Uptake pathways of clinical and healthy animal isolates of Campylobacter jejuni into INT-407 cells

Campylobacter jejuni isolates obtained from human and animal sources showed different invasion levels into human embryonic intestinal (INT-407) cells. There was no significant relation between the degree of invasion and cytot oxins production. The depolymerization of both microfilaments by cytochalas in-D and microtubules by colchicine, demecolcine and nocodazole or stabiliz ation of microtubules by paclitaxel reduced the invasiveness of C. jejuni, although microfilament depolymerization showed greater inhibition than micr otubule depolymerization. Interference with receptor-mediated endocytosis b y G-strophanthin and monodansylcadaverine and inhibition of endosome acidif ication by monensin reduced the number of viable intracellular C. jejuni ce lls. Furthermore inhibition of only host protein kinases by staurosporine, but not phosphoinositide 3-kinase by wortmannin or protein kinase-C by calp hostin-C, significantly reduced invasion of epithelial cells by C. jejuni. These data suggest that the internalization mechanism triggered by C. jejun i is strikingly different from the microfilament-dependent invasion mechani sm exhibited by many of the well-studied enteric bacteria such as enteroinv asive strains of Escherichia coli, Salmonella typhimurium, Shigella flexner i, Yersinia enterocolitica and Yersinia pseudotuberculosis. (C) 2000 Federa tion of European Microbiological Societies. Published by Elsevier Science B .V. All rights reserved.