Modeling the Role of Peroxisome Proliferator-Activated Receptor γ and MicroRNA-146 in Mucosal Immune Responses to Clostridium difficile
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{"title"=>"Modeling the Role of Peroxisome Proliferator-Activated Receptor γ and MicroRNA-146 in Mucosal Immune Responses to Clostridium difficile", "type"=>"journal", "authors"=>[{"first_name"=>"Monica", "last_name"=>"Viladomiu", "scopus_author_id"=>"42962600000"}, {"first_name"=>"Raquel", "last_name"=>"Hontecillas", "scopus_author_id"=>"6602639316"}, {"first_name"=>"Mireia", "last_name"=>"Pedragosa", "scopus_author_id"=>"55017879700"}, {"first_name"=>"Adria", "last_name"=>"Carbo", "scopus_author_id"=>"36637003700"}, {"first_name"=>"Stefan", "last_name"=>"Hoops", "scopus_author_id"=>"15128967000"}, {"first_name"=>"Pawel", "last_name"=>"Michalak", "scopus_author_id"=>"6603442556"}, {"first_name"=>"Katarzyna", "last_name"=>"Michalak", "scopus_author_id"=>"23985874200"}, {"first_name"=>"Richard L.", "last_name"=>"Guerrant", "scopus_author_id"=>"7101799297"}, {"first_name"=>"James K.", "last_name"=>"Roche", "scopus_author_id"=>"7202267890"}, {"first_name"=>"Cirle A.", "last_name"=>"Warren", "scopus_author_id"=>"23767377200"}, {"first_name"=>"Josep", "last_name"=>"Bassaganya-Riera", "scopus_author_id"=>"6603033549"}], "year"=>2012, "source"=>"PLoS ONE", "identifiers"=>{"sgr"=>"84867423956", "doi"=>"10.1371/journal.pone.0047525", "issn"=>"19326203", "pui"=>"365840889", "isbn"=>"1932-6203 (Electronic)\\r1932-6203 (Linking)", "pmid"=>"23071818", "scopus"=>"2-s2.0-84867423956"}, "id"=>"df4819b2-6b77-3a6d-b625-d57e5a5a8d5d", "abstract"=>"Clostridium difficile is an anaerobic bacterium that has re-emerged as a facultative pathogen and can cause nosocomial diarrhea, colitis or even death. Peroxisome proliferator-activated receptor (PPAR) γ has been implicated in the prevention of inflammation in autoimmune and infectious diseases; however, its role in the immunoregulatory mechanisms modulating host responses to C. difficile and its toxins remains largely unknown. To characterize the role of PPARγ in C. difficile-associated disease (CDAD), immunity and gut pathology, we used a mouse model of C. difficile infection in wild-type and T cell-specific PPARγ null mice. The loss of PPARγ in T cells increased disease activity and colonic inflammatory lesions following C. difficile infection. Colonic expression of IL-17 was upregulated and IL-10 downregulated in colons of T cell-specific PPARγ null mice. Also, both the loss of PPARγ in T cells and C. difficile infection favored Th17 responses in spleen and colonic lamina propria of mice with CDAD. MicroRNA (miRNA)-sequencing analysis and RT-PCR validation indicated that miR-146b was significantly overexpressed and nuclear receptor co-activator 4 (NCOA4) suppressed in colons of C. difficile-infected mice. We next developed a computational model that predicts the upregulation of miR-146b, downregulation of the PPARγ co-activator NCOA4, and PPARγ, leading to upregulation of IL-17. Oral treatment of C. difficile-infected mice with the PPARγ agonist pioglitazone ameliorated colitis and suppressed pro-inflammatory gene expression. In conclusion, our data indicates that miRNA-146b and PPARγ activation may be implicated in the regulation of Th17 responses and colitis in C. difficile-infected mice.", "link"=>"http://www.mendeley.com/research/modeling-role-peroxisome-proliferatoractivated-receptor-%CE%B3-microrna146-mucosal-immune-responses-clost-1", "reader_count"=>28, "reader_count_by_academic_status"=>{"Unspecified"=>1, "Professor > Associate Professor"=>2, "Researcher"=>10, "Student > Doctoral Student"=>1, "Student > Ph. D. Student"=>9, "Student > Postgraduate"=>1, "Other"=>1, "Student > Master"=>3}, "reader_count_by_user_role"=>{"Unspecified"=>1, "Professor > Associate Professor"=>2, "Researcher"=>10, "Student > Doctoral Student"=>1, "Student > Ph. D. Student"=>9, "Student > Postgraduate"=>1, "Other"=>1, "Student > Master"=>3}, "reader_count_by_subject_area"=>{"Engineering"=>1, "Unspecified"=>2, "Environmental Science"=>1, "Biochemistry, Genetics and Molecular Biology"=>4, "Agricultural and Biological Sciences"=>12, "Medicine and Dentistry"=>5, "Immunology and Microbiology"=>3}, "reader_count_by_subdiscipline"=>{"Engineering"=>{"Engineering"=>1}, "Medicine and Dentistry"=>{"Medicine and Dentistry"=>5}, "Immunology and Microbiology"=>{"Immunology and Microbiology"=>3}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>12}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>4}, "Unspecified"=>{"Unspecified"=>2}, "Environmental Science"=>{"Environmental Science"=>1}}, "reader_count_by_country"=>{"Austria"=>1, "United States"=>1, "Ireland"=>2, "Chile"=>1}, "group_count"=>0}

