Inflammatory response and its correction in forming a host response to exposure to adverse environmental factors

This study systematically review knowledge about the mechanisms of formation of an inflammatory reaction under the influence of biological, physical, and chemical factors, their similarities and differences, and possible methods of pharmacological correction of pathological conditions associated with excessive activation. The effect of adverse environmental factors, such as biological, physical, and chemical factors, causes a systemic response, which is aimed at maintaining homeostasis and is caused, among other things, by a coordinated reaction of the immune system. Phlogogenic agents result in the activation and regulation of the inflammatory response, which is formed by cellular and humoral components of innate immunity. The activation of innate immunity is characterized by a rapid host response, which diminishes following the elimination of “foreign” invaders, endogenous killer cells, and neogenesis. Depending on the nature of the active factors (biopathogens, allergens, toxins, ionizing radiation, etc.), the mechanisms of immune response arousal have unique features mainly originating from the differences in the recognition of specific molecular patterns and “danger signals” by different receptors. However, inflammatory mediators and inflammatory response patterns at the systemic level are largely similar even under widely different triggers. Inflammation, having evolved as an adaptive reaction directed at the immune response, can lead to the development of chronic inflammation and autoimmune diseases due to a mismatch in mechanisms of its control. A “failure” in the regulation of the inflammatory process is the excessive activation of the immune system, which leads to the cytokine release syndrome (hypercytokinemia, or “cytokine storm”) and can cause self-damage (destruction) of tissues, multiple-organ failure, sepsis, and even death. Modern advances in the study of the pathogenetic bases of the inflammatory response are suggested, such as pharmacological correction using pattern recognition receptor antagonists, pro-inflammatory cytokine inhibitors, or blocking of key control genes or signaling pathways.