Premium
Influence of staphylococcal lipoteichoic acid on the frustrated phagocytosis of neutrophils against opsonized corneocytes
Author(s) -
Kato Taizo,
Terui Tadashi,
Zhen YaXian,
Tagami Hachiro
Publication year - 1993
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.1993.tb00028.x
Subject(s) - lipoteichoic acid , opsonin , phagocytosis , microbiology and biotechnology , staphylococcus aureus , immunology , staphylococcus , corneocyte , chemistry , medicine , biology , bacteria , stratum corneum , genetics
Stratum corneum (SC) exerts a proinflammatory effect in the presence of complement. When Staphylococcus aureus (S. aureus) invades the skin through damaged SC. neutrophils accumulate at the sub‐corneal portion of epidermis to phagocytize the S. aureus as noted in impetigo. Besides the phagocytosis of bacteria. neutrophils interact with opsonized SC in a form of frustrated phagocytosis, increasing a damage of the surrounding tissues. Based on our previous finding that staphylococcal protein A promotes the interaction between SC and neutrophils. we investigated whether lipoteichoic acid (LTA), another cell wall component of S. aureus, also shows similar properties. We found that LTA significantly promoted the binding of neutrophils to opsonized SC, resulting in an increase in SC‐induced respiratory burst of neutrophils assessed by chemiluminescence (CL). The binding of neutrophils to the SC was almost completely inhibited by the blocking of CR3 with anti‐CD11b antibody, suggesting that the binding between SC and neutrophils is mediated by interaction between C3bi and CR3 (Mac‐1). Such enhanced interaction seems to function in the primary host defence mechanism against the invading S. aureus through the skin such as in impetigo.