Scopus | Further Information

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/560258"], "description"=>"<p>CellDesigner-based illustration of the Complex Pathway SImulator model of the model for Clostridium difficile immune response (A). The model represents the interaction between <i>C. difficile</i>, miRNA-146, nuclear receptor coactivator 4 (NCOA4), peroxisome proliferator-activated receptor γ (PPAR γ), interleukin 10 (IL-10) and interleukin 17 (IL-17) in Systems Biology Markup Language format. Inhibition is represented in red and activation in green. COPASI steady state scan showing the variation on the species concentrations with increasing computational concentration of <i>C. difficile</i> (B). In silico simulations show how increasing concentrations of <i>C. difficile</i> increase miRNA-146b levels, thus decreasing NCOA4 and PPAR γ. In line with the experimental data, IL-17 expression also increases with the infection.</p>", "links"=>[], "tags"=>["modeling", "mucosal", "responses"], "article_id"=>230740, "categories"=>["Chemistry", "Genetics", "Infectious Diseases", "Immunology"], "users"=>["Monica Viladomiu", "Raquel Hontecillas", "Mireia Pedragosa", "Adria Carbo", "Stefan Hoops", "Pawel Michalak", "Katarzyna Michalak", "Richard L. Guerrant", "James K. Roche", "Cirle A. Warren", "Josep Bassaganya-Riera"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0047525.g004", "stats"=>{"downloads"=>0, "page_views"=>2, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Computational_modeling_of_mucosal_immune_responses_to_Clostridium_difficile_infection_/230740", "title"=>"Computational modeling of mucosal immune responses to <i>Clostridium difficile</i> infection.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-11 00:12:20"}
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  • {"files"=>["https://ndownloader.figshare.com/files/560402"], "description"=>"<p>Representative photomicrographs of colons of uninfected (A and E), infected wild type mice (B and F), infected CD4cre+ mice (C and G) and infected wild-type mice treated orally with pioglitazone (70 mg/kg) (D and H) (n = 8). Original magnification at 40× (top panel) and 100× (bottom panel).</p>", "links"=>[], "tags"=>["cells", "pharmacological", "activation", "colonic", "inflammatory", "lesions"], "article_id"=>230881, "categories"=>["Chemistry", "Genetics", "Infectious Diseases", "Immunology"], "users"=>["Monica Viladomiu", "Raquel Hontecillas", "Mireia Pedragosa", "Adria Carbo", "Stefan Hoops", "Pawel Michalak", "Katarzyna Michalak", "Richard L. Guerrant", "James K. Roche", "Cirle A. Warren", "Josep Bassaganya-Riera"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0047525.g005", "stats"=>{"downloads"=>1, "page_views"=>7, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Impact_of_the_loss_of_PPAR_in_T_cells_and_pharmacological_activation_of_PPAR_colonic_inflammatory_lesions_in_Clostridium_difficile_infected_mice_/230881", "title"=>"Impact of the loss of PPARγ in T cells and pharmacological activation of PPARγ colonic inflammatory lesions in <i>Clostridium difficile</i>-infected mice.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-11 00:14:41"}
  • {"files"=>["https://ndownloader.figshare.com/files/559968"], "description"=>"<p>Ordinary Differential Equations (ODE) triggering activation and inhibition of the different reactions in the model. Briefly, mass action and Hill functions were used to reproduce reaction behaviors <i>in silico</i> based on initial molecule concentrations.</p>", "links"=>[], "tags"=>["controlling"], "article_id"=>230448, "categories"=>["Chemistry", "Genetics", "Infectious Diseases", "Immunology"], "users"=>["Monica Viladomiu", "Raquel Hontecillas", "Mireia Pedragosa", "Adria Carbo", "Stefan Hoops", "Pawel Michalak", "Katarzyna Michalak", "Richard L. Guerrant", "James K. Roche", "Cirle A. Warren", "Josep Bassaganya-Riera"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0047525.g001", "stats"=>{"downloads"=>0, "page_views"=>4, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Equations_controlling_dynamics_of_the_Clostridium_difficile_infection_model_/230448", "title"=>"Equations controlling dynamics of the <i>Clostridium difficile</i> infection model.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-11 00:07:28"}
