ALVEOLAR HYDATID CYST (AHC) - INFLAMMATION-INDUCED REACTIVE GASTROINTESTINAL (GI) AMYLOIDOSIS IN AHC-INFECTED MICE AND CHEMICAL CHARACTERIZATION OF THE GI AMYLOID

A high incidence of GI amyloidosis has been described in patients with various forms of systemic amyloidosis but its evolution and progressi on in different subregions of the GI tract are not well documented. Th ese aspects including the chemical nature of GI amyloid were examined in the AHC mouse model of inflammation-associated reactive amyloidosis . C57BL/6 mice were infected intraperitoneally with 250 AHC. Paraffin sections from the stomach and the small and large intestines of AHC mi ce were stained at different rime intervals with Congo red or immunocy tochemically with monospecific RAA. The submucosal blood vessels at 1 week postinfection were found to be the first target of amyloid deposi tion. With time the amyloid deposits extended to the mucosa and the Pe yer's patches and immunoreacted with RAA; ileum was the most severely affected region. Amyloid was extracted from the GI tract and purified by size exclusion chromatography using 5 M guanidine-formic acid, pH 3 . The purified amyloid was identified by Western blotting using RAA an d by partial N-terminal microsequencing up to 10 cycles. The GI amyloi d showed homology with murine SAA(2), although SAA(2) mRNA is not expr essed in murine GI tract. These results show that (a) the GI amyloid i s derived, similar to that of splenic/hepatic amyloid, from circulatin g SAA(2) and (b) the GI tract submucosal blood vessels are the first t arget of AA deposition. The data also suggest that AA-mediated damage to the submucosal blood capillaries may lead to SAA leakage followed b y cascading of AA deposition in other layers of the GI tract. (C) 1996 Academic Press, Inc.