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Differential induction of apoptosis in lymphoid tissues during sepsis:
variation in onset, frequency, and the nature of the mediators
A Ayala, CD Herdon, DL Lehman, CA Ayala and IH Chaudry
Department of Surgery, Michigan State University, East Lansing, USA.
Apoptosis (Ao), is a process by which cells undergo a form of nonnecrotic
cellular suicide. Although for most cells this is a constitutive process,
it can be induced in immature and differentiating immune cell populations
by stress mediators associated with inflammation. This inducible form of
A(o) is referred to as programmed cell death. However, it is not clear
whether hematopoietic cell populations such as the thymus and bone marrow
are induced to undergo A(o) during polymicrobial sepsis. To assess this,
thymocytes, bone marrow cells, or splenocytes (as a source of comparative
nonhematopoietic cells) were harvested from C3H/HeN mice at 1, 4, or 24
hours after cecal ligation and puncture (CLP; to induce polymicrobial
sepsis) or sham-CLP (Sham). The results showed that mixed bone marrow cells
ex vivo, although not to the same extent as thymus, showed a marked
increase in the percentage of cells in A(o), increased endonuclease
activity, and a significant decrease in cell yield at 24 hours but not at 4
hours after CLP. Similar changes were not evident in splenocytes.
Phenotypic, as well as morphologic assessment, indicated that most of the
increase in apoptotic cells in the thymus was associated with the immature
T cells (CD4+CD8+) and CD8-CD4- cells. In contrast, the increase in bone
marrow cell A(o) was associated with only the B220+ cells, with no
significant contribution from myeloid cells. Treatment of CLP mice in vivo
with either RU-38486 or PEG-(rsTNF- R1)2 was unable to reverse the
increased A(o) in the bone marrow of these animals. Taken together, these
findings indicate that A(o) as a process induced by polymicrobial sepsis is
not limited to the thymus, but can also be detected in the bone marrow.
However, unlike thymic A(o), bone marrow is not affected
directly/indirectly by glucocorticoids or tumor necrosis factor released
during sepsis.
Volume 87,
Issue 10,
pp. 4261-4275,
05/15/1996
Copyright © 1996 by The American Society of Hematology
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