Fig. 1.
Fig. 1. The activation of inflammation-elicited peritoneal macrophages is thrombin dependent in vivo. / (A) The activation-induced adhesion of peritoneal macrophages by antigen-specific Th1 cells is thrombin dependent. OT-II transgenic T-cell receptor Th1 effector cells were adoptively transferred to C57Bl/6 mice that had been primed with TG (3 mL intraperitoneally) 3 days earlier. The next day, Ova peptide (50 μg intraperitoneally) or PBS vehicle (200 μL) were administered, and 5 hours later peritoneal exudate cells were harvested and macrophages were enumerated. Where indicated, mice received Refludan (2 mg/kg intraperitoneally) at the time of Ova administration. The data depicts the averages and standard deviations of groups of 3 mice. Th1 cells induced antigen-specific macrophage activation (P < .01), which was suppressed by Refludan (P = .02). This experiment was replicated twice. (B) The activation-induced adhesion of peritoneal macrophages by LPS is thrombin dependent. Peritoneal macrophages were elicited with TG (3 mL intraperitoneally). Four days later, LPS (1 μg intraperitoneally) or vehicle control (200 μL PBS) were administered, and macrophage numbers in peritoneal exudates were determined 5 hours later. Where indicated, mice also received Relfudan (20 mg/kg intraperitoneally) at the time of LPS administration. The data depicts the averages and standard deviations of groups of 5 mice. LPS induced macrophage activation (P < .0001) that was suppressed by Refludan (P < .0001). This experiment has been replicated 4 times.

The activation of inflammation-elicited peritoneal macrophages is thrombin dependent in vivo.

(A) The activation-induced adhesion of peritoneal macrophages by antigen-specific Th1 cells is thrombin dependent. OT-II transgenic T-cell receptor Th1 effector cells were adoptively transferred to C57Bl/6 mice that had been primed with TG (3 mL intraperitoneally) 3 days earlier. The next day, Ova peptide (50 μg intraperitoneally) or PBS vehicle (200 μL) were administered, and 5 hours later peritoneal exudate cells were harvested and macrophages were enumerated. Where indicated, mice received Refludan (2 mg/kg intraperitoneally) at the time of Ova administration. The data depicts the averages and standard deviations of groups of 3 mice. Th1 cells induced antigen-specific macrophage activation (P < .01), which was suppressed by Refludan (P = .02). This experiment was replicated twice. (B) The activation-induced adhesion of peritoneal macrophages by LPS is thrombin dependent. Peritoneal macrophages were elicited with TG (3 mL intraperitoneally). Four days later, LPS (1 μg intraperitoneally) or vehicle control (200 μL PBS) were administered, and macrophage numbers in peritoneal exudates were determined 5 hours later. Where indicated, mice also received Relfudan (20 mg/kg intraperitoneally) at the time of LPS administration. The data depicts the averages and standard deviations of groups of 5 mice. LPS induced macrophage activation (P < .0001) that was suppressed by Refludan (P < .0001). This experiment has been replicated 4 times.

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