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)
17
Scopus Publications
958
Scholar Citations
12
Scholar h-index
12
Scholar i10-index
Scopus Publications
Oral Microbiota Dysbiosis in Firefighters and the Potential Contributing Environmental and Lifestyle Factors Based on a Case-Control Study Sukanta S. Bhattacharya, Brijesh Yadav, Roman Jandarov, William A. Jetter, Jagjit S. Yadav Microorganisms, 2025 Epidemiological studies show firefighters have increased risks of cancer, diabetes, and cardiovascular disease. To explore links between occupational/environmental exposures and dysbiosis-associated health risks, this case-control study compared oral microbiota of age-matched firefighters (n = 13) and non-firefighters (n = 13) using next-generation sequencing. Firefighters exhibited significantly reduced overall microbial diversity (p ≤ 0.05) and compositional shifts. Firmicutes increased from 53.5% to 68.5%, and Bacteroidetes from 9.5% to 14.1%, while Proteobacteria decreased from 24.6% to 8.3%, and Fusobacteria from 3.3% to 1.1%. This resulted in a higher Firmicutes to Bacteroidetes ratio (5.63 vs. 4.89 in controls), indicating a pro-inflammatory oral microenvironment. At the family level, Streptococcaceae (45.1% to 60.3%) and Prevotellaceae (6.2% to 10.0%) increased, whereas Neisseriaceae (17.7% to 4.9%) and Fusobacteriaceae (2.1% to 0.8%) decreased. The genus Streptococcus dominated firefighters’ microbiota, rising from 45.1% to 60.3%. Diversity indices confirmed reduced microbial evenness and richness in firefighters. Metadata analysis linked frequent fire exposures to perturbations in Comamonadaceae and Carnobacteriaceae (p ≤ 0.05). Barbecue consumption, a source of polycyclic aromatic hydrocarbons, correlated with elevated Spirochaetaceae and Peptostreptococcaceae. This first report on oral dysbiosis in firefighters reveals significant alterations in microbiota abundance, diversity, and evenness, implying potential health risks for this group.
Oro-Respiratory Dysbiosis and Its Modulatory Effect on Lung Mucosal Toxicity during Exposure or Co-Exposure to Carbon Nanotubes and Cigarette Smoke Brijesh Yadav, Sukanta S. Bhattacharya, Lauren Rosen, Ravinder Nagpal, Hariom Yadav, Jagjit S. Yadav Nanomaterials, 2024 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.
Differential modulation of lung aquaporins among other pathophysiological markers in acute (Cl2 gas) and chronic (carbon nanoparticles, cigarette smoke) respiratory toxicity mouse models Sukanta S. Bhattacharya, Brijesh Yadav, Ekta Yadav, Ariel Hus, Niket Yadav, Perminder Kaur, Lauren Rosen, Roman Jandarov, Jagjit S. Yadav Frontiers in Physiology, 2022 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.
Microbial p450 enzymes in bioremediation and drug discovery: Emerging potentials and challenges Sukanta S. Bhattacharya, Jagjit S. Yadav Current Protein and Peptide Science, 2018 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.
Interleukin-10-mediated regenerative postnatal tissue repair is dependent on regulation of hyaluronan metabolism via fibroblast-specific STAT3 signaling 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, Timothy M. Crombleholme, Paul L. Bollyky, Sundeep G. Keswani FASEB Journal, 2017 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
Comparative genomics of early-diverging mushroom-forming fungi provides insights into the origins of lignocellulose decay capabilities László G. Nagy, Robert Riley, Andrew Tritt, Catherine Adam, Chris Daum, Dimitrios Floudas, Hui Sun, Jagjit S. Yadav, Jasmyn Pangilinan, Karl-Henrik Larsson, Kenji Matsuura, Kerrie Barry, Kurt Labutti, Rita Kuo, Robin A. Ohm, Sukanta S. Bhattacharya, Takashi Shirouzu, Yuko Yoshinaga, Francis M. Martin, Igor V. Grigoriev, David S. Hibbett Molecular Biology and Evolution, 2016 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.
The role of interleukin-10 and hyaluronan in murine fetal fibroblast function in Vitro: Implications for recapitulating fetal regenerative wound healing Swathi Balaji, Alice King, Emily Marsh, Maria LeSaint, Sukanta S. Bhattacharya, Nathaniel Han, Yashu Dhamija, Rajeev Ranjan, Louis D. Le, Paul L. Bollyky, Timothy M. Crombleholme, Sundeep G. Keswani Plos One, 2015 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.
