Lipopolysaccharide directly affects pancreatic acinar cells: implications on acute pancreatitis pathophysiology. (citado 36 veces al 2/11/12, indice h=14)

VACCARO MI; CALVO EL; SUBURO AM; SORDELLI DO; LANOSA G; IOVANNA JL

DIGESTIVE DISEASE AND SCIENCES

Springer

Lugar: New York, NY, USA.; Año: 2000 vol. 45 p. 915 - 926

0163-2116

Al 2 de noviembre de 2012, este trabajo fue citado 36 veces segun Scopus que marca un indice h de 14. Este trabajo fue pionero en marcar que la celula acinar responde a la fase aguda cambiando su fenotipo y expresando genes de stress celular. Asimismo, marcó un cambio cualitativo en el trabajo de mi laboratorio que condujo al descubrimiento de VMP1 como gen relacionado a la autofagia.We have explored whether lipopolysaccharide (LPS, endotoxin) induces pancreatic injury on pancreatic acinar cells both in vivo and in vitro. Wistar male rats were treated with four intraperitoneal injections of 10 mg/kg LPS, and AR4-2J cells were exposed to increasing doses of LPS. Expression of pancreatitis-associated-protein (PAP) mRNA was strongly induced in AR4-2J cells exposed to LPS, while amylase mRNA was reduced. LPS also induced apoptosis and expression of TNF-alpha, IL-1beta, and IL-8 mRNA in AR4-2J cells. The in vivo effect of LPS showed structural signs of cellular damage, including numerous cytoplasmic vacuoles, severe nuclear alterations, and high expression of PAP mRNA. This study demonstrated that LPS induced pancreatic damage by directly affecting the pancreatic acinar cells. The role of LPS in the pathophysiology of acute pancreatitis may be partly due to the effect LPS has on the acinar cell.