Sukanta S Bhattacharya
@jisuniversity.ac.in
Associate Professor, Department of Biosciences
JIS University, Kolkata
My research and academic interest are to investigate the potential of microbial systems in the human body (microbiome) in the modulation of health and disease states, as well as in the environment for biotransformation and detoxication. I seek to understand how the exposure to different toxicants impacts the microbiome and human health (using human cohorts and mice models) as well as the mechanism and components of the microbiomes impacted by a health condition. My research efforts (as PI in mentor mentee projects) have been funded by Pilot project grants from NIH and NIEHS, USA for exploring the modulatory role of human microbiome in health and disease (especially Head and Neck Squamous Cell Carcinoma) in individuals exposed to the xenobiotic compounds (such as Cigarette smoke extract, Carbon nanotubes etc.) using both human samples and animal models. Design of experiments for the optimization of enzymatic and microbial processes is another core area of my expertise.
EDUCATION
• Postdoctoral Researcher (Microbial Biotechnology, Toxicology & Cancer Biology)
September 2021- August 2023, University of Cincinnati, Ohio, USA
• Postdoctoral Research Fellow (Microbial Biotechnology, Enzymology & Toxicology)
January 2012-January 2017, University of Cincinnati, Ohio, USA
• Doctor of Philosophy (Microbial Biotechnology),
August 2011, Indian Institute of Technology Kharagpur, India
• Master of Science in Biotechnology (Applied Microbiology spl.),
May, 2004 School of Life Sciences, Sambalpur University, Odisha, India.
(First Class)
• Bachelor of Science in Biosciences,
May, 2002 Sambalpur University, Odisha, India.
(First Class Honors with Distinction)
Scopus Publications
Scholar Citations
Scholar h-index
Scholar i10-index
Scopus Publications
Brijesh Yadav, Sukanta S. Bhattacharya, Lauren Rosen, Ravinder Nagpal, Hariom Yadav, and Jagjit S. Yadav
MDPI AG
The oro-respiratory microbiome is impacted by inhalable exposures such as smoking and has been associated with respiratory health conditions. However, the effect of emerging toxicants, particularly engineered nanoparticles, alone or in co-exposure with smoking, is poorly understood. Here, we investigated the impact of sub-chronic exposure to carbon nanotube (CNT) particles, cigarette smoke extract (CSE), and their combination. The oral, nasal, and lung microbiomes were characterized using 16S rRNA-based metagenomics. The exposures caused the following shifts in lung microbiota: CNT led to a change from Proteobacteria and Bacteroidetes to Firmicutes and Tenericutes; CSE caused a shift from Proteobacteria to Bacteroidetes; and co-exposure (CNT+CSE) had a mixed effect, maintaining higher numbers of Bacteroidetes (due to the CNT effect) and Tenericutes (due to the CSE effect) compared to the control group. Oral microbiome analysis revealed an abundance of the following genera: Acinetobacter (CNT), Staphylococcus, Aggregatibacter, Allobaculum, and Streptococcus (CSE), and Alkalibacterium (CNT+CSE). These proinflammatory microbial shifts correlated with changes in the relative expression of lung mucosal homeostasis/defense proteins, viz., aquaporin 1 (AQP-1), surfactant protein A (SP-A), mucin 5b (MUC5B), and IgA. Microbiota depletion reversed these perturbations, albeit to a varying extent, confirming the modulatory role of oro-respiratory dysbiosis in lung mucosal toxicity. This is the first demonstration of specific oro-respiratory microbiome constituents as potential modifiers of toxicant effects in exposed lungs.
