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Article ; Online: Immune Responses to Defined Plasmodium falciparum Antigens and Disease Susceptibility in Two Subpopulations of Northern India

Sukla Biswas / Mritunjay Saxena / Ratanesh K. Seth / Krishnan Hajela

Journal of Advanced Laboratory Research in Biology, Vol 4, Iss

2013 Volume 2

Abstract: The aim of this study was to investigate the prevalence of naturally acquired immune response to malaria in individuals of different age groups belonging to areas of northern India, Loni PHC (LN) and Dhaulana PHC (SD) of district Ghaziabad. Plasmodium ... ...

Abstract	The aim of this study was to investigate the prevalence of naturally acquired immune response to malaria in individuals of different age groups belonging to areas of northern India, Loni PHC (LN) and Dhaulana PHC (SD) of district Ghaziabad. Plasmodium falciparum-infected erythrocyte lysate and six synthetic peptides from different stages of P. falciparum (CSP, MSP1, AMA1, RAP1, EBA175 and PfG27) were used to determine both humoral and cellular immune responses. Plasma of individual subject was also analyzed for IL-4, IL-10, IFN-γ and TNF-α level. We observed an age-wise increasing trend of immunity in these two populations. There was a significant association between the number of antibody responders and recognition of stage-specific epitopes by antibodies. Peripheral blood mononuclear cells of more than 75% of individuals proliferated in response to stimulation by all the antigens in LN area. IL-4 and IL-10 responses were significantly higher in individuals of LN Area; whereas IFN-g and TNF-a responses were higher in individuals of SD Area. It was also noticed that the frequency of responders to stage-specific antigens was higher in individuals from the LN area where the frequency of malaria was lower. The naturally acquired immune responses to P. falciparum antigens reflected the reduced risk of malaria in the study groups. The results demonstrated immunogenicity of the epitopes to P. falciparum in population of this endemic zone.
Keywords	Malaria ; P. falciparum ; antigen ; peptide ; ELISA ; Immune response ; Biology (General) ; QH301-705.5 ; Microbiology ; QR1-502
Subject code	616
Language	English
Publishing date	2013-04-01T00:00:00Z
Publisher	Society of Open Science
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Trihalomethane exposure and biomonitoring for the liver injury indicator, alanine aminotransferase, in the United States population (NHANES 1999â2006)

Burch, James B / Todd M. Everson / Ratanesh K. Seth / Michael D. Wirth / Saurabh Chatterjee

Science of the total environment. 2015 July 15, v. 521-522

2015

Abstract: Exposure to trihalomethanes (or THMs: chloroform, bromoform, bromodichloromethane, and dibromochloromethane [DBCM]) formed via drinking water disinfection has been associated with adverse reproductive outcomes and cancers of the digestive or ... ...

Abstract	Exposure to trihalomethanes (or THMs: chloroform, bromoform, bromodichloromethane, and dibromochloromethane [DBCM]) formed via drinking water disinfection has been associated with adverse reproductive outcomes and cancers of the digestive or genitourinary organs. However, few studies have examined potential associations between THMs and liver injury in humans, even though experimental studies suggest that these agents exert hepatotoxic effects, particularly among obese individuals. This study examined participants in the National Health and Nutrition Examination Survey (1999â2006, N=2781) to test the hypothesis that THMs are associated with liver injury as assessed by alanine aminotransferase (ALT) activity in circulation. Effect modification by body mass index (BMI) or alcohol consumption also was examined. Associations between blood THM concentrations and ALT activity were assessed using unconditional multiple logistic regression to calculate prevalence odds ratios (ORs) with 95% confidence intervals (CIs) for exposure among cases with elevated ALT activity (men: >40IU/L, women: >30IU/L) relative to those with normal ALT, after adjustment for variables that may confound the relationship between ALT and THMs. Compared to controls, cases were 1.35 times more likely (95% CI: 1.02, 1.79) to have circulating DBCM concentrations exceeding median values in the study population. There was little evidence for effect modification by BMI, although the association varied by alcohol consumption. Among non-drinkers, cases were more likely than controls to be exposed to DBCM (OR: 3.30, 95% CI: 1.37, 7.90), bromoform (OR: 2.88, 95% CI: 1.21, 6.81), or brominated THMs (OR: 4.00, 95% CI: 1.31, 12.1), but no association was observed among participants with low, or moderate to heavy alcohol consumption. Total THM levels exceeding benchmark exposure limits continue to be reported both in the United States and globally. Results from this study suggest a need for further characterization of ALT activity and possibly other hepatic or metabolic diseases in populations with elevated drinking water THM concentrations.
Keywords	National Health and Nutrition Examination Survey ; alanine transaminase ; alcohol drinking ; blood ; body mass index ; chloroform ; confidence interval ; disinfection ; drinking water ; hepatotoxicity ; humans ; liver ; men ; metabolic diseases ; neoplasms ; odds ratio ; regression analysis ; women ; United States
Language	English
Dates of publication	2015-0715
Size	p. 226-234.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	121506-1
ISSN	1879-1026 ; 0048-9697
ISSN (online)	1879-1026
ISSN	0048-9697
DOI	10.1016/j.scitotenv.2015.03.050
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Environmental microcystin targets the microbiome and increases the risk of intestinal inflammatory pathology via NOX2 in underlying murine model of Nonalcoholic Fatty Liver Disease

