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  1. Article: Eat more natural dietary fiber and whole grains to minimize liver disease risk.

    Golonka, Rachel M / Yeoh, Beng San / Vijay-Kumar, Matam

    Hepatobiliary surgery and nutrition

    2022  Volume 11, Issue 4, Page(s) 601–604

    Language English
    Publishing date 2022-08-04
    Publishing country China (Republic : 1949- )
    Document type Editorial ; Comment
    ZDB-ID 2812398-0
    ISSN 2304-389X ; 2304-3881
    ISSN (online) 2304-389X
    ISSN 2304-3881
    DOI 10.21037/hbsn-22-155
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Invited Perspective: PFOS-Pick Fiber, Oust Sulfonate.

    Golonka, Rachel M / Vijay-Kumar, Matam

    Environmental health perspectives

    2022  Volume 130, Issue 11, Page(s) 111301

    MeSH term(s) Alkanesulfonic Acids ; Fluorocarbons ; Alkanesulfonates
    Chemical Substances Alkanesulfonic Acids ; Fluorocarbons ; Alkanesulfonates
    Language English
    Publishing date 2022-11-04
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 195189-0
    ISSN 1552-9924 ; 0091-6765 ; 1078-0475
    ISSN (online) 1552-9924
    ISSN 0091-6765 ; 1078-0475
    DOI 10.1289/EHP12012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Bacterial flagellin is a dominant, stable innate immune activator in the gastrointestinal contents of mice and rats.

    Vijay-Kumar, Matam / Bovilla, Venugopal R / Yeoh, Beng San / Golonka, Rachel M / Saha, Piu / Joe, Bina / Gewirtz, Andrew T

    Gut microbes

    2023  Volume 15, Issue 1, Page(s) 2185031

    Abstract: Intestinal contents comprise the largest repository of immunogenic ligands of microbial origin. We undertook this study to assess the predominant microbe-associated molecular patterns (MAMPs) present therein and the receptors) that mediate the innate ... ...

    Abstract Intestinal contents comprise the largest repository of immunogenic ligands of microbial origin. We undertook this study to assess the predominant microbe-associated molecular patterns (MAMPs) present therein and the receptors) that mediate the innate immune responses to them. Here, we demonstrated that intestinal contents from conventional, but not germ-free, mice and rats triggered robust innate immune responses
    MeSH term(s) Animals ; Rats ; Gastrointestinal Contents ; Flagellin ; Gastrointestinal Microbiome ; Flagella ; Immunity, Innate
    Chemical Substances Flagellin (12777-81-0)
    Language English
    Publishing date 2023-03-07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2575755-6
    ISSN 1949-0984 ; 1949-0984
    ISSN (online) 1949-0984
    ISSN 1949-0984
    DOI 10.1080/19490976.2023.2185031
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Atypical immunometabolism and metabolic reprogramming in liver cancer: Deciphering the role of gut microbiome.

    Golonka, Rachel M / Vijay-Kumar, Matam

    Advances in cancer research

    2020  Volume 149, Page(s) 171–255

    Abstract: Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related mortality worldwide. Much recent research has delved into understanding the underlying molecular mechanisms of HCC pathogenesis, which has revealed to be heterogenous and ... ...

