Absence of direct relationship between intraperitoneal cellular influx and resistance to experimental peritonitis.

Intraperitoneal inflammation is an essential defence mechanism against microbial invasion of the abdominal cavity. We have recently demonstrated that a single contact with heat killed E. Coli or Staphylococcus aureus increased the intraabdominal leukocyte influx in rats later challenged by these microorganisms.

Role of CD18-dependent and CD18-independent mechanisms in the increased leukocyte adhesiveness and in the variations of circulating white blood cell populations induced by anti-CD3 monoclonal antibodies.

Anti-CD3 antibodies induce a quick and profound depletion of peripheral blood mononuclear cells (PBMCs) that is not well understood. We studied the effect of OKT3, a mouse monoclonal antibody against the human CD3 complex, on the in vitro adhesion of human PBMCs to monolayers of fresh and fixed human umbilical vein endothelial cells (HUVECs). OKT3 induced an increased adhesiveness of PBMCs.

Modulation of inflammatory reactions by previous contact with Escherichia coli in rats.

Objective: To find out if contact with Escherichia coli had any effect on a subsequent inflammatory reaction induced by the same micro-organism.

Design: Controlled laboratory study.

Setting: University laboratory.

Modulation of inflammatory reactions by surgical trauma: lack of relationship with corticosteroid secretion.

The effect of surgery on inflammation was studied in male Wistar R/A rats using the carrageenin-induced edema model. Swelling of the paw was measured in standardized arbitrary units 2, 4, and 6 hr after a subcutaneous injection of carrageenin iota in the subplantar region of the right hind limb. It was significantly depressed in rats submitted to laparotomy (5.