Increased Expression of Leucocyte Adherence‐Related Glycoproteins by Polymorphonuclear Leucocytes during Phagocytosis of Staphylococci on an Endothelial Surface

Abstract

Phagocytosis of Staphylococcus aureus by human polymorphonuclear leucocytes (PMN) on the surface of endothelial cells is accompanied by adherence of the PMN to the endothelial surface and detachment of the endothelial cells from the culture monolayer. We studied the role of the leucocyte adherence-related glycoproteins (Leu-CAM: Mo1/LFA-1/150,95 or CD11a-c-CD18 complex) in these processes. Phagocytosis of S. aureus induced increased expression of the common beta chain (CD18) of Leu-CAM as demonstrated by flow cytometric analysis of PMN treated with a monoclonal antibody (MoAb) (CLB-LFA-1/1) directed against CD18 and fluorescein isothiocyanate (FITC)-conjugated anti-MoAb. This same MoAb also inhibited the increased adherence of the PMN to the endothelial cells which occurs during phagocytosis. Blocking of adherence during phagocytosis with MoAb CLT-LFA-1/1 had no effect on the detaching activity of the PMN on the endothelial cells. We conclude that adherence of PMN to endothelial cells during phagocytosis of S. aureus is mediated by the Leu-CAM complex. Adherence through the Leu-CAM, however, is not necessary for endothelial damage by the phagocytosing PMN.

Expression of the CD11/CD18 cell surface adhesion glycoprotein family and MHC class II antigen on blood monocytes and alveolar macrophages in interstitial lung diseases

“…CDlla/ CD18 can bind to its ligand CD54(ICAM-1) present on vascular endothelium and other cells. The importance of this family of molecules is illustrated by the observations that they become upregulated during inflammatory reactions [24,37,43,58] and that monoclonal antibodies against CD11/CDI8 can prevent attachment of cells to vascular endothelium [23,26,36] and activation of granulocytes [30].…”

Involvement of locomotion of granulocytes in the phagocytosis of glass-adherent group B streptococci in the absence of opsonins

“…Serum proteins can bind to the glass surface and, by decreasing cell-substratum interaction, favour the locomotion of phagocytes [21,23], finally leading to efficient uptake of adhered bacteria. On the contrary, there are cases where they are absolutely required: uptake of an encapsulated Staphylococcus aureus strain was poor in the absence of serum [18], production of slime by adherent staphylococci impaired serum-independent phagocytosis [19] and, in the present study, GBS strain 419.19 withstood phagocytosis in the absence of antibody-containing serum. The present study suggests that the promoting effect of serum on the uptake of glass-adherent streptococci may exert itself independently of opsonins.…”

“…Several studies have demonstrated that adherence to a solid substratum renders Staphylococcus aureus and Pseudomonas aeruginosa susceptible to phagocytosis in the absence of serum [1,18]. Variation in susceptibility to surface phagocytosis among strains of S. aureus or Escherichia coli have been documented [7,18], and the culture of S. aureus or Staphylococcus epidermidis on the substratum may render them resistant to phagocytic killing [19,20]. Variation in susceptibility to surface phagocytosis among strains of S. aureus or Escherichia coli have been documented [7,18], and the culture of S. aureus or Staphylococcus epidermidis on the substratum may render them resistant to phagocytic killing [19,20].…”