In-vitro evidence indicating that IL-10 causes aging-related hypoalbuminemia via JAK1/STAT3 and CEBP-β.

Albumin (ALB) has numerous vital physiological outcomes for healthy aging. A decrease in serum albumin, i.e.

Benzo[a]pyrene exposure causes exonal switch resulting in reduced surface CD5 expression in an AHR-dependent manner.

The function of CD5 protein in T cells is well documented, but regulation of its surface-level expression has yet to be fully understood. However, variation in its surface expression is associated with various immunopathological conditions and haematological malignancies. Briefly, expression of an alternate exon E1B of a human endogenous retroviruses (HERV) origin directly downregulates the conventional transcript variant (E1A), as its expression leads to the retention of the resultant protein at the intracellular level (cCD5).

HIF-1α regulates the expression of the non-conventional isoform of the cd5 gene in T cells under the hypoxic condition: A potential mechanism for CD5 phenotype of infiltrating cells in solid tumors.

CD5, a T-cell receptor (TCR) negative regulator, is reduced on the surface of CD8+ lymphocytes in the tumor microenvironment (TME). Reduced surface CD5 expression (sCD5) occurs due to the preferential transcription of HERV-E derived exon E1B, i.e.

Retinoic acid shows direct parasiticidal activity by targeting ergosterol pathway in a potential therapeutic advancement.

Visceral leishmaniasis (VL) is an infectious disease caused by parasite in Indian subcontinent and is life-threatening. It primarily inflicts the malnourished population. There is little therapeutic advancement in the last one decade or more, as the available drugs show adverse effects, complex long treatment, high cost and drug resistance.

Organ-specific immune profiling of Leishmania donovani-infected hamsters.

Visceral leishmaniasis (VL) is a neglected disease with a broad spectrum of clinical manifestations and involvement of visceral organs. Organ-specific immune response against the Leishmania donovani (Ld) complex is not yet understood due to the unavailability of an appropriate experimental model. In reference to our recent work on comparing the hamster model with VL patients, it is now possible to understand immune profiling in different visceral organs.

Retinoic Acid Increases Cellular Cholesterol in Leishmania donovani-Infected Macrophages in an mTOR-Independent Manner.

Infection with Leishmania donovani reduces cellular cholesterol and thus deprives the host cells by inhibiting its synthesis and uptake. Changes in cholesterol levels increase the chance of attachment and internalization of L. donovani in macrophages (Mϕ).

Jurkat T Cells are Immunophenotypically Distinct from T-Cell Acute Lymphoblastic Leukemia Cells Due to High-Level Surface Expression of CD5.

Human leukemic T cells show decreased surface CD5 (sCD5) and increased cytoplasmic CD5 (cCD5). When we examined their expressions in the Jurkat T cells, it showed increased sCD5 and decreased cCD5, which is in sharp contrast with the pattern of CD5 expression observed for human leukemic T cells. Furthermore, this opposite pattern was due to the absence of an exonal switch between E1A and E1B.

Retinoic acid restores the levels of cellular cholesterol in Leishmania donovani infected macrophages by increasing npc1 and npc2 expressions.

Visceral leishmaniasis (VL) is a fatal form among all forms of leishmaniasis and is caused by visceralization of the Leishmania donovani (Ld) parasite to the critical organs. Mild to severe malnutrition is common in VL patients and the deficiency of retinoic acid (RA), an important micronutrient, results in a compromised state of immune response in macrophages (mφ) leading to the increased parasite load. In the continuation of our earlier work, we observed loss of cellular cholesterol in infected mφ in the absence of RA i.

Linoleic Acid Inhibits the Release of Derived Microvesicles and Decreases Its Survival in Macrophages.

Visceral leishmaniasis is a neglected tropical disease caused by parasite in the Indian subcontinent. Macrophages (mϕ) are the harboring cells for parasite and their interactions dictate the pathogenesis of this disease. Polyunsaturated fatty acids are an integral part of the mϕ cell membrane and are derived from linoleic acid (LA), which is a principal essential fatty acid.

Hamster, a close model for visceral leishmaniasis: Opportunities and challenges.

Aim: Visceral leishmaniasis (VL) caused by parasites belonging to genus Leishmania (L.) is classified as a category I disease by the TDR/WHO. The understanding of the pathogenesis of this disease was built from the findings of available experimental models.

Preventive as well as therapeutic significances of linoleic acid in the containment of Leishmania donovani infection.

People suffering from malnutrition show compromised levels of ω-6 fatty acid and malnutrition is frequently observed among visceral leishmaniasis (VL) patients as disease inflicts primarily the socioeconomic destitute communities. Dietary linoleic acid (LA, 18:2; ω-6 fatty acid) is the principal source of essential fatty acid and its derivatives i.e.

Parasitic load determination by differential expressions of 5-lipoxygenase and PGE2 synthases in visceral leishmaniasis.