Sutapa Sarkar / Diana Kimono / Muayad Albadrani / Ratanesh K. Seth / Philip Busbee / Hasan Alghetaa / Dwayne E. Porter / Geoff I. Scott / Bryan Brooks / Mitzi Nagarkatti / Prakash Nagarkatti / Saurabh Chatterjee

Scientific Reports, Vol 9, Iss 1, Pp 1-

2019 Volume 22

Abstract: Abstract With increased climate change pressures likely to influence harmful algal blooms, exposure to microcystin, a known hepatotoxin and a byproduct of cyanobacterial blooms can be a risk factor for NAFLD associated comorbidities. Using both in vivo ... ...

Abstract	Abstract With increased climate change pressures likely to influence harmful algal blooms, exposure to microcystin, a known hepatotoxin and a byproduct of cyanobacterial blooms can be a risk factor for NAFLD associated comorbidities. Using both in vivo and in vitro experiments we show that microcystin exposure in NAFLD mice cause rapid alteration of gut microbiome, rise in bacterial genus known for mediating gut inflammation and lactate production. Changes in the microbiome were strongly associated with inflammatory pathology in the intestine, gut leaching, tight junction protein alterations and increased oxidative tyrosyl radicals. Increased lactate producing bacteria from the altered microbiome was associated with increased NOX-2, an NADPH oxidase isoform. Activationof NOX2 caused inflammasome activation as shown by NLRP3/ASCII and NLRP3/Casp-1 colocalizations in these cells while use of mice lacking a crucial NOX2 component attenuated inflammatory pathology and redox changes. Mechanistically, NOX2 mediated peroxynitrite species were primary to inflammasome activation and release of inflammatory mediators. Thus, in conclusion, microcystin exposure in NAFLD could significantly alter intestinal pathology especially by the effects on microbiome and resultant redox status thus advancing our understanding of the co-existence of NAFLD-linked inflammatory bowel disease phenotypes in the clinic.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2019-06-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The Gut-Microbiome in Gulf War Veterans

Patricia A. Janulewicz / Ratanesh K. Seth / Jeffrey M. Carlson / Joy Ajama / Emily Quinn / Timothy Heeren / Nancy Klimas / Steven M. Lasley / Ronnie D. Horner / Kimberly Sullivan / Saurabh Chatterjee

International Journal of Environmental Research and Public Health, Vol 16, Iss 19, p

A Preliminary Report

2019 Volume 3751

Abstract: Gulf War Illness (GWI) is a chronic multi-symptom disorder affecting the central nervous system (CNS), immune and gastrointestinal (GI) systems of Gulf War veterans (GWV). We assessed the relationships between GWI, GI symptoms, gut microbiome and ... ...