In Silico Investigation Reveals a Potential Functional Role for Human Microbiome in Chronic Obstructive Pulmonary Disease N Jana, O Dhara, SS Bhattacharya BioRxiv, 2025.06.29.660899 , 2025 2025
Oral Microbiota Dysbiosis in Firefighters and the Potential Contributing Environmental and Lifestyle Factors Based on a Case-Control Study SS Bhattacharya, B Yadav, R Jandarov, WA Jetter, JS Yadav Microorganisms 13, 1154. , 2025 2025 Citations: 1
Oro-respiratory dysbiosis and its modulatory effect on lung mucosal toxicity during exposure or Co-exposure to carbon nanotubes and cigarette smoke B Yadav, SS Bhattacharya, L Rosen, R Nagpal, H Yadav, JS Yadav Nanomaterials 14 (3), 314 , 2024 2024 Citations: 9
Differential modulation of lung aquaporins among other pathophysiological markers in acute (Cl 2 gas) and chronic (carbon nanoparticles, cigarette smoke … SS Bhattacharya, B Yadav, E Yadav, A Hus, N Yadav, P Kaur, L Rosen, ... Frontiers in Physiology 13, 880815 , 2022 2022 Citations: 12
Crosstalk between gut microbiota and lung inflammation in murine toxicity models of respiratory exposure or co-exposure to carbon nanotube particles and cigarette smoke extract SS Bhattacharya, B Yadav, L Rosen, R Nagpal, H Yadav, JS Yadav Toxicology and Applied Pharmacology 447, 116066 , 2022 2022 Citations: 30
Microbiome Changes a Markers of Exposure and Stress in Firefighters S Bhattacharya, H Chandra, R Jandarov, B Yadav, J Yadav University of Cincinnati , 2018 2018
Modeling and simulation of colonization of water-based metalworking fluid by Mycobacterium immunogenum SS Bhattacharya, JS Yadav Journal of environmental chemical engineering 6 (4), 4953-4960 , 2018 2018 Citations: 2
Intellectual Property Rights Protection in Plants: Scopes in Lychee Commercialization N Sahoo, SS Bhattacharya The Lychee Biotechnology, 281-299 , 2017 2017 Citations: 2
Interleukin-10-mediated regenerative postnatal tissue repair is dependent on regulation of hyaluronan metabolism via fibroblast-specific STAT3 signaling S Balaji, X Wang, A King, LD Le, SS Bhattacharya, C Moles, MJ Butte, ... The FASEB Journal , 2016 2016 Citations: 89
Oral Microbiome Perturbations and Associated Risks in Firefighters S Bhattacharya, J Yadav University of Cincinnati , 2016 2016
Comparative genomics of early-diverging mushroom-forming fungi provides insights into the origins of lignocellulose decay capabilities LG Nagy, R Riley, A Tritt, C Adam, C Daum, D Floudas, H Sun, JS Yadav, ... Molecular biology and evolution 33 (4), 959-970 , 2016 2016 Citations: 287
Microbial P450 enzymes in bioremediation and drug discovery: Emerging potentials and challenges SS Bhattacharya, JS Yadav Current Protein and Peptide Science 18 , 2016 2016 Citations: 41
Oral Microbiome Perturbations and Associated Risks in Firefighters CS Baxter, S Bhattacharya, SM Langevin, JS Yadav University of Cincinnati , 2015 2015
FIBROBLAST-SPECIFIC STAT3 SIGNALING OF IL-10 MEDIATES REGENERATIVE WOUND HEALING S Balaji, N Han, C Moles, S Bhattacharya, P Bollyky, T Crombleholme, ... Wound Repair and Regeneration 23 (4), A2-A3 , 2015 2015
The role of interleukin-10 and hyaluronan in murine fetal fibroblast function in vitro: implications for recapitulating fetal regenerative wound healing. S Balaji, A King, E Marsh, M LeSaint, SS Bhattacharya, N Han, Y Dhamija, ... PLoS One 10 (5) , 2015 2015 Citations: 49
IL-10 MEDIATED REGENERATIVE WOUND HEALING IS DEPENDENT ON FIBROBLAST-SPECIFIC STAT3 SIGNALING SS Bhattacharya, S Balaji, N Han, FM Bouso, TM Crombleholme, ... Wound Repair and Regeneration 22 (2), A32 , 2014 2014
A Computational Approach For The Development Of A Skin-specific Hyaluronan Knockout Murine Model SS Bhattacharya, S Balaji, N Han, C Klanke, P Bollyky, TM Crombleholme, ... Wound Repair and Regeneration 22 (2), A32 , 2014 2014
Adenoviral-mediated gene transfer of insulin-like growth factor 1 enhances wound healing and induces angiogenesis S Balaji, M LeSaint, SS Bhattacharya, C Moles, Y Dhamija, M Kidd, LD Le, ... Journal of Surgical Research 190 (1), 367-377 , 2014 2014 Citations: 74
Comparison of interleukin 10 homologs on dermal wound healing using a novel human skin< i> ex vivo</i> organ culture model S Balaji, CM Moles, SS Bhattacharya, M LeSaint, Y Dhamija, LD Le, ... Journal of Surgical Research 190 (1), 358-366 , 2014 2014 Citations: 43
Comparison of IL-10 Homologs on Dermal Wound Healing Using a Novel Human Ex Vivo Model CM Moles, S Balaji, S Bhattacharya, M LeSaint, M Kidd, Y Dhamija, ... Journal of Surgical Research 186 (2), 651-651 , 2014 2014
MOST CITED SCHOLAR PUBLICATIONS
