Mechanism of intestinal mucosal immune dysfunction following trauma- hemorrhage: Increased apoptosis associated with elevated Fas expression in Peyer's patches

Academic Article

Abstract

  • Although intestinal mucosal immune dysfunction oc curs after trauma and hemorrhage and appears to con tribute to infectious complications, the mechanism is not known. In this regard, the inappropriate induction of immune cell apoptosis may contribute to the immune dysfunction following trauma and hemorrhage. To study this, we examined Peyer's patch cells for evidence of apoptosis and changes in Fas protein expression, as well as alterations in the relative lymphocyte subpopulations after trauma and hemorrhagic shock. Male C3H/HeN mice underwent sham operation, trauma (i.e., laparot omy), hemorrhagic shock (mean arterial blood pressure of 35 ± 5 mmHg for 90 min, followed by adequate crys talloid resuscitation), or trauma plus hemorrhage. Pey er's patch cells were isolated at 24 and 72 hr after the procedure. The percentage of apoptotic cells, Fas protein expression, and cell percentage of phenotype were determined by flow cytometry. The results indicate that trauma alone induced no significant change in the measured parameters. However, (i) there were a significant decrease in total viable cell yield and an increased apoptosis in Peyer's patch cells at 24 and 72 hr following hemorrhage or trauma plus hemorrhage; (ii) the in creased apoptosis in Peyer's patch was predominantly in cells of the B-cell lineage; (iii) the increased apoptosis was associated with an elevated Fas expression. In con clusion, hemorrhage alone or trauma plus hemorrhage can induce increased apoptosis in Peyer's patch cells, which is associated with the increased Fas expression. Thus, apoptotic involution may play an important role in the depression of intestinal mucosal immune function after trauma and hemorrhagic shock.
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    Digital Object Identifier (doi)

    Author List

  • Xu YX; Ayala A; Monfils B; Cioffi WG; Chaudry IH
  • Start Page

  • 55
  • End Page

  • 60
  • Volume

  • 70
  • Issue

  • 1