Abstract	Gulf War Illness (GWI) is a chronic multi-symptom disorder affecting the central nervous system (CNS), immune and gastrointestinal (GI) systems of Gulf War veterans (GWV). We assessed the relationships between GWI, GI symptoms, gut microbiome and inflammatory markers in GWV from the Boston Gulf War Illness Consortium (GWIC). Three groups of GWIC veterans were recruited in this pilot study; GWV without GWI and no gastrointestinal symptoms (controls), GWV with GWI and no gastrointestinal symptoms (GWI-GI), GWV with GWI who reported gastrointestinal symptoms (GW+GI). Here we report on a subset of the first thirteen stool samples analyzed. Results showed significantly different gut microbiome patterns among the three groups and within the GWI +/−GI groups. Specifically, GW controls had a greater abundance of firmicutes and the GWI+GI group had a greater abundance of the phyla bacteroidetes, actinobacteria, euryarchaeota, and proteobacteria as well as higher abundances of the families Bacteroidaceae, Erysipelotrichaceae, and Bifidobacteriaceae. The GWI+GI group also showed greater plasma levels of the inflammatory cytokine TNF-RI and they endorsed significantly more chemical weapons exposure during the war and reported significantly greater chronic pain, fatigue and sleep difficulties than the other groups. Studies with larger samples sizes are needed to confirm these initial findings.
Keywords	gulf war illness ; microbiome ; gulf war ; veterans ; inflammation ; cytokines ; exposure ; Medicine ; R
Subject code	150
Language	English
Publishing date	2019-10-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Isolation and Purification of C-phycocyanin from Nostoc muscorum (Cyanophyceae and Cyanobacteria) Exhibits Antimalarial Activity In vitro

Sukla Biswas / Pranay P. Pankaj / Ratanesh K. Seth / Nirupama Mallick

Journal of Advanced Laboratory Research in Biology, Vol 1, Iss

2010 Volume 2

Abstract: The phycobilin pigments are intensively fluorescent and water soluble. They are categorized into three types, such as pigments containing high, intermediate and low energies are phycoerythrins (phycoerythrocyanins), phycocyanins and allophycocyanins, ... ...

Abstract	The phycobilin pigments are intensively fluorescent and water soluble. They are categorized into three types, such as pigments containing high, intermediate and low energies are phycoerythrins (phycoerythrocyanins), phycocyanins and allophycocyanins, respectively. Besides light harvesting, the phycobiliproteins have shown industrial and biomedical importance. Among them, C-phycocyanin (C-PC) has been considered to be the most preferred one. The present study was undertaken to evaluate the antimalarial activity of C-PC isolated from a nitrogen-fixing cyanobacterium and Nostoc muscorum. C-PC was extracted and purified by acetone extraction and ammonium sulfate precipitation and dialysis followed by amicon filtration. It was isolated as a~124 kDa water soluble protein molecule. It showed antimalarial activity in vitro against chloroquine sensitive and resistant Plasmodium falciparum strains. Inhibitory concentrations at 50%, 90% and 95% were determined as 10.27±2.79, 53.53±6.26 and 73.78±6.92 µg/ml against the chloroquine-sensitive strains; 10.37±1.43, 56.99±11.07 and 72.79±8.59 µg/ml against chloroquine resistant of Plasmodium falciparum strains. C-PC was found to have antimalarial activity even at a concentration of 3.0µg/ml. The possible mechanism might be relied on the destruction of polymerization of haemozoin by binding of C-PC with ferriprotoporphyrin-IX at the water surface of the plasma membrane.
Keywords	Plasmodium falciparum ; Antimalarial activity ; Nostoc muscorum ; C-phycocyanin ; In vitro culture ; Biology (General) ; QH301-705.5 ; Microbiology ; QR1-502
Subject code	500
Language	English
Publishing date	2010-10-01T00:00:00Z
Publisher	Society of Open Science
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: HMGB1-RAGE pathway drives peroxynitrite signaling-induced IBD-like inflammation in murine nonalcoholic fatty liver disease

Varun Chandrashekaran / Ratanesh K. Seth / Diptadip Dattaroy / Firas Alhasson / Jacek Ziolenka / James Carson / Franklin G. Berger / Balaraman Kalyanaraman / Anna Mae Diehl / Saurabh Chatterjee

Redox Biology, Vol 13, Iss C, Pp 8-

2017 Volume 19

Abstract: Recent clinical studies found a strong association of colonic inflammation and Inflammatory bowel disease (IBD)-like phenotype with NonAlcoholic Fatty liver Disease (NAFLD) yet the mechanisms remain unknown. The present study identifies high mobility ... ...