  • {"files"=>["https://ndownloader.figshare.com/files/299619", "https://ndownloader.figshare.com/files/299670", "https://ndownloader.figshare.com/files/299725", "https://ndownloader.figshare.com/files/299757", "https://ndownloader.figshare.com/files/299798"], "description"=>"<div><p><em>Clostridium difficile</em> is an anaerobic bacterium that has re-emerged as a facultative pathogen and can cause nosocomial diarrhea, colitis or even death. Peroxisome proliferator-activated receptor (PPAR) γ has been implicated in the prevention of inflammation in autoimmune and infectious diseases; however, its role in the immunoregulatory mechanisms modulating host responses to <em>C. difficile</em> and its toxins remains largely unknown. To characterize the role of PPARγ in <em>C. difficile</em>-associated disease (CDAD), immunity and gut pathology, we used a mouse model of <em>C. difficile</em> infection in wild-type and T cell-specific PPARγ null mice. The loss of PPARγ in T cells increased disease activity and colonic inflammatory lesions following <em>C. difficile</em> infection. Colonic expression of IL-17 was upregulated and IL-10 downregulated in colons of T cell-specific PPARγ null mice. Also, both the loss of PPARγ in T cells and <em>C. difficile</em> infection favored Th17 responses in spleen and colonic lamina propria of mice with CDAD. MicroRNA (miRNA)-sequencing analysis and RT-PCR validation indicated that miR-146b was significantly overexpressed and nuclear receptor co-activator 4 (NCOA4) suppressed in colons of <em>C. difficile</em>-infected mice. We next developed a computational model that predicts the upregulation of miR-146b, downregulation of the PPARγ co-activator NCOA4, and PPARγ, leading to upregulation of IL-17. Oral treatment of <em>C. difficile</em>-infected mice with the PPARγ agonist pioglitazone ameliorated colitis and suppressed pro-inflammatory gene expression. In conclusion, our data indicates that miRNA-146b and PPARγ activation may be implicated in the regulation of Th17 responses and colitis in <em>C. difficile</em>-infected mice.</p> </div>", "links"=>[], "tags"=>["modeling", "peroxisome", "proliferator-activated", "receptor", "microrna-146", "mucosal", "responses"], "article_id"=>119068, "categories"=>["Cancer", "Chemistry", "Genetics", "Immunology"], "users"=>["Monica Viladomiu", "Raquel Hontecillas", "Mireia Pedragosa", "Adria Carbo", "Stefan Hoops", "Pawel Michalak", "Katarzyna Michalak", "Richard L. Guerrant", "James K. Roche", "Cirle A. Warren", "Josep Bassaganya-Riera"], "doi"=>["https://dx.doi.org/10.1371/journal.pone.0047525.s001", "https://dx.doi.org/10.1371/journal.pone.0047525.s002", "https://dx.doi.org/10.1371/journal.pone.0047525.s003", "https://dx.doi.org/10.1371/journal.pone.0047525.s004", "https://dx.doi.org/10.1371/journal.pone.0047525.s005"], "stats"=>{"downloads"=>2, "page_views"=>10, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/Modeling_the_Role_of_Peroxisome_Proliferator_Activated_Receptor_and_MicroRNA_146_in_Mucosal_Immune_Responses_to_Clostridium_difficile_/119068", "title"=>"Modeling the Role of Peroxisome Proliferator-Activated Receptor γ and MicroRNA-146 in Mucosal Immune Responses to <em>Clostridium difficile</em>", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2012-10-11 02:31:08"}
  • {"files"=>["https://ndownloader.figshare.com/files/560523"], "description"=>"<p>Colonic expression of interleukin 10 (IL-10) (A), interleukin 17 (IL-17) (B), monocyte chemoattractant protein 1 (MCP-1) (C) and tumor necrosis factor (TNF-α) (D) were assessed by real-time quantitative RT-PCR in wild type and T cell PPARγ null mice infected with <i>C. difficile</i> (n = 8). Data are represented as mean ± standard error. Points with an asterisk are significantly different when compared to the wild type control group (<i>P</i><0.05).</p>", "links"=>[], "tags"=>["cells", "regulates", "colonic", "cytokine", "mice", "infected"], "article_id"=>231004, "categories"=>["Chemistry", "Genetics", "Infectious Diseases", "Immunology"], "users"=>["Monica Viladomiu", "Raquel Hontecillas", "Mireia Pedragosa", "Adria Carbo", "Stefan Hoops", "Pawel Michalak", "Katarzyna Michalak", "Richard L. Guerrant", "James K. Roche", "Cirle A. Warren", "Josep Bassaganya-Riera"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0047525.g006", "stats"=>{"downloads"=>0, "page_views"=>2, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_The_loss_of_PPAR_in_T_cells_regulates_colonic_cytokine_expression_of_mice_infected_with_Clostridium_difficile_/231004", "title"=>"The loss of PPARγ in T cells regulates colonic cytokine expression of mice infected with <i>Clostridium difficile</i>.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-11 00:16:44"}
