Accelerated immunopathological response of mice infected with Mycobacterium tuberculosis disrupted in the mce1 operon negative transcriptional regulator.

Accelerated immunopathological response of mice infected with Mycobacterium tuberculosis disrupted in the mce1 operon negative transcriptional regulator. Research Abstract Details 

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Accelerated immunopathological response of mice infected with Mycobacterium tuberculosis disrupted in the mce1 operon negative transcriptional regulator. Abstract Text:

Yujiro Uchida,Nicola Casali,Amy White,Lisa Morici,Lon V Kendall,Lee W Riley,

Mycobacterium tuberculosis causes a variety of clinical outcomes determined by host as well as bacterial factors. M. tuberculosis disrupted in the mce1 operon causes increased mortality in immunocompetent mice. This operon is negatively regulated by mce1R (Rv0165c). We studied the role of mce1R in infection outcome in mice. At 5 x 10(4) tail vein infectious dose, the median survival time (MST) of mice infected with the mce1R mutant M. tuberculosis H37Rv was 293 days, while mice infected with the wild-type H37Rv survived more than 350 days (P < 0.0001). At a higher dose (5 x 10(6)), the MST of mutant-infected mice was 32 days, compared with 127 days for wild type-infected mice (P < 0.0001). With either tail vein or aerosol infection, mutant-infected mice developed larger granulomatous lesions in their lungs than mice infected with the wild type. Mutant-infected mice were unable to control the bacterial burden in the first 4 weeks of infection, but even after achieving control later, these mice succumbed to granulomatous pneumonia. These observations suggest that the early deregulated expression of the mce1 operon products determines later granulomatous tissue response. mce1 operon may homeostatically regulate the cell wall architecture in vivo that elicits a steady-state granuloma tissue response permitting M. tuberculosis to establish a long-term infection.

Accelerated immunopathological response of mice infected with Mycobacterium tuberculosis disrupted in the mce1 operon negative transcriptional regulator. Publishing Authors By Initials

Y Uchida,N Casali,A White,L Morici,LV Kendall,LW Riley,

For similar cardiovascular system: blood vessels: veins research abstracts see: cardiovascular system: blood vessels: veins research

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Accelerated immunopathological response of mice infected with Mycobacterium tuberculosis disrupted in the mce1 operon negative transcriptional regulator. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Cellular microbiology

VOLUME: 9

Page Numbers: 1275-83

Journal Abbreviation:

ISSN: 1462-5814

DAY: 11

MONTH: 01

YEAR: 2007

Accelerated immunopathological response of mice infected with Mycobacterium tuberculosis disrupted in the mce1 operon negative transcriptional regulator. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100883691

Accelerated immunopathological response of mice infected with Mycobacterium tuberculosis disrupted in the mce1 operon negative transcriptional regulator. Keywords Mesh Terms:

KEYWORDS: Veins

MESH TERMS: pathology

Chemical & Substance for Abstract: Accelerated immunopathological response of mice infected with Mycobacterium tuberculosis disrupted in the mce1 operon negative transcriptional regulator. Information

Substance Name: mammalian cell entry protein Mce1A, Myco

Registry Number: 0

Grant and Affiliation Information for Accelerated immunopathological response of mice infected with Mycobacterium tuberculosis disrupted in the mce1 operon negative transcriptional regulator.

AFFILIATION: Division of Infectious Diseases, School of Public Health, University of California, Berkeley, CA, USA.

Country: England

AGENCY: United States NIAID

GRANT: R01 AI 53266

ACRONYM: AI

MEDLINETA: Cell Microbiol

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