Rhinovirus Attenuates Non-typeable Hemophilus influenzae-stimulated IL-8 Responses via TLR2-dependent Degradation of IRAK-1
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{"title"=>"Rhinovirus Attenuates Non-typeable Hemophilus influenzae-stimulated IL-8 Responses via TLR2-dependent Degradation of IRAK-1", "type"=>"journal", "authors"=>[{"first_name"=>"Benjamin L.", "last_name"=>"Unger", "scopus_author_id"=>"55425569000"}, {"first_name"=>"Andrea N.", "last_name"=>"Faris", "scopus_author_id"=>"36924824600"}, {"first_name"=>"Shyamala", "last_name"=>"Ganesan", "scopus_author_id"=>"35333822700"}, {"first_name"=>"Adam T.", "last_name"=>"Comstock", "scopus_author_id"=>"35333839200"}, {"first_name"=>"Marc B.", "last_name"=>"Hershenson", "scopus_author_id"=>"7006745687"}, {"first_name"=>"Umadevi S.", "last_name"=>"Sajjan", "scopus_author_id"=>"6602091095"}], "year"=>2012, "source"=>"PLoS Pathogens", "identifiers"=>{"sgr"=>"84868148275", "issn"=>"15537366", "isbn"=>"1553-7374 (Electronic)\\r1553-7366 (Linking)", "pmid"=>"23055935", "doi"=>"10.1371/journal.ppat.1002969", "pui"=>"365953706", "scopus"=>"2-s2.0-84868148275"}, "id"=>"8ac8adf4-8b6f-3c11-8a29-ef44f4b34542", "abstract"=>"Bacterial infections following rhinovirus (RV), a common cold virus, are well documented, but pathogenic mechanisms are poorly understood. We developed animal and cell culture models to examine the effects of RV on subsequent infection with non-typeable Hemophilus influenzae (NTHi). We focused on NTHI-induced neutrophil chemoattractants expression that is essential for bacterial clearance. Mice infected with RV1B were superinfected with NTHi and lung bacterial density, chemokines and neutrophil counts determined. Human bronchial epithelial cells (BEAS-2B) or mouse alveolar macrophages (MH-S) were infected with RV and challenged with NHTi, TLR2 or TLR5 agonists. Chemokine levels were measured by ELISA and expression of IRAK-1, a component of MyD88-dependent TLR signaling, assessed by immunoblotting. While sham-infected mice cleared all NTHi from the lungs, RV-infected mice showed bacteria up to 72 h post-infection. However, animals in RV/NTHi cleared bacteria by day 7. Delayed bacterial clearance in RV/NTHi animals was associated with suppressed chemokine levels and neutrophil recruitment. RV-infected BEAS-2B and MH-S cells showed attenuated chemokine production after challenge with either NTHi or TLR agonists. Attenuated chemokine responses were associated with IRAK-1 protein degradation. Inhibition of RV-induced IRAK-1 degradation restored NTHi-stimulated IL-8 expression. Knockdown of TLR2, but not other MyD88-dependent TLRs, also restored IRAK-1, suggesting that TLR2 is required for RV-induced IRAK-1 degradation.In conclusion, we demonstrate for the first time that RV infection delays bacterial clearance in vivo and suppresses NTHi-stimulated chemokine responses via degradation of IRAK-1. Based on these observations, we speculate that modulation of TLR-dependent innate immune responses by RV may predispose the host to secondary bacterial infection, particularly in patients with underlying chronic respiratory disorders.", "link"=>"http://www.mendeley.com/research/rhinovirus-attenuates-nontypeable-hemophilus-influenzaestimulated-il8-responses-via-tlr2dependent-de", "reader_count"=>28, "reader_count_by_academic_status"=>{"Professor > Associate Professor"=>1, "Librarian"=>1, "Researcher"=>6, "Student > Doctoral Student"=>2, "Student > Ph. D. Student"=>8, "Student > Postgraduate"=>2, "Student > Master"=>5, "Other"=>1, "Student > Bachelor"=>1, "Professor"=>1}, "reader_count_by_user_role"=>{"Professor > Associate Professor"=>1, "Librarian"=>1, "Researcher"=>6, "Student > Doctoral Student"=>2, "Student > Ph. D. Student"=>8, "Student > Postgraduate"=>2, "Student > Master"=>5, "Other"=>1, "Student > Bachelor"=>1, "Professor"=>1}, "reader_count_by_subject_area"=>{"Unspecified"=>1, "Medicine and Dentistry"=>8, "Agricultural and Biological Sciences"=>15, "Veterinary Science and Veterinary Medicine"=>1, "Immunology and Microbiology"=>3}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>8}, "Immunology and Microbiology"=>{"Immunology and Microbiology"=>3}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>15}, "Unspecified"=>{"Unspecified"=>1}, "Veterinary Science and Veterinary Medicine"=>{"Veterinary Science and Veterinary Medicine"=>1}}, "reader_count_by_country"=>{"Netherlands"=>1, "United States"=>1, "Norway"=>1, "United Kingdom"=>1, "Australia"=>1}, "group_count"=>2}

