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Disruption of response regulator gene, devR, leads to attenuation in virulence of Mycobacterium tuberculosis (2004)

Malhotra, Vandana ; Sharma, Deepak ; Ramanathan, V.D ; [et al.]

Oxford, UK : Blackwell Publishing Ltd

FEMS microbiology letters 231 (2004), S. 0

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ISSN: 1574-6968

Source: Blackwell Publishing Journal Backfiles 1879-2005

Topics: Biology

Notes: The devR-devS two-component system of Mycobacterium tuberculosis was identified earlier and partially characterized in our laboratory. A devR::kan mutant of M. tuberculosis was constructed by allelic exchange. The devR mutant strain showed reduced cell-to-cell adherence in comparison to the parental strain in laboratory culture media. This phenotype was reversed on complementation with a wild-type copy of devR. The devR mutant and parental strains grew at equivalent rates within human monocytes either in the absence or in the presence of lymphocytic cells. The expression of DevR was not modulated upon entry of M. tuberculosis into human monocytes. However, guinea pigs infected with the mutant strain showed a significant decrease in gross lesions in lung, liver and spleen; only mild pathological changes in liver and lung; and a nearly 3 log lower bacterial burden in spleen compared to guinea pigs infected with the parental strain. Our results suggest that DevR is required for virulence in guinea pigs but is not essential for entry, survival and multiplication of M. tuberculosis within human monocytes in vitro. The attenuation in virulence of the devR mutant in guinea pigs together with DevR-DevS being a bona fide signal transduction system indicates that DevR plays a critical and regulatory role in the adaptation and survival of M. tuberculosis within tissues.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1016/S0378-1097(04)00002-3

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Biochemical and histochemical changes pertaining to active and healed cutaneous tuberculosis (2002)

Jayasankar, K. ; Shakila, H. ; Umapathy, K.C. ; [et al.]

Oxford, UK : Blackwell Science Ltd

British journal of dermatology 146 (2002), S. 0

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ISSN: 1365-2133

Source: Blackwell Publishing Journal Backfiles 1879-2005

Topics: Medicine

Notes: Summary Background Fibrosis is one of the major causes of post-treatment morbidity in tuberculosis. The molecular basis of fibrosis in active and healed tuberculous lesions is yet to be fully characterized. Objectives To measure the tissue levels of collagen, elastin, fibronectin, transforming growth factor-β (TGF-β) and zinc in active and healed lesions of cutaneous tuberculosis. Patients and methods Biopsy lesions obtained from 17 patients with active cutaneous tuberculosis and 12 patients after a 6-month regimen of antituberculous chemotherapy were examined. Collagen, elastin and zinc were estimated biochemically. In addition, the presence of collagen IV, TGF-β and fibronectin were determined immunohistochemically. Results It was found that collagen, elastin, fibronectin and TGF-β levels were higher in the active lesions. The levels of zinc were similar in both active and healed lesions. Clinically, scar tissue or keloid formation was not seen in any of the healed lesions. Conclusions Effective antituberculous chemotherapy will lead to a substantial reduction of fibrosis and the consequent disability that can arise in patients with tuberculosis.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1046/j.1365-2133.2002.04784.x

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Increased Expression of Mycobacterium tuberculosis 19 kDa Lipoprotein Obliterates the Protective Efficacy of BCG by Polarizing Host Immune Responses to the Th2 Subtype (2005)

Rao, V. ; Dhar, N. ; Shakila, H. ; [et al.]

Oxford, UK; Malden, USA : Blackwell Science Ltd

Scandinavian journal of immunology 61 (2005), S. 0

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ISSN: 1365-3083

Source: Blackwell Publishing Journal Backfiles 1879-2005

Topics: Medicine

Notes: Mycobacterium tuberculosis can not only neutralize immune effector functions, but also has the ability to modulate host-signalling cascades involved in the development of these responses. The 19 kDa antigen (Rv3763), a lipoprotein of M. tuberculosis, elicits high levels of interleukin (IL)-12 from macrophages in addition to its powerful immunomodulatory properties, leading to suppression of antigen-presentation signalling cascades. The present study was aimed at analysing the effect of overexpression of this antigen on the immunostimulatory properties of M. bovis Bacille Calmette–Guérin (BCG). We have constructed a recombinant BCG strain (rBCG19N) producing higher levels of the 19 kDa antigen in both the cytoplasmic (approximately eightfold) and extracellular (approximately fivefold) fractions as compared to the wildtype BCG. Immunization of mice with rBCG19N elicited high levels of interferon-gamma (IFN-γ) and relatively low levels of IL-10 against the purified 19 kDa antigen. However, in response to total BCG sonicate, mice immunized with rBCG19N produced significantly high levels of IL-10 with relatively very low levels of IFN-γ. This polarization of the host immune responses towards T-helper 2 subtype resulted in complete abrogation of the protective efficacy of BCG, when rBCG19N was used as a live vaccine against M. tuberculosis challenge in guinea pigs.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1111/j.1365-3083.2005.01569.x

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Disruption of mptpB impairs the ability of Mycobacterium tuberculosis to survive in guinea pigs (2003)

Singh, Ramandeep ; Rao, Vivek ; Shakila, H. ; [et al.]

Oxford, UK : Blackwell Science Ltd

Molecular microbiology 50 (2003), S. 0

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ISSN: 1365-2958

Source: Blackwell Publishing Journal Backfiles 1879-2005

Topics: Biology , Medicine

Notes: Protein tyrosine kinases and tyrosine phosphatases from several bacterial pathogens have been shown to act as virulence factors by modulating the phosphorylation and dephosphorylation of host proteins. The identification and characterization of two tyrosine phosphatases namely MptpA and MptpB from Mycobacterium tuberculosis has been reported earlier. MptpB is secreted by M. tuberculosis into extracellular mileu and exhibits a pH optimum of 5.6, similar to the pH of the lysosomal compartment of the cell. To determine the role of MptpB in the pathogenesis of M. tuberculosis, we constructed a mptpB mutant strain by homologous recombination and compared the ability of parent and the mutant strain to survive intracellularly. We show that disruption of the mptpB gene impairs the ability of the mutant strain to survive in activated macrophages and guinea pigs but not in resting macrophages suggesting the importance of its role in the host–pathogen interaction. Infection of guinea pigs with the mutant strain resulted in a 70-fold reduction in the bacillary load of spleens in infected animals as compared with the bacillary load in animals infected with the parental strain. Upon reintroduction of the mptpB gene into the mutant strain, the complemented strain was able to establish infection and survive in guinea pigs at rates comparable to the parental strain. These observations demonstrate a role of MptpB in the pathogenesis of M. tuberculosis.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1046/j.1365-2958.2003.03712.x

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