Sukanta S. Bhattacharya, Brijesh Yadav, Ekta Yadav, Ariel Hus, Niket Yadav, Perminder Kaur, Lauren Rosen, Roman Jandarov, and Jagjit S. Yadav
Frontiers Media SA
Inhaled toxic chemicals and particulates are known to disrupt lung homeostasis causing pulmonary toxicity and tissue injury. However, biomarkers of such exposures and their underlying mechanisms are poorly understood, especially for emerging toxicants such as engineered nanoparticles and chemical threat agents such as chlorine gas (Cl2). Aquaporins (AQPs), commonly referred to as water channels, are known to play roles in lung homeostasis and pathophysiology. However, little is known on their regulation in toxicant-induced lung injuries. Here, we compared four lung toxicity models namely, acute chemical exposure (Cl2)-, chronic particulate exposure (carbon nanotubes/CNT)-, chronic chemical exposure (cigarette smoke extract/CSE)-, and a chronic co-exposure (CNT + CSE)- model, for modulation of lung aquaporins (AQPs 1, 3, 4, and 5) in relation to other pathophysiological endpoints. These included markers of compromised state of lung mucosal lining [mucin 5b (MUC5B) and surfactant protein A (SP-A)] and lung-blood barrier [protein content in bronchoalveolar lavage (BAL) fluid and, cell tight junction proteins occludin and zona-occludens]. The results showed toxicity model-specific regulation of AQPs measured in terms of mRNA abundance. A differential upregulation was observed for AQP1 in acute Cl2 exposure model (14.71-fold; p = 0.002) and AQP3 in chronic CNT exposure model (3.83-fold; p = 0.044). In contrast, AQP4 was downregulated in chronic CSE model whereas AQP5 showed no significant change in any of the models. SP-A and MUC5B expression showed a decreasing pattern across all toxicity models except the acute Cl2 toxicity model, which showed a highly significant upregulation of MUC5B (25.95-fold; p = 0.003). This was consistent with other significant pathophysiological changes observed in this acute model, particularly a compromised lung epithelial-endothelial barrier indicated by significantly increased protein infiltration and expression of tight junction proteins, and more severe histopathological (structural and immunological) changes. To our knowledge, this is the first report on lung AQPs as molecular targets of the study toxicants. The differentially regulated AQPs, AQP1 in acute Cl2 exposure versus AQP3 in chronic CNT nanoparticle exposure, in conjunction with the corresponding differentially impacted pathophysiological endpoints (particularly MUC5B) could potentially serve as predictive markers of toxicant type-specific pulmonary injury and as candidates for future investigation for clinical intervention.
Sukanta S. Bhattacharya, Brijesh Yadav, Lauren Rosen, Ravinder Nagpal, Hariom Yadav, and Jagjit S. Yadav
Elsevier BV
Sukanta S. Bhattacharya and Jagjit S. Yadav
Elsevier BV
Sukanta S. Bhattacharya and Jagjit S. Yadav
Bentham Science Publishers Ltd.
Cytochrome P450 enzymes are a structurally conserved but functionally diverse group of heme-containing mixed function oxidases found across both prokaryotic and eukaryotic forms of the microbial world. Microbial P450s are known to perform diverse functions ranging from the synthesis of cell wall components to xenobiotic/drug metabolism to biodegradation of environmental chemicals. Conventionally, many microbial systems have been reported to mimic mammalian P450-like activation of drugs and were proposed as the in-vitro models of mammalian drug metabolism. Recent reports suggest that native or engineered forms of specific microbial P450s from these and other microbial systems could be employed for desired specific biotransformation reactions toward natural and synthetic (drug) compounds underscoring their emerging potential in drug improvement and discovery. On the other hand, microorganisms particularly fungi and actinomycetes have been shown to possess catabolic P450s with unusual potential to degrade toxic environmental chemicals including persistent organic pollutants (POPs). Wood-rotting basidiomycete fungi in particular have revealed the presence of exceptionally large P450 repertoire (P450ome) in their genomes, majority of which are however orphan (with no known function). Our pre- and post-genomic studies have led to functional characterization of several fungal P450s inducible in response to exposure to several environmental toxicants and demonstration of their potential in bioremediation of these chemicals. This review is an attempt to summarize the postgenomic unveiling of this versatile enzyme superfamily in microbial systems and investigation of their potential to synthesize new drugs and degrade persistent pollutants, among other biotechnological applications.
Swathi Balaji, Xinyi Wang, Alice King, Louis D. Le, Sukanta S. Bhattacharya, Chad M. Moles, Manish J. Butte, Vinicio A. Jesus Perez, Kenneth W. Liechty, Thomas N. Wight,et al.
