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449 results on '"Jha, Hem Chandra"'

104. Higher expression of ferritin protects Chlamydia trachomatis infected HeLa 229 cells from reactive oxygen species mediated cell death

Author

Vardhan, Harsh, Bhengraj, Apurb Rashmi, Jha, Rajneesh, Srivastava, Pragya, Jha, Hem Chandra, and Mittal, Aruna

Subjects
Biochemistry -- Physiological aspects -- Research, Cell death -- Research -- Prevention -- Physiological aspects, Chlamydia -- Physiological aspects -- Research, Chlamydia infections -- Research -- Physiological aspects -- Prevention, Apoptosis -- Research -- Physiological aspects, Reactive oxygen species -- Research -- Properties -- Physiological aspects, Ferritin -- Research -- Properties -- Physiological aspects, Chlamydia trachomatis -- Research -- Physiological aspects, Biological sciences
Abstract

Apoptosis plays an important role in modulating the pathogenesis of a variety of infectious diseases. Chlamydial infection protects cells against different forms of apoptosis: extrinsic, intrinsic, and granzyme B mediated. Redox reactions are central to the life and death decision of cells and pathogens and an intimate relationship exists between oxidative stress and iron metabolism. The link between redox status and ferritin was largely unexplored in chlamydia-infected cells. In the present study, we showed that Chlamydia trachomatis (CT) infection induced FHC protein in HeLa cells. FHC induction by CT-infected cells stably expressing FHC blunted ROS production compared with mock infected cells, and the infected cells were relatively resistant to apoptosis induced by [H.sub.2][O.sub.2]. We also demonstrated that endogenous FHC overexpression correlates well with the stabilization of the mitochondrial membrane potential in CT-infected cells. Increased expression of FHC is independent of iron supplementation (FAC) and depletion (DFO) in CT-infected cells. These data suggest that FHC up-regulation is an acute response of HeLa cells against CT infection and that FHC exerts anti-apoptotic activity against oxidative stress. Key words: Chlamydia trachomatis, ferritin, reactive oxygen species, apoptosis, mitochondrial membrane potential. L'apoptose joue un role important dans la modulation de la pathogenese d'une variete de maladies infectieuses. L'infection par la chlamydia protege les cellules contre differentes formes d'apoptose : extrinseque, intrinseque et dependante de la granzyme B. Les reactions d'oxydoreduction sont centrales au cheminement vers la survie ou la mort des cellules et des pathogenes, et il existe un lien etroit entre le stress et le metabolisme du fer. Le lien entre le statut d'oxydoreduction et la ferritine a ete largement negligee chez les cellules infectees par la chlamydia. Dans cette etude, nous avons montre; qu'une infection par Chlamydia trachomatis (CT) induisait la proteine FHC chez les cellules HeLa. L'induction de FHC chez les cellules infectees par CT et exprimant la FHC de facjon stable interrompait la production d'ERO comparativement aux cellules infectees a blanc, et ces cellules eetaient relativement resistantes a l'apoptose induite par le [H.sub.2][O.sub.2]. Nous avons aussi demontree que la surexpression de FHC endogene etait bien relieeea la stabilisation du potentiel membranaire mitochondrial chez les cellules infectees par CT. L'augmentation de l'expression de FHC est independante de la supplementation ou de la depletion en fer chez les cellules infectees par CT. Ces resultats suggerent que la stimulation de l'expression de FHC constitue une reponse aigue des cellules HeLa contre l'infection par CT, et que la FHC exerce une activite anti-apoptotique lors d'un stress oxydant. Mots-cles : Chlamydia trachomatis, ferritine, espeeces reactives d'oxygene, apoptose, potentiel membranaire mitochondrial. [Traduit par la Redaction], Introduction Apoptosis, or programmed cell death, is an evolutionary conserved, strictly regulated, genetic and biochemical program that plays critical roles during development and tissue homeostasis in multicellular organisms (Zakeri and [...]

Published
2010
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119. In silicoanalysis of antiviral phytochemicals efficacy against Epstein–Barr virus glycoprotein H

Author

Jakhmola, Shweta, Hazarika, Zaved, Jha, Anupam Nath, and Jha, Hem Chandra

Abstract

AbstractEpstein–Barr virus is a tumor-associated, enveloped virus with glycoprotein receptor gHgL on its surface. gH attaches to epithelial or B cells and mediates internalization. Till date, no specific anti-EBV FDA approved drug is available. Targeting gH may aid in designing virus-specific therapeutics and reducing the drug induced complications in host. We investigated the influence of antiviral phytochemicals on gH using computational approaches. Through molecular docking, we performed binding energy analysis of cellocidin, bruceantin, EGCG, formononetin and sesquiterpene lactones with gH DII/DIII interface, crucial for gH functions. Further, to cause any perturbations in the protein function, the molecules must bind stably to gH. Bruceantin and EGCG interacted with high affinities to gH. Simulation of these two molecules revealed stable binding with gH throughout 100 ns moreover, van der Waal interactions stabilized overall binding. Mutation of amino acids like V265, L269, L315, I423, I459, L474 and F475 involved in stable binding to gH was predicted deleterious to protein function. We obtained no difference in RMSD between these two ligands and minor deviations in the RMSF were noticed compared to gH. Conclusively, our study provided insights into the potential of bruceantin and EGCG to target gH. Different amino acids are involved in binding of each ligand to gH, engagement of certain amino acids may affect the virus binding with epithelial or B cells. The interaction of the ligand with gH may trap it in its native conformation or induce structural flexibility thereby inhibiting the interaction with host receptors or other glycoproteins.Communicated by Ramaswamy H. Sarma

Published
2022
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129. Epstein–Barr virus infection modulates blood–brain barrier cells and its co-infection with Plasmodium falciparum induces RBC adhesion.