  • {"files"=>["https://ndownloader.figshare.com/files/560091"], "description"=>"<p>Colonic expression of monocyte chemotactic Protein 1 (MCP-1) (A), interleukin 6 (IL-6) (B), interleukin 17 (IL-17) (C) and interleukin 1β (IL-1β) (D were assessed by real-time quantitative RT-PCR in mice infected with <i>C. difficile</i> (n = 10). Data are represented as mean ± standard error. Points with an asterisk are significantly different when compared to the control group (<i>P</i><0.05).</p>", "links"=>[], "tags"=>["modulates", "colonic"], "article_id"=>230575, "categories"=>["Chemistry", "Genetics", "Infectious Diseases", "Immunology"], "users"=>["Monica Viladomiu", "Raquel Hontecillas", "Mireia Pedragosa", "Adria Carbo", "Stefan Hoops", "Pawel Michalak", "Katarzyna Michalak", "Richard L. Guerrant", "James K. Roche", "Cirle A. Warren", "Josep Bassaganya-Riera"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0047525.g002", "stats"=>{"downloads"=>1, "page_views"=>5, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Clostridium_difficile_infection_modulates_colonic_gene_expression_in_mice_/230575", "title"=>"<i>Clostridium difficile</i> infection modulates colonic gene expression in mice.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-11 00:09:35"}
  • {"files"=>["https://ndownloader.figshare.com/files/560180"], "description"=>"<p>Colonic expression of miRNA-146b (A) as well as NCOA4 (B), CD36 (C) and GLUT4 (D) were assessed by real-time quantitative RT-PCR in mice infected with <i>C. difficile</i> (n = 10). Data are represented as mean ± standard error. Points with an asterisk are significantly different when compared to the control group (<i>P</i><0.05).</p>", "links"=>[], "tags"=>["colonic", "mir-146b", "genes", "cd36", "glut4", "mrna"], "article_id"=>230657, "categories"=>["Chemistry", "Genetics", "Infectious Diseases", "Immunology"], "users"=>["Monica Viladomiu", "Raquel Hontecillas", "Mireia Pedragosa", "Adria Carbo", "Stefan Hoops", "Pawel Michalak", "Katarzyna Michalak", "Richard L. Guerrant", "James K. Roche", "Cirle A. Warren", "Josep Bassaganya-Riera"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0047525.g003", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Effect_of_Clostridium_difficile_infection_on_the_colonic_expression_of_miR_146b_and_target_genes_NCOA4_CD36_and_GLUT4_mRNA_in_mice_/230657", "title"=>"Effect of <i>Clostridium difficile</i> infection on the colonic expression of miR-146b and target genes NCOA4, CD36 and GLUT4 mRNA in mice.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-11 00:10:57"}
  • {"files"=>["https://ndownloader.figshare.com/files/560588"], "description"=>"<p>Splenocytes and lamina propria lymphocytes from wild type and T cell PPARγnull mice infected with <i>C. difficile</i> (n = 6) were immunophenotyped to identify immune cell subsets by flow cytometry. Data are represented as mean ± standard error. Points with an asterisk are significantly different when compared to the control group (<i>P</i><0.05).</p>", "links"=>[], "tags"=>["cells", "enhances", "th17", "responses", "spleen", "lamina", "propria"], "article_id"=>231071, "categories"=>["Chemistry", "Genetics", "Infectious Diseases", "Immunology"], "users"=>["Monica Viladomiu", "Raquel Hontecillas", "Mireia Pedragosa", "Adria Carbo", "Stefan Hoops", "Pawel Michalak", "Katarzyna Michalak", "Richard L. Guerrant", "James K. Roche", "Cirle A. Warren", "Josep Bassaganya-Riera"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0047525.g007", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_The_loss_of_PPAR_in_T_cells_and_Clostridium_difficile_infection_enhances_Th17_responses_in_spleen_and_lamina_propria_of_mice_/231071", "title"=>"The loss of PPARγ in T cells and <i>Clostridium difficile</i> infection enhances Th17 responses in spleen and lamina propria of mice.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-11 00:17:51"}

PMC Usage Stats | Further Information

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Relative Metric

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