The Host Protein Calprotectin Modulates the Helicobacter pylori cag Type IV Secretion System via Zinc Sequestration
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{"title"=>"The Host Protein Calprotectin Modulates the Helicobacter pylori cag Type IV Secretion System via Zinc Sequestration", "type"=>"journal", "authors"=>[{"first_name"=>"Jennifer A.", "last_name"=>"Gaddy", "scopus_author_id"=>"7004461741"}, {"first_name"=>"Jana N.", "last_name"=>"Radin", "scopus_author_id"=>"55791145900"}, {"first_name"=>"John T.", "last_name"=>"Loh", "scopus_author_id"=>"7005450274"}, {"first_name"=>"M. Blanca", "last_name"=>"Piazuelo", "scopus_author_id"=>"6506196095"}, {"first_name"=>"Thomas E.", "last_name"=>"Kehl-Fie", "scopus_author_id"=>"14035923700"}, {"first_name"=>"Alberto G.", "last_name"=>"Delgado", "scopus_author_id"=>"7201675988"}, {"first_name"=>"Florin T.", "last_name"=>"Ilca", "scopus_author_id"=>"56398508700"}, {"first_name"=>"Richard M.", "last_name"=>"Peek", "scopus_author_id"=>"7101631818"}, {"first_name"=>"Timothy L.", "last_name"=>"Cover", "scopus_author_id"=>"7102102744"}, {"first_name"=>"Walter J.", "last_name"=>"Chazin", "scopus_author_id"=>"7006727022"}, {"first_name"=>"Eric P.", "last_name"=>"Skaar", "scopus_author_id"=>"6701410252"}, {"first_name"=>"Holly M.", "last_name"=>"Scott Algood", "scopus_author_id"=>"6506840903"}], "year"=>2014, "source"=>"PLoS Pathogens", "identifiers"=>{"issn"=>"15537374", "pmid"=>"25330071", "pui"=>"600311124", "scopus"=>"2-s2.0-84908325882", "doi"=>"10.1371/journal.ppat.1004450", "sgr"=>"84908325882"}, "id"=>"1ebad91b-2402-35f6-8201-f5771e2f5948", "abstract"=>"Transition metals are necessary for all forms of life including microorganisms, evidenced by the fact that 30% of all proteins are predicted to interact with a metal cofactor. Through a process termed nutritional immunity, the host actively sequesters essential nutrient metals away from invading pathogenic bacteria. Neutrophils participate in this process by producing several metal chelating proteins, including lactoferrin and calprotectin (CP). As neutrophils are an important component of the inflammatory response directed against the bacterium Helicobacter pylori, a major risk factor for gastric cancer, it was hypothesized that CP plays a role in the host response to H. pylori. Utilizing a murine model of H. pylori infection and gastric epithelial cell co-cultures, the role CP plays in modifying H. pylori -host interactions and the function of the cag Type IV Secretion System (cag T4SS) was investigated. This study indicates elevated gastric levels of CP are associated with the infiltration of neutrophils to the H. pylori-infected tissue. When infected with an H. pylori strain harboring a functional cag T4SS, calprotectin-deficient mice exhibited decreased bacterial burdens and a trend toward increased cag T4SS -dependent inflammation compared to wild-type mice. In vitro data demonstrate that culturing H. pylori with sub-inhibitory doses of CP reduces the activity of the cag T4SS and the biogenesis of cag T4SS-associated pili in a zinc-dependent fashion. Taken together, these data indicate that zinc homeostasis plays a role in regulating the proinflammatory activity of the cag T4SS.", "link"=>"http://www.mendeley.com/research/host-protein-calprotectin-modulates-helicobacter-pylori-cag-type-iv-secretion-system-via-zinc-seques", "reader_count"=>10, "reader_count_by_academic_status"=>{"Professor > Associate Professor"=>1, "Researcher"=>2, "Student > Ph. D. Student"=>3, "Student > Master"=>1, "Student > Bachelor"=>2, "Professor"=>1}, "reader_count_by_user_role"=>{"Professor > Associate Professor"=>1, "Researcher"=>2, "Student > Ph. D. Student"=>3, "Student > Master"=>1, "Student > Bachelor"=>2, "Professor"=>1}, "reader_count_by_subject_area"=>{"Agricultural and Biological Sciences"=>6, "Chemistry"=>2, "Immunology and Microbiology"=>2}, "reader_count_by_subdiscipline"=>{"Chemistry"=>{"Chemistry"=>2}, "Immunology and Microbiology"=>{"Immunology and Microbiology"=>2}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>6}}, "reader_count_by_country"=>{"United Kingdom"=>1}, "group_count"=>0}

