МОРФОФУНКЦІОНАЛЬНІ ЗМІНИ ТИМУСА ТА КІСТКОВОГО МОЗКУ ПРИ ЕКСПЕРИМЕНТАЛЬНОМУ СПАЙКОВОМУ ПРОЦЕСІ КИШЕЧНИКА: ОГЛЯД ЛІТЕРАТУРИ

Intestinal and intra-abdominal adhesions constitute a complex pathological consequence of tissue injury, characterized by persistent inflammation, fibrin deposition, impaired fibrinolysis, extracellular matrix remodeling, angiogenesis, and progressive fibrosis. Local mechanisms of adhesion formation have received extensive study, whereas the systemic consequences of adhesion disease—particularly its potential effects on central immune and hematopoietic organs—have attracted considerably less attention. Aim. This review synthesizes current evidence on possible morphofunctional remodeling of the thymus and bone marrow in experimental intestinal adhesion disease and proposes a framework for their comparative morphometric assessment. Methods. The literature analysis drew on peer-reviewed experimental studies and reviews addressing postoperative abdominal and intestinal adhesions, inflammatory and fibrotic signaling, thymic stress responses, hematopoietic stem and progenitor cell adaptation, bone marrow niche remodeling, and animal experimental models. Particular emphasis was placed on studies published between 2019 and 2026, supplemented where necessary by foundational earlier publications. Particular emphasis was placed on studies published between 2019 and 2026, supplemented where necessary by foundational earlier publications. Literature searches were conducted in the PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar databases (last search: August 2026), using the following keywords and their combinations (in English, applying the Boolean operators AND/OR): postoperative adhesions, intestinal adhesions, peritoneal adhesions, adhesion formation, thymus, thymic involution, bone marrow, hematopoiesis, hematopoietic stem cells, inflammation, fibrosis, wound healing, tissue remodeling, animal model, rat model (спайки кишечника, спайки брюшины, послеоперационные спайки, тимус, инволюция тимуса, костный мозг, гемопоэз, гемопоэтические стволовые клетки, воспаление, фиброз, заживление ран, ремоделирование ткани, экспериментальная модель). This work formed part of the research activity of the Department of Infectious Diseases and Pediatric Infectious Diseases of Bukhara State Medical Institute named after Abu Ali ibn Sino, addressing the systemic morphofunctional consequences of experimental intra-abdominal adhesion formation. Results. Experimental adhesion formation involves a coordinated inflammatory response engaging neutrophils, macrophages, mesothelial cells, fibroblasts, and multiple cytokine systems. Transforming growth factor-β, interleukin-6, tumor necrosis factor-α, vascular endothelial growth factor, and alterations in the tissue plasminogen activator/plasminogen activator inhibitor system represent key components of this local pathological process. Sustained inflammatory signaling may extend beyond the peritoneal cavity and produce systemic effects. The thymus shows particular sensitivity to stress, infection, glucocorticoids, and inflammatory mediators, with depletion of cortical thymocytes emerging as a characteristic response to acute injury. Concurrently, inflammatory signals can activate hematopoietic stem and progenitor cells, promote myeloid hematopoiesis, and alter the bone marrow microenvironment. These observations support the hypothesis that experimental intestinal adhesions may induce coordinated remodeling of central immune and hematopoietic organs. Conclusions. Comparative assessment of thymic and bone marrow morphology may yield broader insight into the systemic component of experimental adhesion disease. Future studies should combine morphometry with immunohistochemistry, hematological analysis, and molecular evaluation of inflammatory, apoptotic, proliferative, and fibrotic pathways.