[afro-nets] Open Learning Web site on Enteric pathogens

[Salvatore Rubino <rubino@uniss.it>]

Open Learning Web site on Enteric pathogens
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Dear Friends of the Open Learning Web site on Enteric pathogens

A new lecture is available at:
http://www.aclisassari.com/acli-openlearning

Piotr Pierzchalski (Poland), Jagiellonian University Collegium
Medicum, Cracow, Poland

Helicobacter pylori and gastric epithelium during inflammation

Gastric mucosa epithelial cells act as the first line of defence
against the noxious action of ingested food; various topical ir-
ritants such as ethanol; non-steroidal anti-inflammatory drugs;
or pathogens such as Helicobacter pylori (Hp) and their toxins.
Maintaining the integrity of the gastric mucosa is important for
its exocrine and endocrine activity. The members of the family
of heat shock factors coordinate the inducible transcription of
heat shock genes in response to diverse stimuli. Any distur-
bances in signal transduction may lead to the attenuation of
heat shock proteins synthesis and to cell death due to apop-
tosis. It has been shown by others that different nuclear fac-
tors, such as nuclear factor interleukine 6 or signal transducer
and activator of transcription 3, co-operate with heat shock
factors, mostly enhancing their activator effect on heat shock
proteins genes expression. Therefore, we sought to determine
whether apoptosis induced in the gastric epithelium exposed to
live Helicobacter pylori might occur due to the elimination of
HSP70 expression and deregulation of the heat shock response of
the cell. Gastric mucosa epithelial cells act as the first line
of defence against the noxious action of ingested food; various
topical irritants such as ethanol; non-steroidal anti-
inflammatory drugs; or pathogens such as Helicobacter pylori
(Hp) and their toxins. Maintaining the integrity of the gastric
mucosa is important for its exocrine and endocrine activity. We
propose a new model of Helicobacter pylori induced HSP70 depend-
ent apoptosis in human gastric epithelium. In KATO III cells ex-
posed to Helicobacter pylori, heat shock factor 1 is bound and
restrained in complexes by phosphorylated signal transducer and
activator of transcription 3 protein. In consequence, heat shock
factor 1 bound up with phosphorylated signal transducer and ac-
tivator of transcription 3 protein is unable to activate HSP70
protein synthesis in KATO III cells under stress conditions.
Helicobacter pylori also causes changes in bax/bcl-2 cellular
equilibrium, leading to the induction of apoptosis. The observed
phenomenon might be the mechanism whereby gastric epithelium
adapts to the infection of Helicobacter pylori, eliminating
cells which are damaged or altered by bacterial cytotoxic prod-
ucts from the tissue.

Ciao Salvatore Rubino

--
Prof. Salvatore Rubino
Dip. di Scienze Biomediche
V.le San Pietro 43/b
07100 Sassari (Italy)
Tel: +39-079-228302
Fax: +39-079-212345
Cell:+39-3383865292
mailto:rubino@uniss.it