Pattern recognition receptors and their role in immunopathogenesis of pneumonia

Non-specific binding of antigens is provided by the so-called pattern recognition receptors (PRR) that may be located on the cell membrane, in the cytosol, or, as soluble molecules in the blood serum. Membrane receptors include: Toll-like receptors, C-type lectin receptors, scavenger receptors. TLR, NOD-like receptors, RIG-I-like receptors, AIM-2-like receptors are located in the cytosol. Soluble receptors include pentraxins, collectins, and ficolins. After entering a microorganism to lung spaces, the non-specific defense factors and innate immunity mechanisms are primarily involved in the immune response. If non-specific recognition of pathogens is ineffective, a pneumonia focus is formed. In this regard, the role of PRR in the development of community-acquired pneumonia is quite significant. To search for literature appropriate publications, an analysis of the research databases Scopus, Web of Science, Pubmed, CyberLeninka, and RINC was conducted. The studies have demonstrated the importance of TLR4 in combating both Gram-positive and Gram-negative microorganisms. In addition, the blood levels of sCD206 lectin receptor have been considered a predictor of severe pneumonia and lethal outcomes. Increased production of a CD5-like scavenger receptor was observed in pneumonia caused by S.aureus. NOD-like receptors play an important role in defense against Acinetobacter baumannii . Pentraxins perform many functions: they exhibit opsonic properties, activate complement via the classical pathway, activate neutrophils, and regulate chemotaxis and apoptosis. In adult patients with pneumonia, elevated blood CRP levels correspond to disease severity; measurement of CRP levels helps differentiate pneumonia from other acute respiratory infections. PTX3 is a factor that can help determine the severity and prognosis of pneumonia. Mannane-binding lectin (MBL) recognizes bacterial lipopolysaccharides (LPS) in capsular layer, or cell wall of Gram-negative bacteria, lipoarabinomannans, fungal mannans, SARSCoV-2 glycoproteins, PAMP of protozoa and helminths. Ficolins interact with viral, bacterial and fungal antigens. L-ficolin recognizes pneumococcal pneumolysin, activates complement via the lectin pathway, thereby neutralizing the toxin. Thus, a critical role of innate immunity factors in pathogenesis of pneumonia is well proven but requires further research. Studying the mechanisms of disease immunopathogenesis will allow development of new prognostic models and improve the efficiency of therapy, especially in severe cases of pneumonia.