The YompC protein of Yersinia enterocolitica: molecular and physiological characterization.

The structural gene coding for YompC has been identified in the genome of a pathogenic strain of Yersinia enterocolitica O:9, and was subsequently cloned and sequenced. Detailed alignment of the deduced amino acid sequence showed that YompC is a member of the OmpC porin family with the highest degree of homology to Klebsiella pneumoniae. The mutant lacking YompC porin was constructed by insertional inactivation of the yompC gene which resulted from the integration of suicide vector at the yompC locus. In intact cells of Y. enterocolitica, loss of the YompC protein reduced the outer membrane permeability for beta-lactam antibiotics and tetracycline and resulted in a 2-5-fold increase in resistance to these compounds, depending on their chemical properties. Mutation in the ompR regulatory gene resulted in the loss of both YompC and YompF porins, which led to a greater increase of resistance to antibiotics, as compared with the YompC mutant strain. Moreover, the binding assay with HEp-2 cells suggests that YompC may play a role in the adhesion properties of Y. enterocolitica strains.

The level of Yop proteins secreted by Yersinia enterocolitica is changed in maltose mutants.

Enteropathogenic Yersinia enterocolitica strains express a set of plasmid-encoded proteins called Yops, involved in pathogenicity. We studied the influence of the maltose system on the production of Yop proteins and found that the level of Yop proteins of Y. enterocolitica O:9 was reduced in the presence of maltose. Transposon insertion mutants impaired with the maltose transport activity showed a decreased level in the production of Yop proteins. The transcription of the yopH gene for YopH phosphatase in these maltose mutants was unchanged and revealed a maltose mutation impaired in the secretion of Yop proteins instead of their expression.

[Influence of nitrates on red blood cell deformability and clinical parameters in patients with silent ischemia]. / Wplyw azotanów na odksztalcalnosc krwinek czerwonych i parametry kliniczne chorych z niemym niedokrwieniem.

In 30 patients after myocardial infarctum with actual silent ischemia (no pain during last 12 months) mononitrate (Olicard 40) was administered and red blood cell deformability was determined. Clinical improvement and decrease of aforementioned deformability were observed after mononitrate therapy.

[Clinical effect of nitrates (Olicard 40) and their influence on deforming of erythrocytes against the background of 24-hour catecholaminuria]. / Kliniczne efekty nitratów (Olicard 40) i ich wplyw na odksztalcalnosc krwinek czerwonych na tle dobowej katecholaminurii.

Progress in the investigations upon factors influencing the course of the ischemic heart disease focused our attention on the deformability of erythrocytes. That attribute of the red blood cells (RBC) is described by their susceptibility to changes in shape without changing volume. Because of that feature, RBC can reach the smallest capillaries of the circulatory system. The aim of the study was to determine the influence of mononitrates (Olicard Ret.) on the deformability of RBC (EDI) in correlation to the clinical course of the ischemic heart disease and to evaluate the role of catecholamines in the course of the disease and their influence upon EDI. 30 patients (pts) treated with mononitrates for 4 weeks were enrolled into the study. In 27 pts clinical improvement was recorded, as evaluated by the results of repeated exercise tests and changes in the number of anginal attacks. Mean weekly number of anginal attacks decreased from 6.2 to 2.1 (p < 0.05), and parameters of exercise tests improved: DP/Wmac decreased from 0.694 to 0.479 (p < 0.001) and maximal workload attained increased from 6.8 to 9.0 METS (p < 0.001). Correspondingly to the clinical improvement, beneficial changes in RBC deformability were seen: 0.033 vs 0.040 (p < 0.01). Correlation factor for changes in EDI (r = 0.628) was higher than that for the number of anginal attacks (r = 0.589), but lower than the correlation factor for exercise test parameters (r = 0.969 for DP/Wmax and r = 0.858 for METS). There were no significant changes in the urinary output of catecholamines and no correlations were seen between urinary output of adrenaline, noradrenaline and EDI.(ABSTRACT TRUNCATED AT 250 WORDS)

Modulation of inv gene expression by the OmpR two-component response regulator protein of Yersinia enterocolitica.

To elucidate the physiological meaning of OmpR-dependent expression of invasin gene (inv) inhibition in Yersinia enterocolitica, the function of the EnvZ/OmpR regulatory pathway in osmoregulation of inv expression was analyzed in detail. The osmoregulation of inv expression was found to be a multifaceted process involving both OmpR-dependent and -independent mechanisms. Analysis of inv transcription in strains lacking OmpR or EnvZ proteins indicated that kinase EnvZ is not the only regulator of OmpR phosphorylation. Using the transcriptional inv::lacZ fusion in a heterologous system (Escherichia coli) we tried to clarify the role of OmpR in the inv regulatory circuit composed of negative (H-NS) and positive (RovA) regulators of inv gene transcription. We were able to show a significant increase in inv expression in E. coli ompR background under H-NS( Ecoli )-repressed condition. Moreover, H-NS-mediated inv repression was relieved when RovA of Y. enterocolitica was expressed from a plasmid. Furthermore, we showed that RovA may activate inv expression irrespective on the presence of H-NS protein. Using this strategy we showed that OmpR of Y. enterocolitica decrease RovA-mediated inv activation.