Differential colitis susceptibility of Th1- and Th2-biased mice: A multi-omics approach
The health and economic burden of colitis is increasing globally. Understanding the role of host genetics and metagenomics is essential to establish the molecular basis of colitis pathogenesis. In the present study, we have used a common composite dose of DSS to compare the differential disease seve...
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description | The health and economic burden of colitis is increasing globally. Understanding the role of host genetics and metagenomics is essential to establish the molecular basis of colitis pathogenesis. In the present study, we have used a common composite dose of DSS to compare the differential disease severity response in C57BL/6 (Th1 biased) and BALB/c (Th2 biased) mice with zero mortality rates. We employed multi-omics approaches and developed a newer vector analysis approach to understand the molecular basis of the disease pathogenesis. In the current report, comparative transcriptomics, metabonomics, and metagenomics analyses revealed that the Th1 background of C57BL/6 induced intense inflammatory responses throughout the treatment period. On the contrary, the Th2 background of BALB/c resisted severe inflammatory responses by modulating the host's inflammatory, metabolic, and gut microbial profile. The multi-omics approach also helped us discover some unique metabolic and microbial markers associated with the disease severity. These biomarkers could be used in diagnostics. |
doi_str_mv | 10.1371/journal.pone.0264400 |
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Understanding the role of host genetics and metagenomics is essential to establish the molecular basis of colitis pathogenesis. In the present study, we have used a common composite dose of DSS to compare the differential disease severity response in C57BL/6 (Th1 biased) and BALB/c (Th2 biased) mice with zero mortality rates. We employed multi-omics approaches and developed a newer vector analysis approach to understand the molecular basis of the disease pathogenesis. In the current report, comparative transcriptomics, metabonomics, and metagenomics analyses revealed that the Th1 background of C57BL/6 induced intense inflammatory responses throughout the treatment period. On the contrary, the Th2 background of BALB/c resisted severe inflammatory responses by modulating the host's inflammatory, metabolic, and gut microbial profile. The multi-omics approach also helped us discover some unique metabolic and microbial markers associated with the disease severity. These biomarkers could be used in diagnostics.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0264400</identifier><identifier>PMID: 35263357</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Bhabha, Homi K ; Bias ; Biological markers ; Biology and Life Sciences ; Biomarkers ; Colitis ; Colitis - chemically induced ; Colitis - genetics ; Colitis - pathology ; Colon ; Disease ; Drinking water ; Experiments ; Gene expression ; Genetic aspects ; Genetics ; Genomics ; Homeostasis ; Immunology ; Inflammation ; Inflammatory bowel disease ; Life sciences ; Lymphocytes T ; Medical research ; Medicine and Health Sciences ; Medicine, Experimental ; Metabolism ; Metabolites ; Metabolomics ; Metagenomics ; Methods ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Microorganisms ; Mortality ; Pathogenesis ; Pathogens ; Risk factors ; Science education ; Th1 Cells - pathology ; Th2 Cells - pathology ; Transcriptomics ; Vector analysis</subject><ispartof>PloS one, 2022-03, Vol.17 (3), p.e0264400-e0264400</ispartof><rights>COPYRIGHT 2022 Public Library of Science</rights><rights>2022 Mukhopadhyay et al. 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These biomarkers could be used in diagnostics.</description><subject>Animals</subject><subject>Bhabha, Homi K</subject><subject>Bias</subject><subject>Biological markers</subject><subject>Biology and Life Sciences</subject><subject>Biomarkers</subject><subject>Colitis</subject><subject>Colitis - chemically induced</subject><subject>Colitis - genetics</subject><subject>Colitis - pathology</subject><subject>Colon</subject><subject>Disease</subject><subject>Drinking water</subject><subject>Experiments</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Genetics</subject><subject>Genomics</subject><subject>Homeostasis</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Inflammatory bowel disease</subject><subject>Life sciences</subject><subject>Lymphocytes T</subject><subject>Medical research</subject><subject>Medicine and Health Sciences</subject><subject>Medicine, Experimental</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Metabolomics</subject><subject>Metagenomics</subject><subject>Methods</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C57BL</subject><subject>Microorganisms</subject><subject>Mortality</subject><subject>Pathogenesis</subject><subject>Pathogens</subject><subject>Risk factors</subject><subject>Science education</subject><subject>Th1 Cells - 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Understanding the role of host genetics and metagenomics is essential to establish the molecular basis of colitis pathogenesis. In the present study, we have used a common composite dose of DSS to compare the differential disease severity response in C57BL/6 (Th1 biased) and BALB/c (Th2 biased) mice with zero mortality rates. We employed multi-omics approaches and developed a newer vector analysis approach to understand the molecular basis of the disease pathogenesis. In the current report, comparative transcriptomics, metabonomics, and metagenomics analyses revealed that the Th1 background of C57BL/6 induced intense inflammatory responses throughout the treatment period. On the contrary, the Th2 background of BALB/c resisted severe inflammatory responses by modulating the host's inflammatory, metabolic, and gut microbial profile. The multi-omics approach also helped us discover some unique metabolic and microbial markers associated with the disease severity. These biomarkers could be used in diagnostics.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>35263357</pmid><doi>10.1371/journal.pone.0264400</doi><orcidid>https://orcid.org/0000-0002-6963-9879</orcidid><orcidid>https://orcid.org/0000-0003-4927-7812</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animals Bhabha, Homi K Bias Biological markers Biology and Life Sciences Biomarkers Colitis Colitis - chemically induced Colitis - genetics Colitis - pathology Colon Disease Drinking water Experiments Gene expression Genetic aspects Genetics Genomics Homeostasis Immunology Inflammation Inflammatory bowel disease Life sciences Lymphocytes T Medical research Medicine and Health Sciences Medicine, Experimental Metabolism Metabolites Metabolomics Metagenomics Methods Mice Mice, Inbred BALB C Mice, Inbred C57BL Microorganisms Mortality Pathogenesis Pathogens Risk factors Science education Th1 Cells - pathology Th2 Cells - pathology Transcriptomics Vector analysis |
title | Differential colitis susceptibility of Th1- and Th2-biased mice: A multi-omics approach |
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