Arabinosylated lipoarabinomannan modulates the impaired cell mediated immune response in Mycobacterium tuberculosis H37Rv infected C57BL/6 mice.

Mycobacterium tuberculosis is a facultative intracellular pathogen that flourishes inside the host macrophages. This organism has the ability to deactivate the cell-mediated immune responses involving the down-regulation of pro-inflammatory cytokines, T cell proliferation, apoptosis of CD4+T cells and impairment of the expression of MHC Class II molecules. We observed that Arabinosylated Lipoarabinomannan (Ara-LAM), a glycolipid present in the cell wall of the avirulent Mycobacterium smegmatis, could effectively restrict the growth of tubercle bacilli, induced the transcription of Th1 cytokines in alveolar macrophages (AMs) and splenocytes, enhanced the frequency of CD4+T cells secreting IFN-gamma and induced the expression of MHC Class II molecules on the splenocyte membrane, compared to that of Mycobacterium tuberculosis H37Rv infected C57BL/6 mice.

Leishmania donovani-induced ceramide as the key mediator of Akt dephosphorylation in murine macrophages: role of protein kinase Czeta and phosphatase.

Leishmania donovani is an intracellular protozoan parasite that impairs the host macrophage immune response to render it suitable for its survival and establishment. L. donovani-induced immunosuppression and alteration of host cell signaling is mediated by ceramide, a pleiotropic second messenger playing an important role in regulation of several kinases, including mitogen-activated protein kinase and phosphatases.

An unusual pro-inflammatory role of interleukin-10 induced by arabinosylated lipoarabinomannan in murine peritoneal macrophages.

Various species of Mycobacteria produce a major cell wall-associated lipoglycan, called Lipoarabinomannan (LAM), which is involved in the virulence of Mycobacterial species. In this study, we tried to establish the role of the increased IL-10 secretion under Arabinosylated-LAM (Ara-LAM) treatment, the LAM that induces apoptosis in host macrophages or PBMC. We have studied the survival and apoptotic factors by western blotting, and estimated nitrite generation by Griess reaction, quantified iNOS mRNA by semi-quantitative RT-PCR, and ultimately the fate of the cells were studied by Flow Cytometric Analysis of AnnexinV-FITC binding.

Regulation of impaired protein kinase C signaling by chemokines in murine macrophages during visceral leishmaniasis.

The protein kinase C (PKC) family regulates macrophage function involved in host defense against infection. In the case of Leishmania donovani infection, the impairment of PKC-mediated signaling is one of the crucial events for the establishment of parasite into the macrophages. Earlier reports established that C-C chemokines mediated protection against leishmaniasis via the generation of nitric oxide after 48 h.