摘要

Duodenum, spleen and liver have a crucial role in iron balance on the whole organism and are the major sites of Ferroportin (FPN) expression. Specific regulations between FPN and hepcidin are responsible for changes seen in physiopathological conditions such as inflammation. We studied in vivo effects of turpentine oil-induced acute inflammation on FPN expression, and its relation with prohepcidin and iron mobilization. Immunohistochemical procedures were performed using rabbit anti-mouse FPN and prohepcidin antibodies with goat-labeled polymer-HRP anti-rabbit (DAB) as secondary antibody. Plasma and tissular iron were also studied. Our results showed a notable expression and redistribution of duodenal FPN to basolateral membrane in turpentine-treated mice, compared with supranuclear and the weak basolateral expression observed in healthy mice. Red pulp macrophages of healthy mice showed FPN-hemosiderin co-localization, compared with turpentine-treated mice which showed lack of FPN. In liver of healthy mice, FPN was seen in Kupffer cells, whereas in turpentine-treated mice decreased. In addition, we observed an increment of hepatic pro-hepcidin with a significant hypoferremia. Our findings demonstrated that acute inflammation induced a differential distribution of FPN, showing a cell type specific response. In macrophages, increased hepatic prohepcidin induced degradation of FPN, resulting in hypoferremia. In enterocytes, the redistribution observed of duodenal FPN reflects a different regulation in this tissue. The observed response of the proteins studied may be part of a cyclical pattern of systemic effects of acute inflammation on mouse tissue. El duodeno, bazo e h赤gado desempe an un rol clave en el balance de Fe del organismo y son los mayores sitios de expresi車n de ferroportina (FPN). Regulaciones espec赤ficas entre FPN y hepcidina son las responsables de los cambios observados en condiciones fisiopatol車gicas como la inflamaci車n. Nuestro objetivo fue estudiar los efectos in vivo de la inflamaci車n aguda inducida con turpentina sobre la expresi車n de FPN y su relaci車n con prohepcidina y la movilizaci車n de hierro. Los procedimientos inmunohistoqu赤micos fueron desarrollados utilizando anticuerpos anti FPN y prohepcidina de rat車n, desarrollados en conejo y un pol赤mero conjugado con anticuerpos secundarios anti conejo desarrollado en cabra (HRP-DAB). Se evaluaron los niveles de Fe plasm芍tico y tisular. Nuestros resultados mostraron una clara expresi車n y redistribuci車n de FPN duodenal hacia la membrana basolateral en ratones tratados con turpentina, con resp

全文