Infection with L. donovani affects mainly visceral organs. Importantly, the parasitic load differs in different visceral organs; therefore there is a need to understand the organ specific immune regulation, particularly in the spleen and liver.

Comparison Between Immuno-Clinicopathological Features of Experimental and Human Visceral Leishmaniasis by Leishmania donovani.

Background: Current understanding of visceral leishmaniasis (VL) depends upon the experimental model. Different species of mouse and hamster have been used as model for VL. It is already evident that the mouse model of VL is not a true reflection of the pathology of human visceral leishmaniasis (HuVL).

Identification of a novel transcript variant of the human CD6 gene that lacks exon 9.

CD6 is a transmembrane glycoprotein, mainly expressed by all T cells and a subset of B cells. It has been shown that the human CD6 gene has six reported transcript isoforms, including full length and Δ3 isoforms. These are CD6a, CD6b, CD6c, CD6d, CD6e and CD6Δ3.

Dependence of parasite on host derived ATP: an overview of extracellular nucleotide metabolism in parasite.

[Image: see text]

Leishmania donovani reduces the levels of retinoic acid-synthesizing enzymes in infected macrophages and favoring its own survival.

People suffering from malnutrition become susceptible to the infection like Leishmania sp., as it results in a compromised immune response. Retinoic acid (RA), an important constituent of nutrition, shows an immune-modulatory activity.

Synthesis of chitin-glucan-aldehyde-quercetin conjugate and evaluation of anticancer and antioxidant activities.

In the present study, we have synthesized chitin-glucan-aldehyde-quercetin (chi-glu-ald-que) conjugate via condensation reaction. Synthesis of chitin-glucan-aldehyde (chi-glu-ald) complex was facilitated by the oxidation of chitin-glucan (chi-glu) complex. Formation of conjugate was confirmed by Proton nuclear magnetic resonance spectroscopy (H NMR) and Fourier-transform infrared spectroscopy (FT-IR).

Characterization of phosphate transporter(s) and understanding their role in Leishmania donovani parasite.

Inorganic phosphate (Pi) is shown to be involved in excretion of methylglyoxal (MG) in the promastigote form of Leishmania donovani parasite. Absence of Pi leads to its accumulation inside the parasite. Accumulation of MG is toxic to the parasite and utilizes glyoxylase as well as excretory pathways for its detoxification.

Decrease in the Frequency of Circulating CD56CD161 NK Cells in Human Visceral Leishmaniasis.

Background: Natural Killer (NK) cell plays an important role in the innate immune system and is known to produce IFN-γ at an early stage of infection that is essential to eliminate intracellular infection like Leishmania spp. It is already established that Leishmania parasite inhibits the activity of NK cells, avoiding the encounter with the early innate immune response. This, in turn, favors establishment and further dissemination of the infection.

Curcumin loaded chitin-glucan quercetin conjugate: Synthesis, characterization, antioxidant, in vitro release study, and anticancer activity.

In this study, we have synthesized chitin-glucan quercetin conjugate (ChGCQ) by an easy and facile free radical grafting reaction. The structure of ChGCQ was confirmed by proton nuclear magnetic resonance (H NMR) and Fourier transforms infrared spectroscopy (FT-IR). Curcumin was loaded into ChGCQ to study its anti-cancer efficiency.

Development of Leishmania donovani stably expressing DsRed for flow cytometry-based drug screening using chalcone thiazolyl-hydrazone as a new antileishmanial target.

Green fluorescent protein produces significant fluorescence and is extremely stable, however its excitation maximum is close to the ultraviolet range and thus can damage living cells. Hence, Leishmania donovani stably expressing DsRed were developed and their suitability for flow cytometry-based antileishmanial screening was assessed by evaluating the efficacies of standard drugs as well as newly synthesised chalcone thiazolyl-hydrazone compounds. The DsRed gene was successfully integrated at the 18S rRNA locus of L.

Increased level of soluble adenosine deaminase in bone marrow of visceral leishmaniasis patients: an inverse relation with parasite load.

Adenosine deaminase (ADA) which degrades adenosine to inosine, is known to be pro-inflammatory molecule in many diseases. Adenosine suppresses the functioning of the immune system and thus promotes dissemination of the parasite. In our previous finding, the level of soluble ADA in serum of visceral leishmaniasis (VL) was found to be increased as compared to healthy controls.

Pi inhibits intracellular accumulation of methylglyoxal in promastigote form of L. donovani.

Similar to their mammalian counterpart, protozoan parasites including Leishmania donovani detoxify methylglyoxal (MG),(1) a toxic ubiquitous product generated in glycolysis pathway. However, it differs in one or more way(s) from the humans. It is known that MG is eliminated either through glyoxalase (GLO)(2) pathway and/or excreted across the cell membrane.