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/1721479"], "description"=>"<p>High resolution FE-SEM analysis of <i>H. pylori</i> co-cultured with AGS human gastric epithelial cells. Bacteria were cultured in medium alone, or medium supplemented with wild-type CP (200 µg/mL) or mutant forms of CP that lack S1, S2 or both metal-binding sites (DS) at 200 µg/mL, 600 µg/mL, or 1200 µg/mL. Pilus formation was also examined using the synthetic zinc chelator, TPEN. Supplementation with 100 µM zinc chloride (+Zinc) restored T4SS pilus formation to levels comparable to medium alone in all samples. Arrows indicate <i>cag</i> T4SS pili formed at the host-pathogen interface. Magnification bars indicate 1 µm. Dot plot graphs indicate enumeration of pili per bacterial cell as quantified from representative micrographs derived from three biological replicates, and at least 20 fields from each replicate. Asterisks indicate *<i>p</i><0.05, ** <i>p</i><0.01, *** <i>p</i><0.001, **** <i>p</i><0.0001, compared to first condition on each graph (Student's <i>t</i> test).</p>", "links"=>[], "tags"=>["cag Type IV Secretion System", "Host Protein Calprotectin Modulates", "bacterium Helicobacter pylori", "Zinc Sequestration Transition metals", "role CP", "host interactions", "zinc homeostasis", "murine model", "pylori infection", "proinflammatory activity", "pylori strain", "metal chelating proteins", "culturing H", "cag T 4SS", "cag T 4SS pili", "Helicobacter pylori cag Type IV Secretion System", "risk factor", "host response", "metal cofactor"], "article_id"=>1207646, "categories"=>["Biological Sciences"], "users"=>["Jennifer A. Gaddy", "Jana N. Radin", "John T. Loh", "M. Blanca Piazuelo", "Thomas E. Kehl-Fie", "Alberto G. Delgado", "Florin T. Ilca", "Richard M. Peek", "Timothy L. Cover", "Walter J. Chazin", "Eric P. Skaar", "Holly M. Scott Algood"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1004450.g006", "stats"=>{"downloads"=>6, "page_views"=>96, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_H_pylori_cag_T4SS_pilus_production_is_modulated_by_the_zinc_sequestration_activity_of_calprotectin_/1207646", "title"=>"<i>H. pylori cag</i> T4SS pilus production is modulated by the zinc sequestration activity of calprotectin.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-16 04:27:08"}
  • {"files"=>["https://ndownloader.figshare.com/files/1721461"], "description"=>"<p>A) WT <i>H. pylori</i> were cultured for 24 hours in medium alone or medium supplemented with 50 µM zinc chloride plus 50 µM manganese chloride (Medium+Zinc+Manganese) and with increasing concentrations of CP. B) WT <i>H. pylori</i> were cultured for 24 hours in medium alone or medium supplemented with 100 µM zinc chloride (Medium+Zinc) and with increasing concentrations of TPEN, a synthetic zinc chelator. Bacterial growth was evaluated by spectrophotometric OD<sub>600</sub> reading. The percent growth was determined by comparing the OD<sub>600</sub> reading of each culture to controls grown in medium alone. *<i>p</i><0.05, **p<0.01, ***p<0.001, Student's <i>t</i>-test, n = 3 biological replicates.</p>", "links"=>[], "tags"=>["cag Type IV Secretion System", "Host Protein Calprotectin Modulates", "bacterium Helicobacter pylori", "Zinc Sequestration Transition metals", "role CP", "host interactions", "zinc homeostasis", "murine model", "pylori infection", "proinflammatory activity", "pylori strain", "metal chelating proteins", "culturing H", "cag T 4SS", "cag T 4SS pili", "Helicobacter pylori cag Type IV Secretion System", "risk factor", "host response", "metal cofactor"], "article_id"=>1207628, "categories"=>["Biological Sciences"], "users"=>["Jennifer A. Gaddy", "Jana N. Radin", "John T. Loh", "M. Blanca Piazuelo", "Thomas E. Kehl-Fie", "Alberto G. Delgado", "Florin T. Ilca", "Richard M. Peek", "Timothy L. Cover", "Walter J. Chazin", "Eric P. Skaar", "Holly M. Scott Algood"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1004450.g002", "stats"=>{"downloads"=>1, "page_views"=>18, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Inhibition_of_H_pylori_growth_in_vitro_by_CP_or_TPEN_is_dose_dependent_/1207628", "title"=>"Inhibition of <i>H. pylori</i> growth <i>in vitro</i> by CP or TPEN is dose dependent.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-16 04:27:08"}
