Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental oral infections of rabbits with a wild-type Yersinia pseudotuberculosis strain (pIB102), and two null-mutants (yopK and ypkA) were carried out with the aim to explore the possibility to use mutant strains of Y. pseudotuberculosis as live carrier vaccine strains. The infectious process of the three strains proceed with passing hyperthermia, leucocytosis with granulocytosis, moderate monocytosis and a transient lymphopenia, better demonstrated at mutant strain infections. Short-term bacterial dissemination into the brain and viscera was observed at yopK infection. An augmented resistance to bactericidal activity of leucocytes at the initial phase of infection was followed by an increased sensitivity discovered earlier in case of yopK strain accompanied by at least 70- and 20-fold, respectively, for ypkA lower virulence for mice. The level of attenuation of yopK was accompanied by significant Yersinia specific IgG and IgM antibody response. Inflammatory foci were found by morphological examination in brain, lung and small intestines after infection with the wild-type strain, while such foci were only observed in brain and mesenterial lymph nodes after infection with the yopK mutant. After infection with the ypkA mutant foci were found in brain and spleen of the infected animals. Morphological changes in the lymphatic tissue of rabbits infected with mutant strains were consistent with induction of immunogenesis. The data suggest that genetically constructed yopK null-mutant exhibits characteristics that makes the strain suitable to be used as a live carrier vaccine to deliver heterologous antigens.
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PMID:Experimental infections with wild and mutant Yersinia pseudotuberculosis strains in rabbits. 1462 99

Peroral infections of rabbits with a virulent Yersinia enterocolitica serotype O:8 wild-type strain (WA-314) and its isogenic Mn-cofactored superoxide dismutase (sodA) mutant were analyzed with respect to the following parameters: clinical findings, bacterial ability to colonize and persist in different tissues, bacterial resistance to the killing effect of leukocytes and blood sera, IgG antibody response, pathomorphological and immunomorphological changes. In comparison to WA-314, the sodA mutant was markedly impaired in its ability to disseminate into the brain and viscera, and to cause hyperthermia, leukocytosis with monocytosis, granulocytosis and initial lymphopenia. The sodA mutant strain was more susceptible to bactericidal activity of leukocytes and blood sera than the parent strain WA-314. Moreover, in comparison to WA-314, the sodA mutant was attenuated for mice after oral, intravenous, and intraperitoneal inoculation and totally avirulent for rats. Strikingly, the sodA mutation led not only to attenuation of virulence but also enhanced immunogenicity (as reflected by the specific antibody response). These features are consistent with the mild immunomorphological changes observed after infection with the sodA mutant as compared to the severe tissue lesions caused by the virulent strain WA-314. In conclusion, this study demonstrates that the sodA mutation in Y. enterocolitica leads to loss of virulence and gain of immunogenicity in rabbits. These are promising features for a live oral vaccine carrier strain.
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PMID:Comparison of the course of infection of virulent Yersinia enterocolitica serotype O:8 with an isogenic sodA mutant in the peroral rabbit model. 1559 88