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• During the first cycle of rotavirus replication in mucosal epithelial cells, the
synthesis of rotaviral proteins in the cell cytoplasm leads to an increase in the
plasma-membrane permeability to Ca2+, to activation of regulatory mechanisms
and to an increase in the concentration of Ca2+ in the endoplasmic reticulum
through SERCA (Sarco- and Endoplasmic Reticulum Ca2+ ATPase). In the
extracellular medium, Ca2+ stabilizes the structure of the viral capsid but the
increased concentration of cytosolic Ca2+ in infected cells promotes the
activation of Ca2+ dependent enzyme, which in turn induces cell lysis and the
release of viral proteins and viral progeny (Ref.5). NSP4 also act as a viral
enterotoxin to induce secretory diarrhea through Ca2+-dependent secretion by
intestinal cells, Ca2+-dependent secretion of peptides and amines to stimulate
the ENS, or by further activation of epithelial-cell chloride (Cl-) secretion by the
ENS. NSP4 increases [Ca2+]i and this elevation in [Ca2+]i is not due to an
increased influx of extracellular Ca2+ but due to result from the increase in Ca2+
efflux from the endoplasmic reticulum through a PLC (Phospholipase-C)-
dependent mechanism. Exogenous NSP4 induce both Ca2+ release from
intracellular stores and plasmalemma Ca2+ influx, through receptor-mediated
PLC activation and IP3 (Inositol 1,4,5-triphosphate) production (Ref.6). In parallel,
released virus infects downstream absorptive cells. This leads to a massive cell
death and, as a consequence, reduction of the absorptive surface of the intestinal
epithelium and an osmotic component of diarrhea.
2.Bakteri non invasif
ETEC ( enterotoxin E.coli)
enterotoksin
Kerusakan jaringan
Leukosit ++++
Eritrosit ++++
4. parasit
Entamoeba histolitica
Lisis jaringan
ulkus ameba
Common rare
Enterotoxin producing Beta toxin producing type
type A strain C strain