  • {"files"=>["https://ndownloader.figshare.com/files/1721452"], "description"=>"<p>A) <i>s100a8/s100a9</i> transcript abundance in RNA extracted from C57BL/6 mice infected with <i>H. pylori</i> PMSS1 or SS1 for 1, 2, or 3 months relative to uninfected animals as determined by real-time RT-PCR analysis. Points indicate mean relative units of transcript abundance +/− SEM (levels of <i>s100a8</i> in PMSS1-infected mice compared to uninfected mice; 1 mo <i>p</i> = 0.0511; 2 mo <i>p</i> = 0.0432; 3 mo <i>p</i> = 0.0127; levels of <i>s100a8</i> in SS1-infected mice compared to uninfected mice at 2 mo <i>p</i> = 0.0623 Student's <i>t</i> test). (B) Inflammation scores of <i>H. pylori</i> infected mice at 1, 2, and 3 months post infection. (C) <i>s100a8/s100a9</i> transcript abundance in RNA extracted from gastric biopsies derived from human patients, which were either <i>H. pylori</i>-positive or <i>H. pylori</i>-negative (<i>s100a8 p</i> = 0.15; <i>s100a9</i> *<i>p</i> = 0.05). Bars indicate mean relative units of transcript abundance +/− SEM. Each experimental group represents≥5 individuals (mice or human samples). D) Gastric samples derived from <i>H. pylori</i> PMSS1-infected WT mice or SS1-infected WT mice at 2 months post-infection were analyzed via immunohistochemistry using a polyclonal antibody to S100A9 (scale bars are 50 microns). E) Real-time RT-PCR was performed on gastric tissue to quantify <i>s100a8</i> and <i>s100a9</i> transcript abundance from WT (C57BL/6 mice) and IL-17RA-/- mice infected with PMSS1. Data represent relative units of transcript abundance +/− SEM in WT mice and IL-17RA-/- mice, *<i>p</i> = 0.0169 and <i>p</i> = 0.0143, respectively.</p>", "links"=>[], "tags"=>["cag Type IV Secretion System", "Host Protein Calprotectin Modulates", "bacterium Helicobacter pylori", "Zinc Sequestration Transition metals", "role CP", "host interactions", "zinc homeostasis", "murine model", "pylori infection", "proinflammatory activity", "pylori strain", "metal chelating proteins", "culturing H", "cag T 4SS", "cag T 4SS pili", "Helicobacter pylori cag Type IV Secretion System", "risk factor", "host response", "metal cofactor"], "article_id"=>1207625, "categories"=>["Biological Sciences"], "users"=>["Jennifer A. Gaddy", "Jana N. Radin", "John T. Loh", "M. Blanca Piazuelo", "Thomas E. Kehl-Fie", "Alberto G. Delgado", "Florin T. Ilca", "Richard M. Peek", "Timothy L. Cover", "Walter J. Chazin", "Eric P. Skaar", "Holly M. Scott Algood"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1004450.g001", "stats"=>{"downloads"=>0, "page_views"=>28, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Host_CP_S100A8_A9_is_elevated_in_H_pylori_infected_stomach_tissue_/1207625", "title"=>"Host CP (S100A8/A9) is elevated in <i>H. pylori</i> infected stomach tissue.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-16 04:27:08"}
  • {"files"=>["https://ndownloader.figshare.com/files/1721469"], "description"=>"<p>Analysis of CagA phosphorylation upon translocation into AGS cells and total CagA. A) Prior to co-culture with AGS cells, bacteria were grown in medium alone or medium supplemented with various additives (100 µM zinc chloride, or with CP (200 µg/mL), or the synthetic zinc chelator TPEN, in the presence or absence of 100 µM zinc chloride). B) Bacteria were grown in the presence of mutant forms of CP that lack S1 or S2 at 200 µg/mL (+) or 600 µg/mL (++) alone or in the presence of 100 µM zinc chloride prior to co-culture with AGS cells. C) Percentage total CagA that is phosphorylated was quantified by densitometry on immunoblots (p-TYR CagA/total CagA×100). Immunoblotting with anti-<i>H. pylori</i> was also performed as a loading control, as described previously <a href=\"http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004450#ppat.1004450-Loh1\" target=\"_blank\">[58]</a>. Conditions of zinc sequestration repressed the CagA translocation activity of the T4SS. Supplementation with 100 µM zinc chloride (zinc) restored CagA phosphorylation to levels comparable to medium alone in all samples. Bars represent the mean +/− SEM per each group (n = 3–5 biological replicates). *<i>p</i><0.05, **<i>p</i><0.01, compared to medium alone (Student's <i>t</i> test).