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Your search keyword '"Mazumder, Md Habibul Hasan"' showing total 14 results
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14 results on '"Mazumder, Md Habibul Hasan"'

4. Redox imbalance in COVID-19 pathophysiology

Author

Majumder, Nairrita, Deepak, Vishal, Hadique, Sarah, Aesoph, Drake, Velayutham, Murugesan, Ye, Qing, Mazumder, Md Habibul Hasan, Lewis, Sara E., Kodali, Vamsi, Roohollahi, Anthony, Guo, Nancy Lan, Hu, Gangqing, Khramtsov, Valery V., Johnson, Richard J., Wen, Sijin, Kelley, Eric E., and Hussain, Salik

Published
2022
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6. Additional file 1 of Lung-gut axis of microbiome alterations following co-exposure to ultrafine carbon black and ozone

Author

Mazumder, Md Habibul Hasan, Gandhi, Jasleen, Majumder, Nairrita, Wang, Lei, Cumming, Robert Ian, Stradtman, Sydney, Velayutham, Murugesan, Hathaway, Quincy A., Shannahan, Jonathan, Hu, Gangqing, Nurkiewicz, Timothy R., Tighe, Robert M., Kelley, Eric E., and Hussain, Salik

Abstract

Additional file 1. Sequence data are available in NCBI database BioProject PRJNA891236. The online version contains additional file available at journal website. It includes. Figure S1: Changes in weight after single and multiple CB, O3 and CB + O3 inhalation exposures. Figure S2: Gating strategy for identifying inflammatory cells in lungs. A Flow gating strategy to detect cell types in lungs after air, CB, O3 or CB + O3 exposure either for 3 h for one day or four days. B Inflammatory cells identification markers. C Inflammatory cell markers, conjugated fluorochrome, clone and vendors. Figure S3: Exposure induce changes in bacterial community in the lungs. A Alterations in the Lactobacillus in response to inhalation exposure in the lungs. B, C Principle Co-ordinate analysis of lung microbial community, Bray–Curtis, and Unweighted Unifrac, respectively. Figure S4: Exposure induce changes in beta diversity indices in colon contents microbiome. A–C Principle Co-ordinate analysis of colon content microbial community, Bray–Curtis, Jaccard distance and Unweighted Unifrac, respectively. D Alterations in the Firmicutes to Bacteroidetes ratio in the colon content. Figure S5: Correlation analysis of absolute bacterial load in the colon contents to oxidative stress.

Published
2023
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7. Mesenchymal PGD2activates an ILC2-Treg axis to promote proliferation of normal and malignant HSPCs

Author

Wu, Limei, Lin, Qiqi, Ma, Zhilin, Chowdhury, Fabliha Ahmed, Mazumder, Md Habibul Hasan, and Du, Wei

Abstract

Cyclooxygenase (COX)-dependent production of prostaglandins (PGs) is known to play important roles in tumorigenesis. PGD2has recently emerged as a key regulator of tumor- and inflammation-associated functions. Here we show that mesenchymal stromal cells (MSCs) from patients with acute myeloid leukemia (AML) or normal MSCs overexpressing COX2 promote proliferation of co-cultured hematopoietic stem and progenitor cells (HSPCs), which can be prevented by treatment with COX2 knockdown or TM30089, a specific antagonist of the PGD2receptor CRTH2. Mechanistically, we demonstrate that PGD2-CRTH2 signaling acts directly on type 2 innate lymphoid cells (ILC2s), potentiating their expansion and driving them to produce Interleukin-5 (IL-5) and IL-13. Furthermore, IL-5 but not IL-13 expands CD4+CD25+IL5Rα+T regulatory cells (Tregs) and promotes HSPC proliferation. Disruption of the PGD2-activated ILC2-Treg axis by specifically blocking the PGD2receptor CRTH2 or IL-5 impedes proliferation of normal and malignant HSPCs. Conversely, co-transfer of CD4+CD25+IL5Rα+Tregs promotes malignant HSPC proliferation and accelerates leukemia development in xenotransplanted mice. Collectively, these results indicate that the mesenchymal source of PGD2promotes proliferation of normal and malignant HSPCs through activation of the ILC2-Treg axis. These findings also suggest that this novel PGD2-activated ILC2-Treg axis may be a valuable therapeutic target for cancer and inflammation-associated diseases.

