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A B B C D e F: 4 General Mechanism of Pathogenesis

The document discusses the mechanisms of apoptotic cell death, highlighting the role of various proteins and caspases in the process. It details the stages of apoptosis, including cell shrinkage, chromatin condensation, and membrane blebbing, as well as the clearance of apoptotic bodies by phagocytic cells. Additionally, it mentions how certain bacterial toxins can induce programmed cell death or, at high concentrations, cause necrosis.

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15 views1 page

A B B C D e F: 4 General Mechanism of Pathogenesis

The document discusses the mechanisms of apoptotic cell death, highlighting the role of various proteins and caspases in the process. It details the stages of apoptosis, including cell shrinkage, chromatin condensation, and membrane blebbing, as well as the clearance of apoptotic bodies by phagocytic cells. Additionally, it mentions how certain bacterial toxins can induce programmed cell death or, at high concentrations, cause necrosis.

Uploaded by

humaxvyoepwxvfbnop
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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106 4 General Mechanism of Pathogenesis

Fig. 4.11 (A) Schematics of different stages of apoptotic (b) zeiosis stage, cell morphology alters and shrinkage
cell death and (B) fluorescence photographs of human continues; (c) chromatin condensation/margination, cres-
hybridoma B cells infected with Listeria monocytogenes cent-shaped nucleus; (d) DNA fragmentation; (e) mem-
and stained with ethidium bromide and acridine orange at brane blebbing of apoptotic bodies; and (f) clearance of
different stages of apoptotic cell death: (a) cell shrinkage; apoptotic bodies by phagocytic cells

leaflet of the cytoplasmic lipid bilayer mem- Procaspase-9 activates caspase-3, caspase-6, and
brane; however, when cells are undergoing apop- caspase-7 (known as executioner caspase), which
totic cell death, the PS translocates from the inner break down nuclear proteins histone, actin/lam-
leaflet of the membrane to the outer leaflet and ins, and poly-ADP-ribose polymerase (PARP)
becomes a target for macrophage-mediated leading to apoptosis. C-Myc and p53 proteins
clearance. induce programmed cell death, while the Bcl-2
Apoptosis is a highly regulated process of pro- protein family, normally present in the malignant
grammed cell death. Apoptotic stimuli such as cells, suppresses apoptosis.
bacterial toxins activate death ligands FADD Shiga toxin and IpaB protein in Shigella,
(Fas-associated death domain) and TRADD LLO in L. monocytogenes, cholera toxin in V.
(TNF receptor-associated death domain), which cholerae, and Clostridium perfringens entero-
in turn activate procaspase-8. Procaspase-8 phos- toxin (CPE) are some examples, which induce
phorylates Bcl-2-associated death domain programmed cell death. In contrast, some tox-
(BAD), which consequently activates DNase and ins such as LLO and CPE at high concentra-
procaspase-9 (cysteine protease). Procaspase-8 tions induce oncosis, a form of necrosis by
and procaspase-9 are known as initiator caspase. causing physical trauma that leads to cell

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