Analysis of the pathogenicity of Yersinia enterocolitica was performed with an experimental model successfully produced in rabbits by intraduodenal inoculation with strains isolated from various sources.
Pathogenic strains easily penetrated the epithelial linings of the intestinal mucous membrane into the target reticuloendothelial tissues of the intestine, such as the lamina propria and lymph follicles, where they multiplied within mononuclear cells and produced granuloma.
Granuloma, in severe infections, underwent necrobiosis and sometimes progressed to ulceration accompanied by colony formation of the organisms.
In mild infections, granulomatous lesions were localized in lymph follicles and never progressed to ulceration.
Nonpathogenic strains were rapidly excreted without penetration of epithelial linings.
Y. enterocolitica should be within the category of invasion type enteropathogenic bacteria such as Shigella and Salmonella. Pathogenic behavior of Y. enterocolitica is discussed in comparison with that of Shigella and Salmonella.

View full abstract

Analysis of the pathogenicity of Yersinia enterocolitica was performed by means of cell culture studies on the interaction of the organisms with HeLa cells and rabbit peritoneal macrophages based on observations of the pathogenic behavior of the organisms in vivo (11). The pathogenic strains, which successfully produced experimental enterocolitis in rabbits (11), had the ability to penetrate HeLa cells and to survive or multiply within the macrophages. The nonpathogenic strains, lacking the ability to produce pathological changes in rabbits (11), failed to penetrate HeLa cells, except for one strain, and also to survive totally or multiply within the macrophages. It was evident that the abilities of the organisms to penetrate epithelial linings which serve as the barrier of intestinal mucosa and to survive or multiply within the host cells appears to be closely related to the pathogenicity of Y. enterocolitica.

View full abstract

Spikeless particles of HVJ (Sendai virus) lacking in hemagglutinating (HA) activity were obtained by enzymatic digestion of virions with trypsin followed by centrifugation through a sucrose gradient. When they were mixed with glycoprotein components of Newcastle disease virus (NDV) obtained by treatment of purified virions with deoxycholate (DOC), the mixture showed hemagglutination reaction, which was inhibited by anti-NDV serum, but not by anti-HVJ serum. Sedimentation profile of the HA active agents was then examined by centrifugation of the mixture of spikeless particles of HVJ (labeled with ³H-uridine) and glycoproteins of NDV (labeled with ¹⁴C-amino acid mixture). The results showed that the peak of HA activity had both of the radioactivities, and that the sedimentation rate of the HA was faster than that of spikeless HVJ but slower than that of intact HVJ. Electron micrographs of such HA active structures showed that they were morphologically closely similar to intact virion of HVJ, although they had neither hemolytic activity nor infectivity. The mixture of spikeless HVJ and glycoproteins of HVJ or NDV which were removed from virions by proteolytic enzymes, on the other hand, did not show any detectable hemagglutinating activity.

View full abstract

Splenic T lymphocytes from mice sensitized to 100 μg of DNP-coupled mycobacterium (DNP-Tbc) showed in vitro proliferative response against DNPor TNP-conjugated protein antigens. The increased uptake of ³H-thymidine induced by DNP-HSA was partially inhibited by the addition of 10^-4M DNP-EACA. DNP-AECM-Ficoll did not induce any significant proliferative responses in DNPTbc-primed T cell population. However, priming with DNP-Tbc augmented anti-DNP IgG antibody response induced with DNP-Ficoll. The augmentation of IgG response was not due to the presence of DNP-primed B cells or anti-DNP antibody. The results showed that the priming with DNP-Tbc induced DNP-reactive T helper cells which could be triggered with DNP-Ficoll. The possible role of mycobacterium in the induction of hapten-specific T helper cells is discussed.

View full abstract