Published
2020
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12. Gut-Lung Axis of the Microbiome Alterations After Ultrafine Particles and Ozone Inhalation

Author

Mazumder, Md Habibul Hasan

Subjects
Lung-gut axis, Inhalation co-exposure, Microbiome, Carbon black, Ozone, Other Pharmacology, Toxicology and Environmental Health, Pharmacology, Toxicology
Abstract

Air pollution poses a significant threat to public health. It is a mixture of particulate matter, gaseous substances, and other secondary substances. Despite epidemiological research indicating the interactive effects of various components of air pollution, existing studies and regulatory limits often focus on single-exposure scenarios. The emerging understanding of the microbiome’s role in regulating immune response, metabolism, and pathophysiology of various diseases points towards interactions between environmental exposures and microbial dysbiosis. In this dissertation, mice were exposed to relevant deposited doses of carbon black (CB) and ozone (O3), and lung inflammation as well as the lung-gut axis of the microbiome alterations were studied. We also studied the role of nucleotide-biding oligomerization domainlike receptor X1 (NLRX1) in mechanistically modulating immune response and microbial balance. Our project involved inhalation exposures, a unique mouse model (NLRX1 knock out), flow cytometric analysis of immune cells, 16s rRNA sequencing, and absolute bacterial load analysis using QIAcuity digital PCR. We demonstrated significant induction of pulmonary inflammatory response after acute CB+O3 co-exposure coupled with reduced diversity indices and a pathogenic bacterial enrichment in the lung microbiome. In contrast, a significant increase in gut bacterial load, abundance of beneficial bacteria, and induction of microbiome-derived secondary metabolites in the systemic circulation indicated a homeostatic shift. Sub-chronic exposure to CB+O3 did not show significant alterations in the inflammatory response and microbiome balance. However, aggravated inflammatory response and microbiome alterations were observed when lungs were challenged with bleomycin post-exposure. A significant role of genetics, exposure, and sex was observed that changed dynamically at different post-exposure time points. In summary, these studies improved the current understanding of particle and gas mixed exposures in terms of their impacts on immune cell profiling, oxidative stress, and microbiome regulation. Furthermore, our project highlighted the role of microbiome alterations in the air pollution-induced exacerbation of lung inflammation and injury identifying a potential role of the lung-gut axis.

Published
2023

13. Air-Pollution-Mediated Microbial Dysbiosis in Health and Disease: Lung-Gut Axis and Beyond.

Author

Mazumder MHH and Hussain S

Abstract

Growing evidence suggests physiological and pathological functions of lung and gut microbiomes in various pathologies. Epidemiological and experimental data associate air pollution exposure with host microbial dysbiosis in the lungs and gut. Air pollution through increased reactive oxygen species generation, the disruption of epithelial barrier integrity, and systemic inflammation modulates microbial imbalance. Microbiome balance is crucial in regulating inflammation and metabolic pathways to maintain health. Microbiome dysbiosis is proposed as a potential mechanism for the air-pollution-induced modulation of pulmonary and systemic disorders. Microbiome-based therapeutic approaches are increasingly gaining attention and could have added value in promoting lung health. This review summarizes and discusses air-pollution-mediated microbiome alterations in the lungs and gut in humans and mice and elaborates on their role in health and disease. We discuss and summarize the current literature, highlight important mechanisms that lead to microbial dysbiosis, and elaborate on pathways that potentially link lung and lung microbiomes in the context of environmental exposures. Finally, we discuss the lung-liver-gut axis and its potential pathophysiological implications in air-pollution-mediated pathologies through microbial dysbiosis.

Published
2024
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14. Mining the Proteome of Fusobacterium nucleatum subsp. nucleatum ATCC 25586 for Potential Therapeutics Discovery: An In Silico Approach.

Author

Habib AM, Islam MS, Sohel M, Mazumder MH, Sikder MO, and Shahik SM

Abstract

The plethora of genome sequence information of bacteria in recent times has ushered in many novel strategies for antibacterial drug discovery and facilitated medical science to take up the challenge of the increasing resistance of pathogenic bacteria to current antibiotics. In this study, we adopted subtractive genomics approach to analyze the whole genome sequence of the Fusobacterium nucleatum , a human oral pathogen having association with colorectal cancer. Our study divulged 1,499 proteins of F. nucleatum , which have no homolog's in human genome. These proteins were subjected to screening further by using the Database of Essential Genes (DEG) that resulted in the identification of 32 vitally important proteins for the bacterium. Subsequent analysis of the identified pivotal proteins, using the Kyoto Encyclopedia of Genes and Genomes (KEGG) Automated Annotation Server (KAAS) resulted in sorting 3 key enzymes of F. nucleatum that may be good candidates as potential drug targets, since they are unique for the bacterium and absent in humans. In addition, we have demonstrated the three dimensional structure of these three proteins. Finally, determination of ligand binding sites of the 2 key proteins as well as screening for functional inhibitors that best fitted with the ligands sites were conducted to discover effective novel therapeutic compounds against F. nucleatum .

Published
2016
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