ВПЛИВ ЕКСПЕРИМЕНТАЛЬНОГО МАТЕРИНСЬКОГО ХРОНІЧНОГО ЗАПАЛЬНОГО ПРОЦЕСУ СЕЧОСТАТЕВОЇ СИСТЕМИ БАКТЕРІАЛЬНОГО ҐЕНЕЗУ НА МОРФОФУНКЦІОНАЛЬНІ ОСОБЛИВОСТІ ЛЕГЕНЬ ПОТОМСТВА

Chronic urogenital inflammation in women of reproductive age frequently complicates pregnancy and childbirth, potentially impairing lung morphogenesis in the offspring. Current literature lacks comprehensive clinical and experimental studies investigating the morphofunctional features and mechanisms of lung injury in offspring exposed to this pathology in utero, stratified by the specific causative infectious agent. The aim of the study was to experimentally determine the morphofunctional features of the lungs in one-week-old offspring exposed in utero to maternal chronic bacterial urogenital inflammation. Materials and Methods. An experimental study was conducted on WAG rats, which were divided into four groups. Group 1 comprised 318 one-week-old rats born to dams with uncomplicated pregnancies. Group 2 included 257 one-week-old rats born to dams with chronic urogenital inflammation induced by Streptococcus pyogenes. Group 3 consisted of 219 one-week-old rats born to dams with inflammation induced by Proteus mirabilis. Group 4 comprised 223 one-week-old rats born to dams with inflammation induced by Klebsiella pneumoniae. Lung tissue from the one-week-old offspring was subjected to morphological examination. Histological sections were stained with hematoxylin and eosin (H&E), Sudan III, Van Gieson’s picrofuchsin, and Mallory’s trichrome. Immunohistochemical examination was performed using monoclonal antibodies against CD3, CD20, and CD68. The experiment complied with the European Convention for the Protection of Vertebrate Animals used for Experimental and other Scientific Purposes (Strasbourg, 1986) and Directive 2010/63/EU of the European Parliament and of the Council of 22 September 2010 on the protection of animals used for scientific purposes. The study protocol was approved by the Ethics and Bioethics Committee of Kharkiv National Medical University (Protocol No. 7 September 12, 2023). Statistical analysis of the obtained data was performed using PAST software (version 4.15, Natural History Museum, University of Oslo, Norway) and Statistica 8.0. Mean values were compared using Student’s t-test and the Mann-Whitney U test. The study was conducted under the research project of the Department of General and Clinical Pathological Physiology named after D.O. Alpern, Kharkiv National Medical University (State Registration No. 0123U100198; project period: January 2023-December 2027). Results. Chronic maternal urogenital inflammation induced by Klebsiella pneumoniae, Streptococcus pyogenes, and Proteus mirabilis resulted in mild, moderate, and severe morphofunctional alterations in the lungs of one-week-old offspring, respectively. In the bronchi and terminal bronchioles, dystrophic and necrotic epithelial changes and desquamation were observed, leading to basement membrane denudation; wall thickening secondary to sclerosis, hypertrophy, and hyperplasia of smooth muscle cells with concurrent luminal narrowing; and pronounced focal and diffuse infiltration of all wall layers by immune cells, including macrophages (CD68+-cells), T-lymphocytes (CD3+-cells), and B-lymphocytes (CD20+-cells). In the respiratory portion of the lungs, dystrophic and necrotic changes in pneumocytes, a reduced number of type II pneumocytes, surfactant deficiency, atelectatic, dystelectasis, and emphysematous alveolar alterations were detected. Sclerotic changes were observed in the interalveolar septa and around the bronchial tree and blood vessels. Hemodynamic disturbances manifested as vascular congestion, intravascular thrombosis, edema, and hemorrhage. Degenerative and desquamative endothelial changes, along with vascular smooth muscle cell hypertrophy, led to vascular luminal narrowing. Pronounced stromal infiltration by immune cells, predominantly macrophages accompanied by T and B lymphocytes, was also observed. Conclusions. Chronic maternal urogenital inflammation induces morphofunctional alterations in the conducting airways and respiratory portion of the lungs in one-week-old offspring, with severity dependent on the specific infectious agent (mild for Klebsiella pneumoniae, moderate for Streptococcus pyogenes, and most pronounced for Proteus mirabilis). The conducting airways of the offspring exhibit focal degenerative and desquamative epithelial changes; wall thickening secondary to sclerosis, hypertrophy, and hyperplasia of smooth muscle cells; and altered local immune responses. The respiratory portion of the lungs exhibits dystrophic and necrotic pneumocyte changes, a reduced number of type II pneumocytes, and decreased surfactant production; alveolar dystelectasis, atelectasis, and emphysematous alterations; stromal sclerosis and hemodynamic disturbances; and altered local immune responses.