PATHOPHYSIOLOGY OF EOSINOPHILIC PNEUMONIA

Abstract

The article is devoted to the study of the pathophysiology of eosinophilic pneumonia. Eosinophilic pneumonia is characterized by massive pulmonary infiltration by eosinophils, includes various lung diseases with heterogeneous origin, and its etiology, pathogenesis and prevalence are not fully understood.

Eosinophilic inflammation can be caused by T-helper type 2 (Th2) cells, which differentiate in response to certain antigens. Th2 cells produce several cytokines, including interleukin (IL)-5, which plays a key role in the proliferation and maturation of eosinophilic precursors. Binding of IL-5 to its receptor activates a network of intracellular signaling pathways, including the JANUS kinase and activator of transcription signaling pathway, which is involved in the regulation of transcription of genes controlling eosinophil proliferation.

Thus, the results show the importance of eosinophils in the development of human diseases in general, and pneumonia in particular. The etiology and pathogenesis of eosinophilic pneumonia have not been fully studied, so further research is needed to understand the role of eosinophils in a healthy and sick organism.