Exaggerated levels of some specific TLRs, cytokines and chemokines in Japanese encephalitis infected BV2 and neuro 2A cell lines associated with worst outcome.

Japanese encephalitis (JE) disease, a viral brain fever is caused by Japanese encephalitis virus (JEV). Despite the availability of effective vaccines against this deadly infection, JE is the leading cause of epidemic viral encephalitis in children in South-east Asia. There is no treatment available for the JE disease which might be due to incomplete understanding of the pathogenesis of JE virus. The JEV infections lead to permanent neurological deficits even in those who survive from the infection. Activated microglia may play a potentially detrimental role by eliciting the expression of pro-inflammatory cytokines such as interleukin (IL)-1ß, IL-6, and tumor necrosis factor-α (TNF-α) influencing the surrounding brain tissue. Microglial activation, proinflammatory cytokine release and leukocytes trafficking are associated following JEV infection in central nervous system (CNS). How the pattern recognition receptors sense the viral nucleic acid and how the microglial and neuronal cells behaves following JEV infection is still unelucidated. There is scarcity of data on the expression levels of toll like receptors (TLRs), cytokines and chemokines in JEV infection in invitro model. To explore the molecular mechanisms of JEV infection of microglial cells and neuronal cells, we studied the expression profile of TLRs, cytokines and chemokines in JEV infected microglial cell line BV2 and Neuronal cell line Neuro 2A. For the present study, we developed the mouse model of encephalitis by intracerebral (IC) injection of JE virus for virus propagation, disease progression and damage study. Our results demonstrate the exaggerated release of some specific TLRs, cytokines and chemokines in invitro cell culture of microglial and Neuro 2A cell line, which are associated with bad outcome in invivo study.

Identification and characterization of chickpea genotypes for early flowering and higher seed germination through molecular markers.

BACKGROUND: Chickpea is the fourth most important legume crop contributing 15.42% to the total legume production and a rich source of proteins, minerals, and vitamins. Determination of genetic diversity of wild and elite cultivars coupled with early flowering and higher seed germination lines are quintessential for variety improvement. METHODS AND RESULTS: In the present study, we have analyzed the genetic diversity, population structure, cross-species transferability, and allelic richness in 50 chickpea collections using 23 Inter simple sequence repeats (ISSR) markers. The observed parameters such as allele number varied from 3 to 16, range of allele size varied from 150 to 1600 bp and polymorphic information content (PIC) range lies in between 0.15 and 0.49. Dendrogram was constructed with ISSR marker genotypic data and classified 50 chickpea germplasms into groups I and II, where the accession P 74 - 1 is in group I and the rest are in group II. Dendrogram, Principal component analysis (PCA), dissimilarity matrix, and Bayesian model-based genetic clustering of 50 chickpea germplasms revealed that P 74 - 1 and P 1883 are very diverse chickpea accessions. CONCLUSION: Based on genetic diversity analysis, 15 chickpea germplasm having been screened for early flowering and higher seed germination and found that the P 1857-1 and P 3971 have early flowering and higher seed germination percentage in comparison to P 1883 and other germplasm. These agronomic traits are essential for crop improvement and imply the potential of ISSR markers in crop improvement.

Role of P-gp and HDAC2 and their Reciprocal Relationship in Uncontrolled Asthma.

INTRODUCTION: Resistance to corticosteroid is an essential mechanism in uncontrolled asthma as the corticosteroid is the mainstay of therapy. There are recent reports that epigenetic factors play a crucial role in the regulation of steroid action. Overexpression of P glycoprotein (P-gp) and reduced expression of Histone Deacetylase 2 (HDAC2) have been linked to regulating the steroid action in other diseases like Nephrotic Syndrome (NS). However, their role in uncontrolled asthma is still not clear and warrants further investigation. We evaluated the expression and activity of P-gp and HDAC2 in patients with Controlled Asthma (CA) and Uncontrolled Asthma (UA). METHODS: A total of 60 CA (mean age 51.72±17.02 years, male=38), and 38 of UA (mean age=53.55±11.90 years, male=17) were recruited. The level of control was defined according to (Global Initiative for Asthma) GINA 2016 criteria. The mRNA expression of HDAC2 and P-gp was studied by quantitative real-time Polymerase Chain Reaction (PCR), the functional activity of P-gp was evaluated by a commercially available kit via flow cytometry, and HDAC2 enzymatic activity was measured by commercially available kit by Enzyme-Linked Immunosorbent Assay (ELISA). RESULTS: P-gp expression and the functionality were significantly higher in the UA group of patients as compared to the CA group of patients (p<0.005), moreover HDAC2 expression was significantly reduced in UA patients as compared to CA patients, (p<0.005). The enzymatic activity of HDAC2 was also significantly reduced in UA patients as compared to CA patients (p<0.005). CONCLUSION: P-gp overexpression and HDAC2 under expression play an essential role in uncontrolled asthma by impairing the response to corticosteroid.