Abstract

It is generally accepted that Pantone-Valentine leucocidin (PVL)-mediated pore formation in the cytoplasmic membrane of leukocytes (polymorphonuclear neutrophils—PMNs) in vitro eventually leads to cytolysis. However, this hypothesis has not been confirmed in vivo. Furthermore, the studies performed to date indicate that PVL concentration in vivo is probably insufficient to cause cell lysis. On the other hand, sublytic amounts of PVL prime neutrophil production of reactive oxygen species release pro-inflammatory molecules and cause exocytosis of granules. Although the molecular basis of the PVL-mediated PMNs priming is still unclear, infections caused by community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) isolates are closely related to the presence of the toxin. The PVL-producing S. aureus are often isolated from human CA-MRSA infections; however, little is still known regarding PVL-positive strains from animals. An explanation of PVL’s impact in S. aureus diseases is an important issue in the field of infectious diseases. Therefore, understanding the structure and function of PVL in S. aureus pathology is considered to be crucial for the development of new diagnostic tools, as well as drugs and vaccines. This chapter provides detailed information concerning the genetic basis for PVL synthesis and secretion, along with its chemical structure and pathogenic role.

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