PSEUDOTUBERCULOSIS: PATHOGENETIC VALUE OF INNATE IMMUNITY CELLS

Abstract

Novel data on mechanisms of innate immunity during infections with pathogenic Yersiniae are summarized in the review, that was mostly determined by complex developments regarding a unique pair of genetically related causative agents Y. pseudotuberculosis/Y. pestis. Our previous studies have revealed a morphological substrate of relative granulocyte immune deficiency that determines characteristic pathomorphologic features of pseudotuberculosis. To date, evidence has been obtained, that pathogenic for human Yersinia predominately activate protective function of innate immunity cells that is an important strategy to avoid elimination and cause the disease for the bacteria. Neutrophils (PMNs) play a fundamental role in response to infection by pathogenic Yersiniae in primary immune response and limit of primary spread of bacteria that use several mechanisms of eradication ofbacteria, e.g.: phagocytosis, oxidative stress, secretory degranulation, formation of neutrophil extracellular traps, efferocytosis. Infected PMNs can act as an intermediate host for consequent non-inflammatory infection of macrophages. Further elaboration of questions relating to primary anti-infection protection during Yersinia infections gives a key to understanding of immune pathogenesis of epidemic pseudotuberculosis (far Eastern scarlet-like fever) and yersiniosis in general.