    Abstract Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related mortality worldwide. Much recent research has delved into understanding the underlying molecular mechanisms of HCC pathogenesis, which has revealed to be heterogenous and complex. Two major hallmarks of HCC include: (i) a hijacked immunometabolism and (ii) a reprogramming in metabolic processes. We posit that the gut microbiota is a third component in an entanglement triangle contributing to HCC progression. Besides metagenomic studies highlighting the diagnostic potential in the gut microbiota profile, recent research is pinpointing the gut microbiota as an instigator, not just a mere bystander, in HCC. In this chapter, we discuss mechanistic insights on atypical immunometabolism and metabolic reprogramming in HCC, including the examination of tumor-associated macrophages and neutrophils, tumor-infiltrating lymphocytes (e.g., T-cell exhaustion, regulatory T-cells, natural killer T-cells), the Warburg effect, rewiring of the tricarboxylic acid cycle, and glutamine addiction. We further discuss the potential involvement of the gut microbiota in these characteristics of hepatocarcinogenesis. An immediate highlight is that microbiota metabolites (e.g., short chain fatty acids, secondary bile acids) can impair anti-tumor responses, which aggravates HCC. Lastly, we describe the rising 'new era' of immunotherapies (e.g., immune checkpoint inhibitors, adoptive T-cell transfer) and discuss for the potential incorporation of gut microbiota targeted therapeutics (e.g., probiotics, fecal microbiota transplantation) to alleviate HCC. Altogether, this chapter invigorates for continuous research to decipher the role of gut microbiome in HCC from its influence on immunometabolism and metabolic reprogramming.
    MeSH term(s) Animals ; Carcinoma, Hepatocellular/immunology ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/microbiology ; Carcinoma, Hepatocellular/pathology ; Gastrointestinal Microbiome ; Humans ; Immune System/immunology ; Liver Neoplasms/immunology ; Liver Neoplasms/metabolism ; Liver Neoplasms/microbiology ; Liver Neoplasms/pathology
    Language English
    Publishing date 2020-11-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 127-2
    ISSN 2162-5557 ; 0065-230X
    ISSN (online) 2162-5557
    ISSN 0065-230X
    DOI 10.1016/bs.acr.2020.10.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Crosstalk between Gut Microbiota and Host Immunity: Impact on Inflammation and Immunotherapy.

    Campbell, Connor / Kandalgaonkar, Mrunmayee R / Golonka, Rachel M / Yeoh, Beng San / Vijay-Kumar, Matam / Saha, Piu

    Biomedicines

    2023  Volume 11, Issue 2

    Abstract: Gut microbes and their metabolites are actively involved in the development and regulation of host immunity, which can influence disease susceptibility. Herein, we review the most recent research advancements in the gut microbiota-immune axis. We discuss ...

    Abstract Gut microbes and their metabolites are actively involved in the development and regulation of host immunity, which can influence disease susceptibility. Herein, we review the most recent research advancements in the gut microbiota-immune axis. We discuss in detail how the gut microbiota is a tipping point for neonatal immune development as indicated by newly uncovered phenomenon, such as maternal imprinting, in utero intestinal metabolome, and weaning reaction. We describe how the gut microbiota shapes both innate and adaptive immunity with emphasis on the metabolites short-chain fatty acids and secondary bile acids. We also comprehensively delineate how disruption in the microbiota-immune axis results in immune-mediated diseases, such as gastrointestinal infections, inflammatory bowel diseases, cardiometabolic disorders (e.g., cardiovascular diseases, diabetes, and hypertension), autoimmunity (e.g., rheumatoid arthritis), hypersensitivity (e.g., asthma and allergies), psychological disorders (e.g., anxiety), and cancer (e.g., colorectal and hepatic). We further encompass the role of fecal microbiota transplantation, probiotics, prebiotics, and dietary polyphenols in reshaping the gut microbiota and their therapeutic potential. Continuing, we examine how the gut microbiota modulates immune therapies, including immune checkpoint inhibitors, JAK inhibitors, and anti-TNF therapies. We lastly mention the current challenges in metagenomics, germ-free models, and microbiota recapitulation to a achieve fundamental understanding for how gut microbiota regulates immunity. Altogether, this review proposes improving immunotherapy efficacy from the perspective of microbiome-targeted interventions.
    Language English
    Publishing date 2023-01-20
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines11020294
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Sex Dimorphic Effects of Bile Acid Metabolism in Liver Cancer in Mice.

