NISCAIR Online Periodicals Repository Collection: IJEB Vol.47(06) [June 2009]

Cross-resistance of Mycobacterium tuberculosis isolates among streptomycin, kanamycin and amikacin

Fri, 29 May 2009 22:58:59 GMT

Title: Cross-resistance of Mycobacterium tuberculosis isolates among streptomycin, kanamycin and amikacin

Authors: Sugawara, I; Zhang, J; Li, C

Abstract: Seventy-four streptomycin (SM)-resistant M. tuberculosis clinical isolates were subjected to cross-resistance drug testing against two major aminoglycosides, kanamycin (KM) and amikacin (AMK). Among them, 15 clinical isolates (20.3%) were resistant to both KM and AMK. Fifteen (80%) of 19 KM-resistant isolates were AMK-resistant. Fifteen SM, KM, and AMK resistant isolates harbored rrs mutation, but only two had rrs and rpsL double mutations. Low-level SM resistance was associated with rpsL mutation, whereas high-level SM resistance was linked to rrs mutation.

Page(s): 520-522

Mycobacterium tuberculosis secreted antigen (MTSA-10) inhibits macrophage response to lipopolysaccharide by redox regulation of phosphatases

Fri, 29 May 2009 22:58:59 GMT

Title: Mycobacterium tuberculosis secreted antigen (MTSA-10) inhibits macrophage response to lipopolysaccharide by redox regulation of phosphatases

Authors: Basu, Sandip Kumar; Kumar, Dhiraj; Ganguly, Niladri; Rao, Kanury Venkata Subba; Sharma, Pawan

Abstract: The present study was undertaken to investigate the possible role of a 10-kDa, secretory antigenic protein of Mtb (MTSA-10) in regulating macrophase response to lipopolysacchride (LPS). MTSA-10 inhibited the lipopolysaccharide (LPS)-induced oxidant species generation in the macrophage. Treatment of macrophages with MTSA-10 activated their protein tyrosine phosphatases (PTPs) in a redox-regulated fashion. These activated phosphatases then interfered with the early events of LPS signaling and lower the strength and magnitude of the signal generated, thereby preventing macrophages from making an effective immune response. Mycobacterium tuberculosis Region of Deletion-1 (RD-1)-specific secretory antigen MTSA-10 (encoded by ORF Rv3874 of Mtb genome) modulated the macrophage signaling machinery and prevented it from responding to further activation by LPS.

Page(s): 505-519

Identification of Mycobacterium tuberculosis-specific genomic regions encoding antigens inducing protective cellular immune responses

Fri, 29 May 2009 22:58:59 GMT

Title: Identification of Mycobacterium tuberculosis-specific genomic regions encoding antigens inducing protective cellular immune responses

Authors: Mustafa, Abu Salim; Al-Attiyah, Rajaa

Abstract: Comparative genomic studies have identified 11 regions of difference (RD1, RD4, RD5, RD6, RD7, RD9, RD10, RD11, RD12, RD13 and RD15) in Mycobacterium tuberculosis genome which are absent in all vaccine strains of M. bovis BCG. The proteins encoded by genes predicted in these RDs could be useful as protective vaccines and/or exacerbate the disease process by inducing cellular immune responses involved in protection and pathogenesis of tuberculosis. In our studies, by using pools of overlapping synthetic peptides covering the sequence of putative proteins encoded by genes predicted in each RD, we have determined the cellular immune responses in relation to antigen-induced proliferation and secretion of the protective Th1 cytokine IFN-g and the pathologic Th2 cytokine IL-10 by peripheral blood mononuclear cells of tuberculosis patients and healthy humans. It has been observed that peptides of RD1_pool induced the highest antigen-induced proliferation and IFN-g responses, whereas the peptides of RD12_pool and RD13_pool induced the highest IL-10 responses. Furthermore, addition of RD12_pool and RD13_pool to peripheral blood mononuclear cells (PBMCs) cultures inhibited the RD1_pool-induced secretion of IFN-g by PBMCs of healthy humans. These results suggest the relevance of RD1-encoded proteins in protection and RD12- and RD13-encoded proteins in pathogenesis of tuberculosis.

Page(s): 498-504

Anti-IL-10 mAb protection against experimental visceral leishmaniasis via induction of Th1 cytokines and nitric oxide

Fri, 29 May 2009 22:58:59 GMT

Title: Anti-IL-10 mAb protection against experimental visceral leishmaniasis via induction of Th1 cytokines and nitric oxide

Authors: Bhattacharjee, Surajit; Gupta, Gaurav; Bhattacharya, Parna; Adhikari, Anupam; Majumdar, Suchandra Bhattacharya; Majumdar, Subrata

Abstract: Visceral leishmaniasis is characterized by severe immune suppression of the host. This suppression of the host immune system is primarily mediated by the immunosuppressive cytokine Interleukin-10 (IL-10), whose levels are significantly up-regulated during leishmaniasis. This immune suppression is reflected at the level of T-cell dysfunction and abrogation of leishmaniacidal molecules along with a dampened Th1 cytokine response. In the present study, we showed in vivo neutralization of IL-10 by administration of anti IL-10 monoclonal antibodies (mAb) could confer protection against leishmanial pathogenesis. This protective response was primarily mediated by a strong induction of T cell proliferation along with a Th1 biased cytokine response which was further aided by the generation of, leishmanicidal molecules, nitric oxide.

Page(s): 489-497