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Biomedical subjects

Dejiang Tan

Publications and source records attributed to Dejiang Tan.

5 recordsLinked to original sources
PubMed2004

In vitro activity of protegrin-1 and beta-defensin-1, alone and in combination with isoniazid, against Mycobacterium tuberculosis.

The antimicrobial peptide protegrin-1 (PG-1) inhibited the growth in vitro of drug-susceptible and multidrug-resistant Mycobacterium tuberculosis; a lower activity was shown by human beta-defensin-1 (HBD-1) against both strains. The combination of PG-1 or HBD-1 with isoniazid significantly reduced M. tuberculosis growth in comparison with the peptides or isoniazid alone.

Anti-Infective Agents↗
PubMed2003

Activities of moxifloxacin alone and in combination with other antimicrobial agents against multidrug-resistant Mycobacterium tuberculosis infection in BALB/c mice.

The activity of moxifloxacin was enhanced by the addition of ethionamide but not by that of cycloserine, thiacetazone, capreomycin, para-aminosalicylic acid, or linezolid in BALB/c mice infected with a strain of Mycobacterium tuberculosis resistant to isoniazid, rifampin, and six other drugs. These observations are important for the therapy of multidrug-resistant tuberculosis.

Animals↗
PubMed2002

Exposure of BALB/c mice to low doses of Mycobacterium avium increases resistance to a subsequent high-dose infection.

BALB/c mice exposed intranasally (i.n.), intradermally (i.d.) or intraperitoneally (i.p.) to low doses of Mycobacterium avium (20 c.f.u. at three different times two weeks apart) showed an increased resistance to a subsequent high-dose (10(5) c.f.u.) infection. I.n.-exposed mice had few mycobacteria in the tissues (>100 c.f.u.) and showed an expansion of CD4(+) T cells associated with overproduction of IL-12 and IFN-gamma, but not IL-4 and IgG antibodies. Parenterally (i.p. and i.d.) exposed animals showed c.f.u. numbers higher than i.n.-exposed mice, together with overproduction of IL-12, IFN-gamma and IL-4 in the case of i.p.-exposed mice, and of IL-12, IFN-gamma and IgG2a and IgG1 antibodies in the case of i.d.-exposed mice. Low-dose exposures were not contained by athymic BALB/c nude mice; however, naive nude mice reconstituted with i.n.-primed CD4(+) T cells of BALB/c mice were protected against high-dose infection, indicating that CD4(+) T cells are essential to control even low-dose infections by M. avium. Overall, these data suggest that continuous i.n. exposure to M. avium doses commonly found in the environment may play a role in determining the natural resistance of normal hosts against this organism.

Administration, Cutaneous↗
PubMed2002

Involvement of the fadD33 gene in the growth of Mycobacterium tuberculosis in the liver of BALB/c mice.

The potential pathogenic role of Mycobacterium tuberculosis H37Rv fadD33, a gene encoding an acyl-CoA synthase that is underexpressed in the attenuated strain H37Ra, was investigated. In a first approach, fadD33 was cloned and expressed in strain H37Ra to restore gene expression and fadD33-complemented bacteria were used to investigate whether fadD33 might confer any growth advantage to M. tuberculosis H37Ra in an infection model of BALB/c mice. No differences were found in the growth rates of M. tuberculosis H37Rv, H37Ra and fadD33-complemented H37Ra in the lungs and spleen. In contrast, in the liver, where the attenuated strain H37Ra showed impaired growth compared to the virulent strain H37Rv, complementation of the attenuated strain H37Ra with fadD33 restored bacterial replication. In a further approach, the fadD33 gene of strain H37Rv was disrupted by allelic exchange mutagenesis and the virulence of the mutant strain was tested by mouse infection. It was found that disruption of fadD33 decreased M. tuberculosis H37Rv growth in the liver, but not in the lungs or spleen, and complementation of the fadD33-disrupted mutant with fadD33 restored bacterial replication in the liver, but did not affect replication in the lungs and spleen. These findings suggest that fadD33 plays a role in M. tuberculosis virulence by supporting bacterial growth in the liver.

Animals↗