Publication: Epithelia1 integrity, cell death and cell loss in mammalian small intestine
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Date
1999
Authors
Mayhew, T.M. ; Myklebust, R. ; Whybrow, A. ; Jenkins, R.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
In recent years, the different mechanisms of
epithelial cell loss which occur in mammalian and avian
small intestine have been re-investigated. Information is
now available for a variety of mammalian types and
mechanisms can be divided into two major classes: [i]
those preserving epithelial integrity by maintaining
intercellular tight junctions throughout early-to-late
stages of cell extrusion; and [ii] those which compromise
integrity by introducing breaches in epithelial continuity.
Both classes are associated with the activity andtor
proximity of non-epithelia1 cells (mainly lymphocytes
and mononuclear phagocytes) located in the epithelium
or underlying lamina propria. Intraepithelial lymphocytes
may be involved in enterocyte targetting and
killing whilst lamina propria (LP) macrophages
sequester cell debris. Where epithelial integrity is
maintained, two types of loss can be identified. In the
first (type l), complete cells are extruded into the lumen.
In the second (type 2), only anucleate apical cell
fragments pass into the lumen . There are two variants of
type 2 loss distinguishable by the fate of the nucleated
basal portions of cells. One variant (type 2a) creates
large intercellular spaces extending from the preserved
apical cap to the basal lamina and containing enterocyte
debris for phagocytosis. The second (type 2b) involves
the gradual shrinkage of individual cells (which become
more electron-dense) and in situ degeneration of their
nucleated subapical portions in increasingly narrower intercellular spaces between adjacent healthy
enterocytes. The mechanism of removal of these
fragments is unclear but may be via macrophages or
surrounding enterocytes. Apoptosis has been implicated
in both type 1 and type 2 extrusion. In contrast, type 3
loss involves morphological changes in enterocytes
which are reminiscent of those seen in necrosis and is
accompanied by breaks in epithelial continuity following
cell swelling, a decrease in cell electron density and total or subtotal degradation of organelles and membranes. It
ends in loss of either an abnormal cell apex (with
subsequent exposure of the degraded cell contents and
their spillage into the lumen) or a complete cell remnant
(extruded into the lumen before total disintegration of
plasma membranes).
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