Abstract	Recent clinical studies found a strong association of colonic inflammation and Inflammatory bowel disease (IBD)-like phenotype with NonAlcoholic Fatty liver Disease (NAFLD) yet the mechanisms remain unknown. The present study identifies high mobility group box 1 (HMGB1) as a key mediator of intestinal inflammation in NAFLD and outlines a detailed redox signaling mechanism for such a pathway. NAFLD mice showed liver damage and release of elevated HMGB1 in systemic circulation and increased intestinal tyrosine nitration that was dependent on NADPH oxidase. Intestines from NAFLD mice showed higher Toll like receptor 4 (TLR4) activation and proinflammatory cytokine release, an outcome strongly dependent on the existence of NAFLD pathology and NADPH oxidase. Mechanistically intestinal epithelial cells showed the HMGB1 activation of TLR-4 was both NADPH oxidase and peroxynitrite dependent with the latter being formed by the activation of NADPH oxidase. Proinflammatory cytokine production was significantly blocked by the specific peroxynitrite scavenger phenyl boronic acid (FBA), AKT inhibition and NADPH oxidase inhibitor Apocynin suggesting NADPH oxidase-dependent peroxynitrite is a key mediator in TLR-4 activation and cytokine release via an AKT dependent pathway. Studies to ascertain the mechanism of HMGB1-mediated NADPH oxidase activation showed a distinct role of Receptor for advanced glycation end products (RAGE) as the use of inhibitors targeted against RAGE or use of deformed HMGB1 protein prevented NADPH oxidase activation, peroxynitrite formation, TLR4 activation and finally cytokine release. Thus, in conclusion the present study identifies a novel role of HMGB1 mediated inflammatory pathway that is RAGE and redox signaling dependent and helps promote ectopic intestinal inflammation in NAFLD.
Keywords	Nonalcoholic steatohepatitis ; DAMP ; FBA ; TLR4 ; Flotillin ; NADPH oxidase ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2017-10-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Association between exposures to brominated trihalomethanes, hepatic injury and type II diabetes mellitus

Makris, Konstantinos C / Androniki Ioannou / Costas A. Christophi / James B. Burch / Michael Picolos / Pantelis Charisiadis / Ratanesh K. Seth / Saurabh Chatterjee / Xanthi D. Andrianou

Elsevier Ltd Environment international. 2016 July, Aug., v. 92-93

2016

Abstract: Non-alcoholic fatty liver disease (NAFLD) is considered the most common liver disorder in the Western world, commonly diagnosed in the majority of obese patients with type 2 diabetes mellitus (T2DM). Metabolic disrupting chemicals with short half-lives, ... ...

