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  1. Article ; Online: Cyanobacterial Harmful Algal Bloom Toxin Microcystin and Increased

    Chatterjee, Saurabh / More, Madhura

    Toxins

    2023  Volume 15, Issue 4

    Abstract: The effects of global warming are not limited to rising global temperatures and have set in motion a complex chain of events contributing to climate change. A consequence of global warming and the resultant climate change is the rise in cyanobacterial ... ...

    Abstract The effects of global warming are not limited to rising global temperatures and have set in motion a complex chain of events contributing to climate change. A consequence of global warming and the resultant climate change is the rise in cyanobacterial harmful algal blooms (cyano-HABs) across the world, which pose a threat to public health, aquatic biodiversity, and the livelihood of communities that depend on these water systems, such as farmers and fishers. An increase in cyano-HABs and their intensity is associated with an increase in the leakage of cyanotoxins. Microcystins (MCs) are hepatotoxins produced by some cyanobacterial species, and their organ toxicology has been extensively studied. Recent mouse studies suggest that MCs can induce gut resistome changes. Opportunistic pathogens such as
    MeSH term(s) Humans ; Animals ; Mice ; Microcystins/toxicity ; Harmful Algal Bloom ; Diabetes Mellitus, Type 2 ; Cyanobacteria Toxins ; Cyanobacteria ; Climate Change ; Liver ; Brain
    Chemical Substances microcystin (77238-39-2) ; Microcystins ; Cyanobacteria Toxins
    Language English
    Publishing date 2023-04-17
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2518395-3
    ISSN 2072-6651 ; 2072-6651
    ISSN (online) 2072-6651
    ISSN 2072-6651
    DOI 10.3390/toxins15040289
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Host microbiome associated low intestinal acetate correlates with progressive NLRP3-dependent hepatic-immunotoxicity in early life microcystin-LR exposure.

    More, Madhura / Chatterjee, Somdatta / Saha, Punnag / Bose, Dipro / Trivedi, Ayushi / Roy, Subhajit / Chatterjee, Saurabh

    BMC pharmacology & toxicology

    2023  Volume 24, Issue 1, Page(s) 78

    Abstract: Background: Microcystins (MCs), potent hepatotoxins pose a significant health risk to humans, particularly children, who are more vulnerable due to higher water intake and increased exposure during recreational activities.: Methods: Here, we ... ...

    Abstract Background: Microcystins (MCs), potent hepatotoxins pose a significant health risk to humans, particularly children, who are more vulnerable due to higher water intake and increased exposure during recreational activities.
    Methods: Here, we investigated the role of host microbiome-linked acetate in modulating inflammation caused by early-life exposure to the cyanotoxin Microcystin-LR (MC-LR) in a juvenile mice model.
    Results: Our study revealed that early-life MC-LR exposure disrupted the gut microbiome, leading to a depletion of key acetate-producing bacteria and decreased luminal acetate concentration. Consequently, the dysbiosis hindered the establishment of a gut homeostatic microenvironment and disrupted gut barrier function. The NOD-like receptor family pyrin domain - containing 3 (NLRP3) inflammasome, a key player in MC-induced hepatoxicity emerged as a central player in this process, with acetate supplementation effectively preventing NLRP3 inflammasome activation, attenuating hepatic inflammation, and decreasing pro-inflammatory cytokine production. To elucidate the mechanism underlying the association between early-life MC-LR exposure and the progression of metabolic dysfunction associated steatotic liver disease (MASLD), we investigated the role of acetate binding to its receptor -G-protein coupled receptor 43 (GPR43) on NLRP3 inflammasome activation. Our results demonstrated that acetate-GPR43 signaling was crucial for decreasing NLRP3 protein levels and inhibiting NLRP3 inflammasome assembly. Further, acetate-induced decrease in NLRP3 protein levels was likely mediated through proteasomal degradation rather than autophagy. Overall, our findings underscore the significance of a healthy gut microbiome and its metabolites, particularly acetate, in the progression of hepatotoxicity induced by early life toxin exposure, crucial for MASLD progression.
    Conclusions: This study highlights potential therapeutic targets in gut dysbiosis and NLRP3 inflammasome activation for mitigating toxin-associated inflammatory liver diseases.
    MeSH term(s) Animals ; Mice ; Acetates ; Dysbiosis/chemically induced ; Gastrointestinal Microbiome ; Inflammasomes ; Inflammation/drug therapy ; Microcystins/toxicity ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
    Chemical Substances Acetates ; cyanoginosin LR (EQ8332842Y) ; Inflammasomes ; Microcystins ; NLR Family, Pyrin Domain-Containing 3 Protein
    Language English
    Publishing date 2023-12-13
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2680259-4
    ISSN 2050-6511 ; 2050-6511
    ISSN (online) 2050-6511
    ISSN 2050-6511
    DOI 10.1186/s40360-023-00721-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Hepatic NLRP3-Derived Hsp70 Binding to TLR4 Mediates MASLD to MASH Progression upon Inhibition of PP2A by Harmful Algal Bloom Toxin Microcystin, a Second Hit.

