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Endotoxin suppresses matrix protein-induced upregulation of PMN candicidal activity: an effect reversed by low-dose

H H Simms1, R D'Amico

  • 1Division of Surgical Research, Rhode Island Hospital/Brown University School of Medicine, Providence 02903.

The Journal of Surgical Research
|May 1, 1992
PubMed

Insights

Lipopolysaccharide (LPS) impairs polymorphonuclear leukocyte (PMN) killing of Candida, even with matrix proteins present. Low-dose TNF-alpha can restore PMN function by increasing fibronectin receptor expression.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Matrix proteins like fibronectin enhance polymorphonuclear leukocyte (PMN) candicidal activity.
  • Lipopolysaccharide (LPS) is known to modulate immune cell function.

Purpose of the Study:

  • To investigate how LPS affects the interaction between matrix proteins and PMN candicidal activity.
  • To elucidate the mechanisms by which LPS modulates PMN function in the presence of matrix proteins.

Main Methods:

  • Assessing PMN candicidal activity in the presence of matrix proteins and LPS.
  • Measuring CD11b/CD18 expression on PMN using antibody-coated erythrocytes.
  • Quantifying fibronectin and RGDS binding to PMN using radiolabeled ligands.
  • Investigating the effects of PMA, FMLP, staurosporine, and TNF-alpha on PMN function and receptor expression.

Main Results:

  • LPS reduced PMN candicidal activity and CD11b/CD18 expression when PMN were adhered to fibronectin or laminin.
  • LPS decreased fibronectin and RGDS binding to PMN, indicating reduced receptor availability.
  • PMN oxidative burst stimulation reduced fibronectin and RGDS binding, while staurosporine blocked this decrease.
  • Low-dose TNF-alpha restored fibronectin and RGDS binding and CD11b/CD18 expression, enhancing PMN candicidal activity.

Conclusions:

  • Matrix proteins enhance PMN candicidal activity.
  • LPS diminishes PMN candicidal activity in the presence of matrix proteins.
  • Oxidative burst stimulation, particularly via protein kinase C, reduces fibronectin receptor bioavailability.
  • Low-dose TNF-alpha can restore PMN candicidal activity by upregulating fibronectin receptor expression.

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