Defining the temporal evolution of gut dysbiosis and inflammatory responses leading to hepatocellular carcinoma in Mdr2 −/− mouse model View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2021-04-15

AUTHORS

J. Behary, A. E. Raposo, N. M. L. Amorim, H. Zheng, L. Gong, E. McGovern, J. Chen, K. Liu, J. Beretov, C. Theocharous, M. T. Jackson, J. Seet-Lee, G. W. McCaughan, E. M. El-Omar, A. Zekry

ABSTRACT

BackgroundEmerging evidence implicates the gut microbiome in liver inflammation and hepatocellular carcinoma (HCC) development. We aimed to characterize the temporal evolution of gut dysbiosis, in relation to the phenotype of systemic and hepatic inflammatory responses leading to HCC development. In the present study, Mdr2 −/− mice were used as a model of inflammation-based HCC. Gut microbiome composition and function, in addition to serum LPS, serum cytokines/chemokines and intrahepatic inflammatory genes were measured throughout the course of liver injury until HCC development.ResultsEarly stages of liver injury, inflammation and cirrhosis, were characterized by dysbiosis. Microbiome functional pathways pertaining to gut barrier dysfunction were enriched during the initial phase of liver inflammation and cirrhosis, whilst those supporting lipopolysaccharide (LPS) biosynthesis increased as cirrhosis and HCC ensued. In parallel, serum LPS progressively increased during the course of liver injury, corresponding to a shift towards a systemic Th1/Th17 proinflammatory phenotype. Alongside, the intrahepatic inflammatory gene profile transitioned from a proinflammatory phenotype in the initial phases of liver injury to an immunosuppressed one in HCC. In established HCC, a switch in microbiome function from carbohydrate to amino acid metabolism occurred.ConclusionIn Mdr2 −/− mice, dysbiosis precedes HCC development, with temporal evolution of microbiome function to support gut barrier dysfunction, LPS biosynthesis, and redirection of energy source utilization. A corresponding shift in systemic and intrahepatic inflammatory responses occurred supporting HCC development. These findings support the notion that gut based therapeutic interventions could be beneficial early in the course of liver disease to halt HCC development. More... »

PAGES

113

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s12866-021-02171-9

DOI

http://dx.doi.org/10.1186/s12866-021-02171-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1137217970

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/33858327


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25 schema:description BackgroundEmerging evidence implicates the gut microbiome in liver inflammation and hepatocellular carcinoma (HCC) development. We aimed to characterize the temporal evolution of gut dysbiosis, in relation to the phenotype of systemic and hepatic inflammatory responses leading to HCC development. In the present study, Mdr2 −/− mice were used as a model of inflammation-based HCC. Gut microbiome composition and function, in addition to serum LPS, serum cytokines/chemokines and intrahepatic inflammatory genes were measured throughout the course of liver injury until HCC development.ResultsEarly stages of liver injury, inflammation and cirrhosis, were characterized by dysbiosis. Microbiome functional pathways pertaining to gut barrier dysfunction were enriched during the initial phase of liver inflammation and cirrhosis, whilst those supporting lipopolysaccharide (LPS) biosynthesis increased as cirrhosis and HCC ensued. In parallel, serum LPS progressively increased during the course of liver injury, corresponding to a shift towards a systemic Th1/Th17 proinflammatory phenotype. Alongside, the intrahepatic inflammatory gene profile transitioned from a proinflammatory phenotype in the initial phases of liver injury to an immunosuppressed one in HCC. In established HCC, a switch in microbiome function from carbohydrate to amino acid metabolism occurred.ConclusionIn Mdr2 −/− mice, dysbiosis precedes HCC development, with temporal evolution of microbiome function to support gut barrier dysfunction, LPS biosynthesis, and redirection of energy source utilization. A corresponding shift in systemic and intrahepatic inflammatory responses occurred supporting HCC development. These findings support the notion that gut based therapeutic interventions could be beneficial early in the course of liver disease to halt HCC development.
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31 schema:keywords BackgroundEmerging evidence
32 HCC
33 HCC development
34 LPS
35 LPS biosynthesis
36 Mdr2
37 Th1
38 acid metabolism
39 addition
40 amino acid metabolism
41 barrier dysfunction
42 biosynthesis
43 carbohydrates
44 carcinoma
45 carcinoma development
46 chemokines
47 cirrhosis
48 composition
49 corresponding shift
50 course
51 cytokines/chemokines
52 development
53 disease
54 dysbiosis
55 dysfunction
56 energy source utilization
57 evidence
58 evolution
59 findings
60 function
61 functional pathways
62 gene profiles
63 genes
64 gut
65 gut barrier dysfunction
66 gut dysbiosis
67 gut microbiome
68 gut microbiome composition
69 hepatic inflammatory response
70 hepatocellular carcinoma
71 hepatocellular carcinoma development
72 inflammation
73 inflammatory gene profiles
74 inflammatory genes
75 inflammatory response
76 initial phase
77 injury
78 intervention
79 intrahepatic inflammatory response
80 lipopolysaccharide biosynthesis
81 liver disease
82 liver inflammation
83 liver injury
84 metabolism
85 mice
86 microbiome
87 microbiome composition
88 microbiome function
89 model
90 mouse model
91 notion
92 parallel
93 pathway
94 phase
95 phenotype
96 present study
97 profile
98 proinflammatory phenotype
99 redirection
100 relation
101 response
102 serum LPS
103 serum cytokines/chemokines
104 shift
105 source utilization
106 stage
107 study
108 switch
109 systemic Th1
110 temporal evolution
111 therapeutic interventions
112 utilization
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