Wiley
The cytokine IL‐10 has potent antifibrotic effects in models of adult fibrosis, but the mechanisms of action are unclear. Here, we report a novel finding that IL‐10 triggers a signal transducer and activator of transcription 3(STAT3)–dependent signaling pathway that regulates hyaluronan (HA) metabolism and drives adult fibroblasts to synthesize an HA‐rich pericellular matrix, which mimics the fetal regenerative wound healing phenotype with reduced fibrosis. By using cre‐lox‐mediated novel, inducible, fibroblast‐, keratinocyte‐, and wound‐specific STAT3‐knockdown postnatal mice—plus syngeneic fibroblast cell‐transplant models—we demonstrate that the regenerative effects of IL‐10 in postnatal wounds are dependent on HA synthesis and fibroblast‐specific STAT3‐dependent signaling. The importance of IL‐10‐induced HA synthesis for regenerative wound healing is demonstrated by inhibition of HA synthesis in a murine wound model by administering 4‐methylumbelliferone. Although IL‐10 and STAT3 signaling were intact, the antifibrotic repair phenotype that is induced by IL‐10 overexpression was abrogated in this model. Our data show a novel role for IL‐10 beyond its accepted immune‐regulatory mechanism. The opportunity for IL‐10 to regulate a fibroblast‐specific formation of a regenerative, HA‐rich wound extracellular matrix may lead to the development of innovative therapies to attenuate postnatal fibrosis in organ systems or diseases in which dysregulated inflammation and HA intersect.—Balaji, S., Wang, X., King, A., Le, L. D., Bhattacharya, S. S., Moles, C. M., Butte, M. J., de Jesus Perez, V.A., Liechty, K. W., Wight, T. N., Crombleholme, T. M., Bollyky, P. L., Keswani, S. G. Interleukin‐10‐mediated regenerative postnatal tissue repair is dependent on regulation of hyaluronan metabolism via fibroblast‐specific STAT3 signaling. FASEB J. 31, 868–881 (2017). www.fasebj.org
Niharika Sahoo and Sukanta S. Bhattacharya
Springer Singapore
László G. Nagy, Robert Riley, Andrew Tritt, Catherine Adam, Chris Daum, Dimitrios Floudas, Hui Sun, Jagjit S. Yadav, Jasmyn Pangilinan, Karl-Henrik Larsson,et al.
Oxford University Press (OUP)
Evolution of lignocellulose decomposition was one of the most ecologically important innovations in fungi. White-rot fungi in the Agaricomycetes (mushrooms and relatives) are the most effective microorganisms in degrading both cellulose and lignin components of woody plant cell walls (PCW). However, the precise evolutionary origins of lignocellulose decomposition are poorly understood, largely because certain early-diverging clades of Agaricomycetes and its sister group, the Dacrymycetes, have yet to be sampled, or have been undersampled, in comparative genomic studies. Here, we present new genome sequences of ten saprotrophic fungi, including members of the Dacrymycetes and early-diverging clades of Agaricomycetes (Cantharellales, Sebacinales, Auriculariales, and Trechisporales), which we use to refine the origins and evolutionary history of the enzymatic toolkit of lignocellulose decomposition. We reconstructed the origin of ligninolytic enzymes, focusing on class II peroxidases (AA2), as well as enzymes that attack crystalline cellulose. Despite previous reports of white rot appearing as early as the Dacrymycetes, our results suggest that white-rot fungi evolved later in the Agaricomycetes, with the first class II peroxidases reconstructed in the ancestor of the Auriculariales and residual Agaricomycetes. The exemplars of the most ancient clades of Agaricomycetes that we sampled all lack class II peroxidases, and are thus concluded to use a combination of plesiomorphic and derived PCW degrading enzymes that predate the evolution of white rot.
Swathi Balaji, Alice King, Emily Marsh, Maria LeSaint, Sukanta S. Bhattacharya, Nathaniel Han, Yashu Dhamija, Rajeev Ranjan, Louis D. Le, Paul L. Bollyky,et al.