Abstract	Non-alcoholic fatty liver disease (NAFLD) is considered the most common liver disorder in the Western world, commonly diagnosed in the majority of obese patients with type 2 diabetes mellitus (T2DM). Metabolic disrupting chemicals with short half-lives, such as those of halogenated structure (trihalomethanes, THM) have been linked with hepatic insulin resistance phenomena in animal studies. However, human studies evaluating the role of THM exposure on liver pathogenesis and T2DM disease process are scarce. The objectives of this study were to: i) determine the association of urinary brominated THM (BrTHM) levels and T2DM disease status, and ii) investigate the association between urinary BrTHM levels and serum alanine aminotransferase (ALT) concentrations, often used as surrogate markers of NAFLD. A pilot case–control study was conducted in Nicosia, Cyprus (n=95). Cases were physician-diagnosed T2DM patients and controls were healthy individuals. Liver enzymes, leptin and TNF-α were measured in sera, while urinary THM levels were measured using tandem mass spectrometry. Diabetics had higher levels of serum leptin, body mass index and ALT than the controls. Among all study participants those with serum ALT levels above the median (17IU/L) had higher mean tribromomethane (TBM) concentrations compared to those with serum ALT below 17IU/L. A significant increase in the odds of having above the median serum ALT levels [OR 6.38, 95% CI: 1.11, 42.84 (p=0.044)] was observed for each unit increase in creatinine-unadjusted urinary TBM levels, along with BMI and past smoking, after adjusting for possible confounders, such as urinary creatinine, age, sex, and leptin; no other THM compound showed a significant association with serum ALT. Logistic regression models for T2DM using the urinary BrTHM as exposure variables did not reach the predetermined level of significance. The interplay between exposures to BrTHM and the initiation of key pathophysiological events relating to hepatic injury (ALT) and inflammation (leptin) was recognized via the use of selected biomarkers of effect. Our evidence that THM could act as hepatic toxins with a further initiation of diabetogenic effects call for additional studies to help us better understand the disease process of the two co-morbidities (NAFLD and T2DM).
Keywords	alanine transaminase ; biomarkers ; blood serum ; body mass index ; bromination ; case-control studies ; creatinine ; fatty liver ; glycemic effect ; half life ; humans ; inflammation ; insulin resistance ; leptin ; liver ; pathogenesis ; patients ; regression analysis ; tandem mass spectrometry ; toxins ; tumor necrosis factor-alpha ; Cyprus
Language	English
Dates of publication	2016-07
Size	p. 486-493.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	554791-x
ISSN	1873-6750 ; 0160-4120
ISSN (online)	1873-6750
ISSN	0160-4120
DOI	10.1016/j.envint.2016.04.012
Database	NAL-Catalogue (AGRICOLA)

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Zs.A 3131: Show issues

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Article ; Online: Association between exposures to brominated trihalomethanes, hepatic injury and type II diabetes mellitus

Konstantinos C. Makris / Xanthi D. Andrianou / Pantelis Charisiadis / James B. Burch / Ratanesh K. Seth / Androniki Ioannou / Michael Picolos / Costas A. Christophi / Saurabh Chatterjee

Environment International, Vol 92, Iss , Pp 486-

2016 Volume 493

Abstract	Non-alcoholic fatty liver disease (NAFLD) is considered the most common liver disorder in the Western world, commonly diagnosed in the majority of obese patients with type 2 diabetes mellitus (T2DM). Metabolic disrupting chemicals with short half-lives, such as those of halogenated structure (trihalomethanes, THM) have been linked with hepatic insulin resistance phenomena in animal studies. However, human studies evaluating the role of THM exposure on liver pathogenesis and T2DM disease process are scarce. The objectives of this study were to: i) determine the association of urinary brominated THM (BrTHM) levels and T2DM disease status, and ii) investigate the association between urinary BrTHM levels and serum alanine aminotransferase (ALT) concentrations, often used as surrogate markers of NAFLD. A pilot case–control study was conducted in Nicosia, Cyprus (n = 95). Cases were physician-diagnosed T2DM patients and controls were healthy individuals. Liver enzymes, leptin and TNF-α were measured in sera, while urinary THM levels were measured using tandem mass spectrometry. Diabetics had higher levels of serum leptin, body mass index and ALT than the controls. Among all study participants those with serum ALT levels above the median (17 IU/L) had higher mean tribromomethane (TBM) concentrations compared to those with serum ALT below 17 IU/L. A significant increase in the odds of having above the median serum ALT levels [OR 6.38, 95% CI: 1.11, 42.84 (p = 0.044)] was observed for each unit increase in creatinine-unadjusted urinary TBM levels, along with BMI and past smoking, after adjusting for possible confounders, such as urinary creatinine, age, sex, and leptin; no other THM compound showed a significant association with serum ALT. Logistic regression models for T2DM using the urinary BrTHM as exposure variables did not reach the predetermined level of significance. The interplay between exposures to BrTHM and the initiation of key pathophysiological events relating to hepatic injury (ALT) and inflammation (leptin) was recognized via the use of selected biomarkers of effect. Our evidence that THM could act as hepatic toxins with a further initiation of diabetogenic effects call for additional studies to help us better understand the disease process of the two co-morbidities (NAFLD and T2DM). Keywords: Brominated trihalomethanes, Fatty liver, Non-alcoholic, Diabetes, Disinfection byproducts, Inflammation, Obesity
Keywords	Environmental sciences ; GE1-350
Subject code	630
Language	English
Publishing date	2016-07-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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