</p>", "links"=>[], "tags"=>["cag Type IV Secretion System", "Host Protein Calprotectin Modulates", "bacterium Helicobacter pylori", "Zinc Sequestration Transition metals", "role CP", "host interactions", "zinc homeostasis", "murine model", "pylori infection", "proinflammatory activity", "pylori strain", "metal chelating proteins", "culturing H", "cag T 4SS", "cag T 4SS pili", "Helicobacter pylori cag Type IV Secretion System", "risk factor", "host response", "metal cofactor"], "article_id"=>1207636, "categories"=>["Biological Sciences"], "users"=>["Jennifer A. Gaddy", "Jana N. Radin", "John T. Loh", "M. Blanca Piazuelo", "Thomas E. Kehl-Fie", "Alberto G. Delgado", "Florin T. Ilca", "Richard M. Peek", "Timothy L. Cover", "Walter J. Chazin", "Eric P. Skaar", "Holly M. Scott Algood"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1004450.g004", "stats"=>{"downloads"=>0, "page_views"=>12, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Calprotectin_inhibits_CagA_translocation_into_gastric_epithelial_cells_/1207636", "title"=>"Calprotectin inhibits CagA translocation into gastric epithelial cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-16 04:27:08"}
  • {"files"=>["https://ndownloader.figshare.com/files/1721483"], "description"=>"<p>In the presence of available zinc, <i>H. pylori</i> elaborates a functional <i>cag</i> T4SS and translocates CagA into host epithelial cells, resulting in increased NFκB activation and IL-8 secretion. The chemokine IL-8 recruits neutrophils to the site of infection, increasing the amount of CP present. CP sequesters the nutrient zinc away from the bacterial cell, downregulating the activity of the <i>cag</i> T4SS, and thereby decreasing the translocation of CagA, NFκB activation and IL-8 secretion.</p>", "links"=>[], "tags"=>["cag Type IV Secretion System", "Host Protein Calprotectin Modulates", "bacterium Helicobacter pylori", "Zinc Sequestration Transition metals", "role CP", "host interactions", "zinc homeostasis", "murine model", "pylori infection", "proinflammatory activity", "pylori strain", "metal chelating proteins", "culturing H", "cag T 4SS", "cag T 4SS pili", "Helicobacter pylori cag Type IV Secretion System", "risk factor", "host response", "metal cofactor"], "article_id"=>1207650, "categories"=>["Biological Sciences"], "users"=>["Jennifer A. Gaddy", "Jana N. Radin", "John T. Loh", "M. Blanca Piazuelo", "Thomas E. Kehl-Fie", "Alberto G. Delgado", "Florin T. Ilca", "Richard M. Peek", "Timothy L. Cover", "Walter J. Chazin", "Eric P. Skaar", "Holly M. Scott Algood"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1004450.g007", "stats"=>{"downloads"=>4, "page_views"=>396, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Model_of_H_pylori_cag_T4SS_regulation_in_response_to_neutrophil_recruitment_and_deposition_of_calprotectin_at_the_site_of_infection_/1207650", "title"=>"Model of <i>H. pylori cag</i> T4SS regulation in response to neutrophil recruitment and deposition of calprotectin at the site of infection.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-16 04:27:08"}
