Influence of staphylococcal lipoteichoic acid on the frustrated phagocytosis of neutrophils against opsonized corneocytes

Abstract

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 subcorneal 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.

Pseudomonas aeruginosa biofilm is a potent inducer of phagocyte hyperinflammation

“…It has been well documented that hyperinflammatory response, the effect of activation of neutrophils and macrophages with limited access to targets, does favor chronic inflammation without effective bacterial clearance [ 15 – 18 ]. Such reaction was also named as “ frustrated phagocytosis ” [ 19 , 20 ].…”

Lipoteichoic acid improves the capability of mast cells in the host defense system against bacteria

“…CR3 (CD11b/CD18) on the surface of MCs recognizes and phagocytose a wide variety of opsonized bacteria [11,12]. CR3 stimulation affects the release of humoral factors such as TNF-a [13], and it is essential for killing, phagocytosis and elimination of Gram-positive bacteria [14,15]. FccRI are also expressed on MCs in response to IFN-c, which is an inflammatory response to bacterial entry, and bacterial recognition and/or internalization by these surface receptors on MCs induces the release of numerous inflammatory mediators [16,17].…”

Release of monocyte chemoattractants by polymorphonuclear leukocytes stimulated by their adhesion to stratum corneum opsonized via complement activation, measured with a human acute monocytic leukemic cell line, THP‐1

“…In certain inflammatory processes a polymorphonuclear leukocyte (PMN) infiltration predominates in the acute phase, and monocytes/macrophages infiltrate and form granulomas with multinucleated giant cells in the later phase. When pathogenic materials cannot be phagocytized or are resistant to digestion by the phagocytes, PMNs secrete active oxygens and other tissue-destructive substances (1). Such a phenomenon is often found in tuberculosis and deep mycoses like chromomycosis and sporotrichosis.…”