    Golonka, Rachel M / Yeoh, Beng San / Saha, Piu / Tian, Yuan / Chiang, John Y L / Patterson, Andrew D / Gewirtz, Andrew T / Joe, Bina / Vijay-Kumar, Matam

    Cellular and molecular gastroenterology and hepatology

    2024  Volume 17, Issue 5, Page(s) 719–735

    Abstract: Background & aims: Hepatocellular carcinoma (HCC) is a male-dominant disease, but targeted sex hormone therapies have not been successful. Bile acids are a potential liver carcinogen and are biomolecules with hormone-like effects. A few studies ... ...

    Abstract Background & aims: Hepatocellular carcinoma (HCC) is a male-dominant disease, but targeted sex hormone therapies have not been successful. Bile acids are a potential liver carcinogen and are biomolecules with hormone-like effects. A few studies highlight their potential sex dimorphism in physiology and disease. We hypothesized that bile acids could be a potential molecular signature that explains sex disparity in HCC.
    Methods & results: We used the farnesoid X receptor knockout (FxrKO) mouse model to study bile acid-dependent HCC. Temporal tracking of circulating bile acids determined more than 80% of FxrKO females developed spontaneous cholemia (ie, serum total bile acids ≥40 μmol/L) as early as 8 weeks old. Opposingly, FxrKO males were highly resistant to cholemia, with ∼23% incidence even when 26 weeks old. However, FxrKO males demonstrated higher levels of deoxycholate than females. Compared with males, FxrKO females had more severe cholestatic liver injury and further aberrancies in bile acid metabolism. Yet, FxrKO females expressed more detoxification transcripts and had greater renal excretion of bile acids. Intervention with CYP7A1 (rate limiting enzyme for bile acid biosynthesis) deficiency or taurine supplementation either completely or partially normalized bile acid levels and liver injury in FxrKO females. Despite higher cholemia prevalence in FxrKO females, their tumor burden was less compared with FxrKO males. An exception to this sex-dimorphic pattern was found in a subset of male and female FxrKO mice born with congenital cholemia due to portosystemic shunt, where both sexes had comparable robust HCC.
    Conclusions: Our study highlights bile acids as sex-dimorphic metabolites in HCC except in the case of portosystemic shunt.
    MeSH term(s) Mice ; Male ; Female ; Animals ; Liver Neoplasms ; Carcinoma, Hepatocellular/genetics ; Bile Acids and Salts ; Mice, Knockout
    Chemical Substances Bile Acids and Salts
    Language English
    Publishing date 2024-01-21
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2819778-1
    ISSN 2352-345X ; 2352-345X
    ISSN (online) 2352-345X
    ISSN 2352-345X
    DOI 10.1016/j.jcmgh.2024.01.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: IL-10 Receptor Neutralization-Induced Colitis in Mice: A Comprehensive Guide.

    Saha, Piu / Golonka, Rachel M / Abokor, Ahmed A / Yeoh, Beng San / Vijay-Kumar, Matam

    Current protocols

    2021  Volume 1, Issue 8, Page(s) e227

    Abstract: Interleukin-10 (IL-10) and its receptor (IL-10R) have been foremost targets to understand inflammatory bowel disease (IBD) pathogenesis. For the past several decades, IL-10-deficient ( ... ...

    Abstract Interleukin-10 (IL-10) and its receptor (IL-10R) have been foremost targets to understand inflammatory bowel disease (IBD) pathogenesis. For the past several decades, IL-10-deficient (Il10
    MeSH term(s) Animals ; Antibodies, Monoclonal ; Colitis ; Crohn Disease ; Humans ; Inflammatory Bowel Diseases ; Mice ; Receptors, Interleukin-10
    Chemical Substances Antibodies, Monoclonal ; Receptors, Interleukin-10
    Language English
    Publishing date 2021-08-16
    Publishing country United States
    Document type Journal Article
    ISSN 2691-1299
    ISSN (online) 2691-1299
    DOI 10.1002/cpz1.227
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Urine-based Detection of Congenital Portosystemic Shunt in C57BL/6 Mice.