  • {"files"=>["https://ndownloader.figshare.com/files/1721463"], "description"=>"<p>WT mice and calprotectin-deficient mice (A9-/-) were infected with either WT <i>H. pylori</i> strain SS1, PMSS1 or an isogenic mutant with an inactivation of the <i>cagE</i> locus, and sacrificed 6 weeks post-infection. A) Bacterial burden was higher in A9-/- mice compared to WT mice in groups infected with WT <i>H. pylori</i> SS1 strain. B) There is no significant difference in inflammation in A9-/- mice compared to WT mice in <i>H. pylori</i> SS1 infected mice. C) Bacterial burden was lower in A9-/- mice compared to WT mice in groups infected with WT <i>H. pylori</i> PMSS1 strain (<i>p</i> = 0.0325). D) Histological analyses of inflammation demonstrate that PMSS1 infected A9-/- mice had significantly higher inflammation than PMSS1 infected WT mice. Statistical analyses were performed for inflammation scores using Mann Whitney U test. E) Bacterial burden was diminished in A9-/- mice compared to WT mice in groups infected with WT <i>H. pylori</i> PMSS1 strain (<i>p</i> = 0.038), but not in groups infected with the PMSS1 <i>cagE</i> mutant (<i>p</i> = 0.4699). Data represent the mean +/− SEM per each group (n = 8–9 animals per group). Statistical analyses were performed for bacterial burden using Student's <i>t</i> test. *<i>p</i><0.05.</p>", "links"=>[], "tags"=>["cag Type IV Secretion System", "Host Protein Calprotectin Modulates", "bacterium Helicobacter pylori", "Zinc Sequestration Transition metals", "role CP", "host interactions", "zinc homeostasis", "murine model", "pylori infection", "proinflammatory activity", "pylori strain", "metal chelating proteins", "culturing H", "cag T 4SS", "cag T 4SS pili", "Helicobacter pylori cag Type IV Secretion System", "risk factor", "host response", "metal cofactor"], "article_id"=>1207630, "categories"=>["Biological Sciences"], "users"=>["Jennifer A. Gaddy", "Jana N. Radin", "John T. Loh", "M. Blanca Piazuelo", "Thomas E. Kehl-Fie", "Alberto G. Delgado", "Florin T. Ilca", "Richard M. Peek", "Timothy L. Cover", "Walter J. Chazin", "Eric P. Skaar", "Holly M. Scott Algood"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1004450.g003", "stats"=>{"downloads"=>0, "page_views"=>25, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_The_presence_of_calprotectin_increases_bacterial_burden_and_reduces_inflammation_in_WT_mice_in_a_cag_T4SS_dependent_manner_/1207630", "title"=>"The presence of calprotectin increases bacterial burden and reduces inflammation in WT mice in a <i>cag</i> T4SS-dependent manner.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-16 04:27:08"}
  • {"files"=>["https://ndownloader.figshare.com/files/1721472"], "description"=>"<p>Bacteria were grown in medium alone or medium supplemented with the synthetic zinc chelator TPEN (TPEN), wild-type CP (CP) at 200 µg/mL, or mutant forms of CP [ΔS1 or ΔS2 at 200 µg/mL or 600 µg/mL, or a double-site mutant (DS) at 1200 µg/mL] alone or in the presence of 100 µM zinc chloride (+Zinc) prior to co-culture with AGS cells. A) NFκB activation in human gastric epithelial cells co-cultured with <i>H. pylori</i> for 4 hours was quantified using a luciferase reporter assay. B) IL-8 secretion by human gastric epithelial cells was quantified using an IL-8 ELISA assay. Bars represent the mean +/− SEM per each group (n = 3–5 biological replicates). Asterisks indicate *<i>p</i><0.05, ** <i>p</i><0.01, *** <i>p</i><0.001, **** <i>p</i><0.0001, compared to medium alone (Student's <i>t</i> test).</p>", "links"=>[], "tags"=>["cag Type IV Secretion System", "Host Protein Calprotectin Modulates", "bacterium Helicobacter pylori", "Zinc Sequestration Transition metals", "role CP", "host interactions", "zinc homeostasis", "murine model", "pylori infection", "proinflammatory activity", "pylori strain", "metal chelating proteins", "culturing H", "cag T 4SS", "cag T 4SS pili", "Helicobacter pylori cag Type IV Secretion System", "risk factor", "host response", "metal cofactor"], "article_id"=>1207639, "categories"=>["Biological Sciences"], "users"=>["Jennifer A. Gaddy", "Jana N. Radin", "John T. Loh", "M. Blanca Piazuelo", "Thomas E. Kehl-Fie", "Alberto G. Delgado", "Florin T. Ilca", "Richard M. Peek", "Timothy L. Cover", "Walter J. Chazin", "Eric P. Skaar", "Holly M. Scott Algood"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1004450.g005", "stats"=>{"downloads"=>1, "page_views"=>18, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_NF_B_activation_and_IL_8_secretion_in_response_to_co_culture_with_H_pylori_is_dependent_on_zinc_availability_/1207639", "title"=>"NFκB activation and IL-8 secretion in response to co-culture with <i>H. pylori</i> is dependent on zinc availability.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-10-16 04:27:08"}