Public Library of Science (PLoS)
Background Mid-gestation fetal cutaneous wounds heal scarlessly and this has been attributed in part to abundant hyaluronan (HA) in the extracellular matrix (ECM) and a unique fibroblast phenotype. We recently reported a novel role for interleukin 10 (IL-10) as a regulator of HA synthesis in the fetal ECM, as well as the ability of the fetal fibroblast to produce an HA-rich pericellular matrix (PCM). We hypothesized that IL-10-mediated HA synthesis was essential to the fetal fibroblast functional phenotype and, moreover, that this phenotype could be recapitulated in adult fibroblasts via supplementation with IL-10 via an HA dependent process. Methodology/Principal Findings To evaluate the differences in functional profile, we compared metabolism (MTS assay), apoptosis (caspase-3 staining), migration (scratch wound assay) and invasion (transwell assay) between C57Bl/6J murine fetal (E14.5) and adult (8 weeks) fibroblasts. We found that fetal fibroblasts have lower rates of metabolism and apoptosis, and an increased ability to migrate and invade compared to adult fibroblasts, and that these effects were dependent on IL-10 and HA synthase activity. Further, addition of IL-10 to adult fibroblasts resulted in increased fibroblast migration and invasion and recapitulated the fetal phenotype in an HA-dependent manner. Conclusions/Significance Our data demonstrates the functional differences between fetal and adult fibroblasts, and that IL-10 mediated HA synthesis is essential for the fetal fibroblasts' enhanced invasion and migration properties. Moreover, IL-10 via an HA-dependent mechanism can recapitulate this aspect of the fetal phenotype in adult fibroblasts, suggesting a novel mechanism of IL-10 in regenerative wound healing.
Swathi Balaji, Maria LeSaint, Sukanta S. Bhattacharya, Chad Moles, Yashu Dhamija, Mykia Kidd, Louis D. Le, Alice King, Aimen Shaaban, Timothy M. Crombleholme,et al.
Elsevier BV
Swathi Balaji, Chad M. Moles, Sukanta S. Bhattacharya, Maria LeSaint, Yashu Dhamija, Louis D. Le, Alice King, Mykia Kidd, Muhammad F. Bouso, Aimen Shaaban,et al.
Elsevier BV
Sukanta S. Bhattacharya, Khajamohiddin Syed, Jodi Shann, and Jagjit S. Yadav
Elsevier BV
Sukanta Shekhar Bhattacharya, Vijay Kumar Garlapati, and Rintu Banerjee
Elsevier BV
S.S. Bhattacharya, S. Karmakar, and R. Banerjee
Elsevier BV
S.S. Bhattacharya and R. Banerjee
Elsevier BV
S.S. Bhattacharya and R. Banerjee
Elsevier BV
RECENT SCHOLAR PUBLICATIONS
MOST CITED SCHOLAR PUBLICATIONS
GRANT DETAILS
1. CEG-NIS P30-ES006096 Sukanta S. Bhattacharya, Ph.D (PI) 05/21/2016-02/28/17
Murine Model to investigate the role of oral microbiome in PAH Exposure linked Head and Neck Cancer:
Role: Principal Investigator
Funding Agency: National Institute of Health via Center of Environmental Genetics, University of Cincinnati
Lab location: University of Cincinnati, Cincinnati, Ohio, USA
Amount:$5000.00
2. NIEHS P30ES006096-24 Sukanta S. Bhattacharya, Ph.D (PI) 05/10/2016-02/28/17
Metallic Nanoparticles interactions with xenobiotic-metabolizing P450 genes via modulation of microbiome in mice
Role: Principal Investigator
Funding Agency: National Institute of Health via Center of Environmental Genetics, University of Cincinnati
Lab location: University of Cincinnati, Cincinnati, Ohio, USA
Amount:$15000.00
3. CEG-NIS P30-ES006096 Sukanta S. Bhattacharya, Ph.D (PI) 05/21/2015-02/28/16 Oral Microbiome in PAH exposure-linked Head and Neck Cancer
Role: Principal Investigator
Funding Agency: National Institute of Health, USA via Center of Environmental Genetics, University of
Cincinnati
Lab location: University of Cincinnati, Cincinnati, Ohio, USA Amount:$5000
4. ERC-PRP T42/OH008432-10 Sukanta S. Bhattacharya, Ph.D (PI) 08/05/2015-06/30/16 Oral Microbiome perturbations and associated risks in firefighters
Role: Principal Investigator
Funding Agency: National Institute for Occupational Safety and Health, USA, Pilot Research Project Training Program of the University of