Author

Indari, Omkar, Chandramohanadas, Rajesh, and Jha, Hem Chandra

Subjects
EPSTEIN-Barr virus diseases, BLOOD-brain barrier, MIXED infections, CEREBRAL malaria, PLASMODIUM falciparum, MALARIA
Abstract

Plasmodium falciparum infection-mediated Epstein–Barr virus (EBV) reactivation is well established in malaria-endemic countries. We hypothesize that, during malaria onset, the reactivated EBV can infect human brain microvascular endothelial cells (HBECs). This may cause severe cerebral manifestations. We infected HBECs with EBV in vitro. The subsequent gene expression pattern of EBV, inflammatory and endothelial markers was analysed using qRT-PCR. Further, a wound-healing assay for cells maintaining blood–brain barrier (BBB) integrity was performed to investigate the effect of EBV-infected HBECs secretions. The RBC adhesion assay was conducted to assess RBC attachment onto HBECs during EBV and P. falciparum mono- and co-infection. Our experiments revealed that EBV infection of HBECs significantly elevated several inflammatory (TNFα, CCL2) and endothelial (integrin β3, PECAM, VEGFA, VWF, claudin-5, cx37) markers. The EBV-infected HBECs secretion significantly reduced migration of HBECs, glial and neuronal cells. Additionally, EBV– P. falciparum co-infection significantly (P  < 0.05) enhanced RBC adhesion to HBECs compared to mono-infection scenarios. Conclusively, the EBV infection of HBECs led to endothelial activation and modulated the BBB microenvironment. The EBV- P. falciparum co-infection scenario increased RBC adhesion on ECs which is a hallmark of cerebral malaria. Together with malaria, EBV infection can aid in exacerbation of cerebral malaria pathology. [ABSTRACT FROM AUTHOR]

Published
2021
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130. Status of Epstein-Barr Virus Coinfection with Helicobacter pylori in Gastric Cancer

Author

Singh, Shyam and Jha, Hem Chandra

Subjects
Article Subject
Abstract

Epstein-Barr virus is a ubiquitous human herpesvirus whose primary infection causes mononucleosis, Burkett’s lymphoma, nasopharyngeal carcinoma, autoimmune diseases, and gastric cancer (GC). The persistent infection causes malignancies in lymph and epithelial cells. Helicobacter pylori causes gastritis in human with chronic inflammation. This chronic inflammation is thought to be the cause of genomic instability. About 45%-word population have a probability of having both pathogens, namely, H. pylori and EBV. Approximately 180 per hundred thousand population is developing GC along with many gastric abnormalities. This makes GC the third leading cause of cancer-related death worldwide. Although lots of research are carried out individually for EBV and H. pylori, still there are very few reports available on coinfection of both pathogens. Recent studies suggested that EBV and H. pylori coinfection increases the occurrence of GC as well as the early age of GC detection comparing to individual infection. The aim of this review is to present status on coinfection of both pathogens and their association with GC.

Published
2017
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136. Prediction of three-dimensional structure of Chlamydia trachomatis heat shock protein 60: an immunodominant antigen

Author

Jha, Rajneesh, Jha, Hem Chandra, Biswas, Sumit, and Mittal, Aruna

Subjects
Chlamydia infections -- Risk factors, Chlamydia infections -- Genetic aspects, Chlamydia infections -- Research, Chlamydia trachomatis -- Health aspects, Chlamydia trachomatis -- Genetic aspects, Chlamydia trachomatis -- Research, Heat shock proteins -- Structure, Heat shock proteins -- Genetic aspects, Heat shock proteins -- Research, Health
Abstract

Chlamydia trachomatis infections are the most prevalent sexually transmitted infection in the world and are often associated with various fertility disorders. C. trachomatis heat shock protein 60 (cHSP60) or GroEL has been identified as an immunodominant antigen, being strong target of both humoral and cell mediated immune responses. A homology modeling was used for the prediction of three-dimensional (3-D) structure of cHSP60 by using the comparative modeling module of MODELLER. Since the MODELLER-aligned alignments led to asymmetric matching, the necessary sequence alignments were done using ClustalW and mGenTHREADER. The template used was the file with code 1kp8 from the Protein Data Bank (PDB), which gives the crystal structure of GroEL of Escherichia coli. The structure was energy minimized by MODELLER's inherent minimization module. From the Ramachandran plot analysis, it was found that 91.8% of residues falls in the most favoured region. Further, this study could shed light on characterizing cHSP60 in wet laboratory. Keywords: Heat shock protein 60 | homology modeling | 3-D model | mGenTHREADER | Ramachandran plot, Introduction Chlamydia trachomatis infections are the most prevalent sexually transmitted disease recognized throughout the world. According to World Health Organization (WHO), annually 92 million C. trachomatis infections are detected worldwide, [...]

Published
2009

140. Gammaherpesvirus Infection of Human Neuronal Cells

Author

Jha, Hem Chandra, primary, Mehta, Devan, additional, Lu, Jie, additional, El-Naccache, Darine, additional, Shukla, Sanket K., additional, Kovacsics, Colleen, additional, Kolson, Dennis, additional, and Robertson, Erle S., additional

Published
2015
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