    Yeoh, Beng San / Golonka, Rachel M / Saha, Piu / Kandalgaonkar, Mrunmayee R / Tian, Yuan / Osman, Islam / Patterson, Andrew D / Gewirtz, Andrew T / Joe, Bina / Vijay-Kumar, Matam

    Function (Oxford, England)

    2023  Volume 4, Issue 5, Page(s) zqad040

    Abstract: Sporadic occurrence of congenital portosystemic shunt (PSS) at a rate of ∼1 out of 10 among C57BL/6 J mice, which are widely used in biomedical research, results in aberrancies in serologic, metabolic, and physiologic parameters. Therefore, mice with PSS ...

    Abstract Sporadic occurrence of congenital portosystemic shunt (PSS) at a rate of ∼1 out of 10 among C57BL/6 J mice, which are widely used in biomedical research, results in aberrancies in serologic, metabolic, and physiologic parameters. Therefore, mice with PSS should be identified as outliers in research. Accordingly, we sought methods to, reliably and efficiently, identify PSS mice. Serum total bile acids ≥ 40 µm is a
    MeSH term(s) Animals ; Mice ; Portasystemic Shunt, Transjugular Intrahepatic ; Mice, Inbred C57BL ; Portal System/abnormalities ; Vascular Malformations ; Biomarkers
    Chemical Substances Biomarkers
    Language English
    Publishing date 2023-07-28
    Publishing country England
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ISSN 2633-8823
    ISSN (online) 2633-8823
    DOI 10.1093/function/zqad040
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Loss of toll-like receptor 5 potentiates spontaneous hepatocarcinogenesis in farnesoid X receptor-deficient mice.

    Golonka, Rachel M / Yeoh, Beng San / Saha, Piu / Gohara, Amira / Tummala, Ramakumar / Stepkowski, Stanislaw / Tiwari, Amit K / Joe, Bina / Gonzalez, Frank J / Gewirtz, Andrew T / Vijay-Kumar, Matam

    Hepatology communications

    2023  Volume 7, Issue 6

    Abstract: Background: HCC is the most common primary liver cancer and a leading cause of cancer-related mortality. Gut microbiota is a large collection of microbes, predominately bacteria, that harbor the gastrointestinal tract. Changes in gut microbiota that ... ...

    Abstract Background: HCC is the most common primary liver cancer and a leading cause of cancer-related mortality. Gut microbiota is a large collection of microbes, predominately bacteria, that harbor the gastrointestinal tract. Changes in gut microbiota that deviate from the native composition, that is, "dysbiosis," is proposed as a probable diagnostic biomarker and a risk factor for HCC. However, whether gut microbiota dysbiosis is a cause or a consequence of HCC is unknown.
    Methods: To better understand the role of gut microbiota in HCC, mice deficient of toll-like receptor 5 (TLR5, a receptor for bacterial flagellin) as a model of spontaneous gut microbiota dysbiosis were crossed with farnesoid X receptor knockout mice (FxrKO), a genetic model for spontaneous HCC. Male FxrKO/Tlr5KO double knockout (DKO), FxrKO, Tlr5KO, and wild-type (WT) mice were aged to the 16-month HCC time point.
    Results: Compared with FxrKO mice, DKO mice had more severe hepatooncogenesis at the gross, histological, and transcript levels and this was associated with pronounced cholestatic liver injury. The bile acid dysmetabolism in FxrKO mice became more aberrant in the absence of TLR5 due in part to suppression of bile acid secretion and enhanced cholestasis. Out of the 14 enriched taxon signatures seen in the DKO gut microbiota, 50% were dominated by the Proteobacteria phylum with expansion of the gut pathobiont γ-Proteobacteria that is implicated in HCC.
    Conclusions: Collectively, introducing gut microbiota dysbiosis by TLR5 deletion exacerbated hepatocarcinogenesis in the FxrKO mouse model.
    MeSH term(s) Animals ; Male ; Mice ; Bile Acids and Salts ; Carcinogenesis ; Carcinoma, Hepatocellular ; Cholestasis ; Dysbiosis ; Liver Neoplasms ; Mice, Knockout ; Toll-Like Receptor 5/genetics
    Chemical Substances Bile Acids and Salts ; Toll-Like Receptor 5 ; Tlr5 protein, mouse
    Language English
    Publishing date 2023-05-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2471-254X
    ISSN (online) 2471-254X
    DOI 10.1097/HC9.0000000000000166
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Altered nutrient status reprograms host inflammation and metabolic health via gut microbiota.

