Mechanisms of damaging effects of atypical pathogens on respiratory epithelium: infectious and post-infectious airway hyperresponsiveness in children

The aim of this review was to analyze and summarize the current literature on the role of atypical respiratory pathogens ( Mycoplasma pneumoniae and Chlamydia pneumoniae ) in the development of airway hyperresponsiveness in children. The article presents the main mechanisms through which M. pneumoniae and Ch. pneumoniae can damage respiratory epithelial cells and contribute to the formation of bronchial hyperresponsiveness. It is shown that epithelial damage occurs both directly, through the depletion of nutrient resources, oxidative stress, and disruption of repair mechanisms, and indirectly, through immune mechanisms, including the production of specific immunoglobulin E antibodies and cytokine imbalance. Key characteristics of atypical pathogens leading to severe complications are highlighted, including: the production of the community-acquired respiratory distress syndrome (CARDS TX) toxin by M. pneumoniae , and the production of lipopolysaccharides and heat shock protein 60 (HSP60) by Ch. pneumoniae . A separate section is dedicated to the ability of atypical pathogens to form biofilms to enhance survival and pathogenicity. It is emphasized that damaged epithelium, in turn, induces the production of pro-inflammatory mediators, thereby exacerbating airway inflammation and contributing, in some cases, to the development of bronchial hyperresponsiveness. The authors believe that elucidating the mechanisms by which atypical pathogens damage the respiratory tract will facilitate the development of new approaches to the diagnosis, prevention, and treatment of respiratory diseases in children.