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Th1-type immune response to infection by pYV-cured phoP-phoQ null mutant of Yersinia pseudotuberculosis is defective in mouse model

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Abstract

The PhoP-PhoQ two-component system of Yersinia pseudotuberculosis, a Gram-negative enteric pathogen which causes a variety of gastrointestinal and extraintestinal infections in humans, has been shown to be necessary for virulence. A phoP-phoQ null mutant of a strain of Y. pseudotuberculosis cured of its native plasmid pYV was obtained and studied for generation of immune response in mouse model following intravenous inoculation. The phoP-phoQ null mutant elicited much weaker IgG antibody response to whole cell sonicated (WCS) antigen, in particular that of IgG2a isotype. Interferon-γ levels were also significantly reduced in cultured splenocytes of mice immunized with phoP-phoQ null mutant. The null mutant was found to be about 72-fold less virulent than the parent isogenic strain of Y. pseudotuberculosis. Average counts in spleen of mice inoculated with the null mutant were observed to reduce by at least four logs when compared with the counts in the spleen of mice inoculated with parent isogenic strain. We can thus suggest that the Th1-type immune response of the phoP-phoQ null mutant of Y. pseudotuberculosis is diminished in mice.

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Abbreviations

CFU:

Colony-forming units

ELISA:

Enzyme-linked immunosorbent assay

LFR:

Long flanking region

LD50 :

Lethal dose 50

PBS:

Phosphate buffer saline

YOPs:

Yersinia outer proteins

WCS:

Whole cell sonicated

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Acknowledgments

The authors are thankful to the Director of DRDE for providing the necessary facilities and encouragement. Authors are also grateful to Dr. Elisabeth Carniel of the Pasteur Institute, Paris, for the kind gift of plasmid pKOBEG-sacB.

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Correspondence to Subodh Kumar.

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Kumar, S., Balakrishna, K., Agarwal, G.S. et al. Th1-type immune response to infection by pYV-cured phoP-phoQ null mutant of Yersinia pseudotuberculosis is defective in mouse model. Antonie van Leeuwenhoek 95, 91–100 (2009). https://doi.org/10.1007/s10482-008-9292-5

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