermis and in granulomatous infiltrate; in the dermis and subcutis, many were close to fungal structures. In four cases, intra-epidermal CD1a+ cell number was slightly lower than in control skin. CD68+ cells were not found in the epidermis.