    Golonka, Rachel M / Xiao, Xia / Abokor, Ahmed A / Joe, Bina / Vijay-Kumar, Matam

    The Journal of nutritional biochemistry

    2020  Volume 80, Page(s) 108360

    Abstract: The metabolism of macro- and micronutrients is a complex and highly regulated biological process. An imbalance in the metabolites and their signaling networks can lead to nonresolving inflammation and consequently to the development of chronic ... ...

    Abstract The metabolism of macro- and micronutrients is a complex and highly regulated biological process. An imbalance in the metabolites and their signaling networks can lead to nonresolving inflammation and consequently to the development of chronic inflammatory-associated diseases. Therefore, identifying the accumulated metabolites and altered pathways during inflammatory disorders would not only serve as "real-time" markers but also help in the development of nutritional therapeutics. In this review, we explore recent research that has delved into elucidating the effects of carbohydrate/calorie restriction, protein malnutrition, lipid emulsions and micronutrient deficiencies on metabolic health and inflammation. Moreover, we describe the integrated stress response in terms of amino acid starvation and lipemia and how this modulates new age diseases such as inflammatory bowel disease and atherosclerosis. Lastly, we explain the latest research on metaflammation and inflammaging. This review focuses on multiple signaling pathways, including, but not limited to, the FGF21-β-hydroxybutryate-NLRP3 axis, the GCN2-eIF2α-ATF4 pathway, the von Hippel-Lindau/hypoxia-inducible transcription factor pathway and the TMAO-PERK-FoxO1 axis. Additionally, throughout the review, we explain how the gut microbiota responds to altered nutrient status and also how antimicrobial peptides generated from nutrient-based signaling pathways can modulate the gut microbiota. Collectively, it must be emphasized that metabolic starvation and inflammation are strongly regulated by both environmental (i.e., nutrition, gut microbiome) and nonenvironmental (i.e., genetics) factors, which can influence the susceptibility to inflammatory disorders.
    MeSH term(s) Anemia, Iron-Deficiency/epidemiology ; Anemia, Iron-Deficiency/metabolism ; Animals ; Diet, Ketogenic/methods ; Dietary Carbohydrates/administration & dosage ; Gastrointestinal Microbiome ; Humans ; Inflammation/epidemiology ; Inflammation/metabolism ; Inflammation/therapy ; Inflammatory Bowel Diseases/epidemiology ; Inflammatory Bowel Diseases/metabolism ; Malnutrition/epidemiology ; Malnutrition/metabolism ; Metabolic Syndrome/epidemiology ; Metabolic Syndrome/metabolism ; Micronutrients/administration & dosage ; Micronutrients/deficiency ; Nutrients/administration & dosage ; Nutritional Status ; Vitamin A Deficiency/epidemiology ; Vitamin A Deficiency/metabolism
    Chemical Substances Dietary Carbohydrates ; Micronutrients
    Language English
    Publishing date 2020-02-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1014929-6
    ISSN 1873-4847 ; 0955-2863
    ISSN (online) 1873-4847
    ISSN 0955-2863
    DOI 10.1016/j.jnutbio.2020.108360
    Database MEDical Literature Analysis and Retrieval System OnLINE

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