    Roy, Subhajit / Saha, Punnag / Bose, Dipro / Trivedi, Ayushi / More, Madhura / Xiao, Shuo / Diehl, Anna Mae / Chatterjee, Saurabh

    International journal of molecular sciences

    2023  Volume 24, Issue 22

    Abstract: Harmful algal bloom toxin microcystin has been associated with metabolic dysfunction-associated steatotic liver disease (MASLD) progression and hepatocellular carcinoma, though the mechanisms remain unclear. Using an established mouse model of MASLD, we ... ...

    Abstract Harmful algal bloom toxin microcystin has been associated with metabolic dysfunction-associated steatotic liver disease (MASLD) progression and hepatocellular carcinoma, though the mechanisms remain unclear. Using an established mouse model of MASLD, we show that the NLRP3-Hsp70-TLR4 axis drives in part the inflammation of the liver lobule that results in the progression of MASLD to metabolic dysfunction-associated steatohepatitis (MASH). Results showed that mice deficient in NLRP3 exhibited decreased MASH pathology, blocked Hsp70 expression, and co-binding with NLRP3, a crucial protein component of the liver inflammasome. Hsp70, both in the liver lobule and extracellularly released in the liver vasculature, acted as a ligand to TLR4 in the liver, primarily in hepatocytes to activate the NF-κB pathway, ultimately leading to hepatic cell death and necroptosis, a crucial pathology of MASH progression. The above studies show a novel insight into an inflammasome-triggered Hsp70-mediated inflammation that may have broader implications in MASLD pathology. MASLD to MASH progression often requires multiple hits. One of the mediators of progressive MASLD is environmental toxins. In this research report, we show for the first time a novel mechanism where microcystin-LR, an environmental toxin, advances MASLD to MASH by triggering the release of Hsp70 as a DAMP to activate TLR4-induced inflammation in the liver.
    MeSH term(s) Mice ; Animals ; Inflammasomes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/metabolism ; Harmful Algal Bloom ; Microcystins/toxicity ; Non-alcoholic Fatty Liver Disease/metabolism ; Inflammation/metabolism
    Chemical Substances Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Toll-Like Receptor 4 ; Microcystins
    Language English
    Publishing date 2023-11-15
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms242216354
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Prolonged Antibiotic Use in a Preclinical Model of Gulf War Chronic Multisymptom-Illness Causes Renal Fibrosis-like Pathology via Increased micro-RNA 21-Induced PTEN Inhibition That Is Correlated with Low Host

    Trivedi, Ayushi / Bose, Dipro / Saha, Punnag / Roy, Subhajit / More, Madhura / Skupsky, Jonathan / Klimas, Nancy G / Chatterjee, Saurabh

    Cells

    2023  Volume 13, Issue 1

    Abstract: Gulf War (GW) veterans show gastrointestinal disturbances and gut dysbiosis. Prolonged antibiotic treatments commonly employed in veterans, especially the use of fluoroquinolones and aminoglycosides, have also been associated with dysbiosis. This study ... ...

    Abstract Gulf War (GW) veterans show gastrointestinal disturbances and gut dysbiosis. Prolonged antibiotic treatments commonly employed in veterans, especially the use of fluoroquinolones and aminoglycosides, have also been associated with dysbiosis. This study investigates the effect of prolonged antibiotic exposure on risks of adverse renal pathology and its association with gut bacterial species abundance in underlying GWI and aims to uncover the molecular mechanisms leading to possible renal dysfunction with aging. Using a GWI mouse model, administration of a prolonged antibiotic regimen involving neomycin and enrofloxacin treatment for 5 months showed an exacerbated renal inflammation with increased NF-κB activation and pro-inflammatory cytokines levels. Involvement of the high mobility group 1 (HMGB1)-mediated receptor for advanced glycation end products (RAGE) activation triggered an inflammatory phenotype and increased transforming growth factor-β (TGF-β) production. Mechanistically, TGF-β- induced microRNA-21 upregulation in the renal tissue leads to decreased phosphatase and tensin homolog (PTEN) expression. The above event led to the activation of protein kinase-B (AKT) signaling, resulting in increased fibronectin production and fibrosis-like pathology. Importantly, the increased miR-21 was associated with low levels of
    MeSH term(s) Animals ; Mice ; Anti-Bacterial Agents/adverse effects ; Proto-Oncogene Proteins c-akt ; Dysbiosis ; Gulf War ; HMGB1 Protein ; Kidney Diseases ; Chronic Disease ; Clostridiales ; Fibrosis ; Inflammation ; Transforming Growth Factor beta ; MicroRNAs
    Chemical Substances Anti-Bacterial Agents ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; HMGB1 Protein ; Transforming Growth Factor beta ; MicroRNAs
    Language English
    Publishing date 2023-12-27
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells13010056
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Subchronic Oral Cylindrospermopsin Exposure Alters the Host Gut Microbiome and Is Associated with Progressive Hepatic Inflammation, Stellate Cell Activation, and Mild Fibrosis in a Preclinical Study.