Comparative genomics of early-diverging mushroom-forming fungi provides insights into the origins of lignocellulose decay capabilities LG Nagy, R Riley, A Tritt, C Adam, C Daum, D Floudas, H Sun, JS Yadav, ... Molecular biology and evolution 33 (4), 959-970 , 2016 2016 Citations: 287
Laccase mediated biodegradation of 2, 4-dichlorophenol using response surface methodology SS Bhattacharya, R Banerjee Chemosphere 73 (1), 81-85 , 2008 2008 Citations: 115
Optimization of laccase production using response surface methodology coupled with differential evolution SS Bhattacharya, VK Garlapati, R Banerjee New biotechnology 28 (1), 31-39 , 2011 2011 Citations: 98
Interleukin-10-mediated regenerative postnatal tissue repair is dependent on regulation of hyaluronan metabolism via fibroblast-specific STAT3 signaling S Balaji, X Wang, A King, LD Le, SS Bhattacharya, C Moles, MJ Butte, ... The FASEB Journal , 2016 2016 Citations: 89
Adenoviral-mediated gene transfer of insulin-like growth factor 1 enhances wound healing and induces angiogenesis S Balaji, M LeSaint, SS Bhattacharya, C Moles, Y Dhamija, M Kidd, LD Le, ... Journal of Surgical Research 190 (1), 367-377 , 2014 2014 Citations: 74
A novel P450-initiated biphasic process for sustainable biodegradation of benzo [a] pyrene in soil under nutrient-sufficient conditions by the white rot fungus Phanerochaete … SS Bhattacharya, K Syed, J Shann, JS Yadav Journal of hazardous materials 261, 675-683 , 2013 2013 Citations: 65
The role of interleukin-10 and hyaluronan in murine fetal fibroblast function in vitro: implications for recapitulating fetal regenerative wound healing. S Balaji, A King, E Marsh, M LeSaint, SS Bhattacharya, N Han, Y Dhamija, ... PLoS One 10 (5) , 2015 2015 Citations: 49
Comparison of interleukin 10 homologs on dermal wound healing using a novel human skin< i> ex vivo</i> organ culture model S Balaji, CM Moles, SS Bhattacharya, M LeSaint, Y Dhamija, LD Le, ... Journal of Surgical Research 190 (1), 358-366 , 2014 2014 Citations: 43
Microbial P450 enzymes in bioremediation and drug discovery: Emerging potentials and challenges SS Bhattacharya, JS Yadav Current Protein and Peptide Science 18 , 2016 2016 Citations: 41
Optimization of laccase mediated biodegradation of 2, 4-dichlorophenol using genetic algorithm SS Bhattacharya, S Karmakar, R Banerjee Water Research 43 (14), 3503-3510 , 2009 2009 Citations: 41
Crosstalk between gut microbiota and lung inflammation in murine toxicity models of respiratory exposure or co-exposure to carbon nanotube particles and cigarette smoke extract SS Bhattacharya, B Yadav, L Rosen, R Nagpal, H Yadav, JS Yadav Toxicology and Applied Pharmacology 447, 116066 , 2022 2022 Citations: 30
Differential modulation of lung aquaporins among other pathophysiological markers in acute (Cl 2 gas) and chronic (carbon nanoparticles, cigarette smoke … SS Bhattacharya, B Yadav, E Yadav, A Hus, N Yadav, P Kaur, L Rosen, ... Frontiers in Physiology 13, 880815 , 2022 2022 Citations: 12
Oro-respiratory dysbiosis and its modulatory effect on lung mucosal toxicity during exposure or Co-exposure to carbon nanotubes and cigarette smoke B Yadav, SS Bhattacharya, L Rosen, R Nagpal, H Yadav, JS Yadav Nanomaterials 14 (3), 314 , 2024 2024 Citations: 9
Modeling and simulation of colonization of water-based metalworking fluid by Mycobacterium immunogenum SS Bhattacharya, JS Yadav Journal of environmental chemical engineering 6 (4), 4953-4960 , 2018 2018 Citations: 2
Intellectual Property Rights Protection in Plants: Scopes in Lychee Commercialization N Sahoo, SS Bhattacharya The Lychee Biotechnology, 281-299 , 2017 2017 Citations: 2
Oral Microbiota Dysbiosis in Firefighters and the Potential Contributing Environmental and Lifestyle Factors Based on a Case-Control Study SS Bhattacharya, B Yadav, R Jandarov, WA Jetter, JS Yadav Microorganisms 13, 1154. , 2025 2025 Citations: 1
In Silico Investigation Reveals a Potential Functional Role for Human Microbiome in Chronic Obstructive Pulmonary Disease N Jana, O Dhara, SS Bhattacharya BioRxiv, 2025.06.29.660899 , 2025 2025
Microbiome Changes a Markers of Exposure and Stress in Firefighters S Bhattacharya, H Chandra, R Jandarov, B Yadav, J Yadav University of Cincinnati , 2018 2018
Oral Microbiome Perturbations and Associated Risks in Firefighters S Bhattacharya, J Yadav University of Cincinnati , 2016 2016
Oral Microbiome Perturbations and Associated Risks in Firefighters CS Baxter, S Bhattacharya, SM Langevin, JS Yadav University of Cincinnati , 2015 2015
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