  • {"files"=>["https://ndownloader.figshare.com/files/1721486", "https://ndownloader.figshare.com/files/1721487", "https://ndownloader.figshare.com/files/1721488", "https://ndownloader.figshare.com/files/1721489", "https://ndownloader.figshare.com/files/1721490", "https://ndownloader.figshare.com/files/1721491"], "description"=>"<div><p>Transition metals are necessary for all forms of life including microorganisms, evidenced by the fact that 30% of all proteins are predicted to interact with a metal cofactor. Through a process termed nutritional immunity, the host actively sequesters essential nutrient metals away from invading pathogenic bacteria. Neutrophils participate in this process by producing several metal chelating proteins, including lactoferrin and calprotectin (CP). As neutrophils are an important component of the inflammatory response directed against the bacterium <i>Helicobacter pylori</i>, a major risk factor for gastric cancer, it was hypothesized that CP plays a role in the host response to <i>H. pylori</i>. Utilizing a murine model of <i>H. pylori</i> infection and gastric epithelial cell co-cultures, the role CP plays in modifying <i>H. pylori</i> -host interactions and the function of the <i>cag</i> Type IV Secretion System (<i>cag</i> T4SS) was investigated. This study indicates elevated gastric levels of CP are associated with the infiltration of neutrophils to the <i>H. pylori</i>-infected tissue. When infected with an <i>H. pylori</i> strain harboring a functional <i>cag</i> T4SS, calprotectin-deficient mice exhibited decreased bacterial burdens and a trend toward increased <i>cag</i> T4SS -dependent inflammation compared to wild-type mice. <i>In vitro</i> data demonstrate that culturing <i>H. pylori</i> with sub-inhibitory doses of CP reduces the activity of the <i>cag</i> T4SS and the biogenesis of <i>cag</i> T4SS-associated pili in a zinc-dependent fashion. Taken together, these data indicate that zinc homeostasis plays a role in regulating the proinflammatory activity of the <i>cag</i> T4SS.</p></div>", "links"=>[], "tags"=>["cag Type IV Secretion System", "Host Protein Calprotectin Modulates", "bacterium Helicobacter pylori", "Zinc Sequestration Transition metals", "role CP", "host interactions", "zinc homeostasis", "murine model", "pylori infection", "proinflammatory activity", "pylori strain", "metal chelating proteins", "culturing H", "cag T 4SS", "cag T 4SS pili", "Helicobacter pylori cag Type IV Secretion System", "risk factor", "host response", "metal cofactor"], "article_id"=>1207653, "categories"=>["Biological Sciences"], "users"=>["Jennifer A. Gaddy", "Jana N. Radin", "John T. Loh", "M. Blanca Piazuelo", "Thomas E. Kehl-Fie", "Alberto G. Delgado", "Florin T. Ilca", "Richard M. Peek", "Timothy L. Cover", "Walter J. Chazin", "Eric P. Skaar", "Holly M. Scott Algood"], "doi"=>["https://dx.doi.org/10.1371/journal.ppat.1004450.s001", "https://dx.doi.org/10.1371/journal.ppat.1004450.s002", "https://dx.doi.org/10.1371/journal.ppat.1004450.s003", "https://dx.doi.org/10.1371/journal.ppat.1004450.s004", "https://dx.doi.org/10.1371/journal.ppat.1004450.s005", "https://dx.doi.org/10.1371/journal.ppat.1004450.s006"], "stats"=>{"downloads"=>21, "page_views"=>12, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/The_Host_Protein_Calprotectin_Modulates_the_Helicobacter_pylori_cag_Type_IV_Secretion_System_via_Zinc_Sequestration/1207653", "title"=>"The Host Protein Calprotectin Modulates the <i>Helicobacter pylori cag</i> Type IV Secretion System via Zinc Sequestration", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2014-10-16 04:27:08"}

PMC Usage Stats | Further Information

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