    Saha, Punnag / Upright, Macayla / Bose, Dipro / Roy, Subhajit / Trivedi, Ayushi / More, Madhura / Scott, Geoff I / Brooks, Bryan W / Chatterjee, Saurabh

    Toxins

    2022  Volume 14, Issue 12

    Abstract: Epidemiological studies have reported a strong association between liver injury and incidences of hepatocellular carcinoma in sections of humans globally. Several preclinical studies have shown a strong link between cyanotoxin exposure and the ... ...

    Abstract Epidemiological studies have reported a strong association between liver injury and incidences of hepatocellular carcinoma in sections of humans globally. Several preclinical studies have shown a strong link between cyanotoxin exposure and the development of nonalcoholic steatohepatitis, a precursor of hepatocellular carcinoma. Among the emerging threats from cyanotoxins, new evidence shows cylindrospermopsin release in freshwater lakes. A known hepatotoxin in higher concentrations, we examined the possible role of cylindrospermopsin in causing host gut dysbiosis and its association with liver pathology in a mouse model of toxico-pharmacokinetics and hepatic pathology. The results showed that oral exposure to cylindrospermopsin caused decreased diversity of gut bacteria phyla accompanied by an increased abundance of
    MeSH term(s) Animals ; Mice ; Humans ; Carcinoma, Hepatocellular/metabolism ; Kupffer Cells/metabolism ; Kupffer Cells/pathology ; Gastrointestinal Microbiome/physiology ; Dysbiosis ; Liver/metabolism ; Liver Cirrhosis/pathology ; Liver Neoplasms/metabolism ; Inflammation/metabolism
    Chemical Substances cylindrospermopsin (2JIZ556BA3)
    Language English
    Publishing date 2022-12-01
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2518395-3
    ISSN 2072-6651 ; 2072-6651
    ISSN (online) 2072-6651
    ISSN 2072-6651
    DOI 10.3390/toxins14120835
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Microbiome Dysbiosis Shows Strong Association of Gut-Derived Altered Metabolomic Profile in Gulf War Chronic Multisymptom Illness Symptom Persistence Following Western Diet Feeding and Development of Obesity.

    Bose, Dipro / Stebliankin, Vitalli / Cickovski, Trevor / Saha, Punnag / Trivedi, Ayushi / Roy, Subhajit / More, Madhura / Tuteja, Ashok / Mathee, Kalai / Narasimhan, Giri / Chatterjee, Saurabh

    International journal of molecular sciences

    2023  Volume 24, Issue 4

    Abstract: The pathophysiology of Gulf War Illness (GWI) remains elusive even after three decades. The persistence of multiple complex symptoms along with metabolic disorders such as obesity worsens the health of present Gulf War (GW) Veterans often by the ... ...

    Abstract The pathophysiology of Gulf War Illness (GWI) remains elusive even after three decades. The persistence of multiple complex symptoms along with metabolic disorders such as obesity worsens the health of present Gulf War (GW) Veterans often by the interactions of the host gut microbiome and inflammatory mediators. In this study, we hypothesized that the administration of a Western diet might alter the host metabolomic profile, which is likely associated with the altered bacterial species. Using a five-month symptom persistence GWI model in mice and whole-genome sequencing, we characterized the species-level dysbiosis and global metabolomics, along with heterogenous co-occurrence network analysis, to study the bacteriome-metabolomic association. Microbial analysis at the species level showed a significant alteration of beneficial bacterial species. The beta diversity of the global metabolomic profile showed distinct clustering due to the Western diet, along with the alteration of metabolites associated with lipid, amino acid, nucleotide, vitamin, and xenobiotic metabolism pathways. Network analysis showed novel associations of gut bacterial species with metabolites and biochemical pathways that could be used as biomarkers or therapeutic targets to ameliorate symptom persistence in GW Veterans.
    MeSH term(s) Mice ; Animals ; Dysbiosis ; Gulf War ; Diet, Western ; Gastrointestinal Microbiome/physiology ; Bacteria ; Obesity
    Language English
    Publishing date 2023-02-20
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24044245
    Database MEDical Literature Analysis and Retrieval System OnLINE

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