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/300235", "https://ndownloader.figshare.com/files/300271", "https://ndownloader.figshare.com/files/300307", "https://ndownloader.figshare.com/files/300342"], "description"=>"<div><p>Bacterial infections following rhinovirus (RV), a common cold virus, are well documented, but pathogenic mechanisms are poorly understood. We developed animal and cell culture models to examine the effects of RV on subsequent infection with non-typeable <em>Hemophilus influenzae</em> (NTHi). We focused on NTHI-induced neutrophil chemoattractants expression that is essential for bacterial clearance. Mice infected with RV1B were superinfected with NTHi and lung bacterial density, chemokines and neutrophil counts determined. Human bronchial epithelial cells (BEAS-2B) or mouse alveolar macrophages (MH-S) were infected with RV and challenged with NHTi, TLR2 or TLR5 agonists. Chemokine levels were measured by ELISA and expression of IRAK-1, a component of MyD88-dependent TLR signaling, assessed by immunoblotting. While sham-infected mice cleared all NTHi from the lungs, RV-infected mice showed bacteria up to 72 h post-infection. However, animals in RV/NTHi cleared bacteria by day 7. Delayed bacterial clearance in RV/NTHi animals was associated with suppressed chemokine levels and neutrophil recruitment. RV-infected BEAS-2B and MH-S cells showed attenuated chemokine production after challenge with either NTHi or TLR agonists. Attenuated chemokine responses were associated with IRAK-1 protein degradation. Inhibition of RV-induced IRAK-1 degradation restored NTHi-stimulated IL-8 expression. Knockdown of TLR2, but not other MyD88-dependent TLRs, also restored IRAK-1, suggesting that TLR2 is required for RV-induced IRAK-1 degradation.</p> <p>In conclusion, we demonstrate for the first time that RV infection delays bacterial clearance <em>in vivo</em> and suppresses NTHi-stimulated chemokine responses via degradation of IRAK-1. Based on these observations, we speculate that modulation of TLR-dependent innate immune responses by RV may predispose the host to secondary bacterial infection, particularly in patients with underlying chronic respiratory disorders.</p> </div>", "links"=>[], "tags"=>["rhinovirus", "attenuates", "non-typeable", "il-8", "responses", "tlr2-dependent", "degradation", "irak-1"], "article_id"=>119200, "categories"=>["Cancer", "Microbiology", "Immunology"], "users"=>["Benjamin L. Unger", "Andrea N. Faris", "Shyamala Ganesan", "Adam T. Comstock", "Marc B. Hershenson", "Umadevi S. Sajjan"], "doi"=>["https://dx.doi.org/10.1371/journal.ppat.1002969.s001", "https://dx.doi.org/10.1371/journal.ppat.1002969.s002", "https://dx.doi.org/10.1371/journal.ppat.1002969.s003", "https://dx.doi.org/10.1371/journal.ppat.1002969.s004"], "stats"=>{"downloads"=>3, "page_views"=>13, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/Rhinovirus_Attenuates_Non_typeable_Hemophilus_influenzae_stimulated_IL_8_Responses_via_TLR2_dependent_Degradation_of_IRAK_1/119200", "title"=>"Rhinovirus Attenuates Non-typeable <em>Hemophilus influenzae</em>-stimulated IL-8 Responses via TLR2-dependent Degradation of IRAK-1", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2012-10-04 02:33:20"}
  • {"files"=>["https://ndownloader.figshare.com/files/564698"], "description"=>"<p>(A) BEAS-2B cells were infected with RV39 or sham as described under <a href=\"http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1002969#ppat-1002969-g002\" target=\"_blank\">figure 2</a> and then treated with Pam3CSK4 (TLR2 agonist), or flagellin (TLR5 agonist) and incubated for 6 h. IL-8 protein levels in the cell culture supernatants were determined by ELISA. (B, C and D) BEAS-2B cells were infected with RV39 or sham, blocked and incubated with antibodies to TLR2 or TLR5 followed second antibody conjugated with Alexafluor-488 and analyzed by flow cytometry. Histograms are representative of three independent experiments. Data in A and D represents mean ± SEM calculated from 3 independent experiments performed in duplicate (* p≤0.05, ANOVA, different from sham; #, p≤0.05, ANOVA, different from sham/TLR2 or sham/TLR5 treated cells).</p>", "links"=>[], "tags"=>["suppresses", "tlr2", "tlr5", "ligands-elicited", "il-8", "affecting"], "article_id"=>235181, "categories"=>["Virology", "Microbiology", "Immunology"], "users"=>["Benjamin L. Unger", "Andrea N. Faris", "Shyamala Ganesan", "Adam T. Comstock", "Marc B. Hershenson", "Umadevi S. Sajjan"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1002969.g004", "stats"=>{"downloads"=>1, "page_views"=>12, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_RV_suppresses_TLR2_or_TLR5_ligands_elicited_IL_8_production_without_affecting_TLR2_or_TLR5_expression_/235181", "title"=>"RV suppresses TLR2 or TLR5 ligands-elicited IL-8 production without affecting TLR2 or TLR5 expression.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-04 01:26:21"}
  • {"files"=>["https://ndownloader.figshare.com/files/565509"], "description"=>"<p>(A and B) MH-S cells were infected with sham, RV1B or UV-RV1B as described in <a href=\"http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1002969#ppat-1002969-g002\" target=\"_blank\">figure 2</a> and incubated for 24 h. Cells were lysed in RIPA buffer and aliquots of cell lysates containing equal amounts of protein was subjected to Western blot analysis with IRAK-1 antibody. (C and D) Mice were infected with sham or RV1B, sacrificed two days later and lung lysates subjected to Western blot analysis to determine IRAK-1 expression. (A and C) Image presented is a representative of three independent experiments and 3 different animals respectively. (B and D) Band intensities of IRAK-1 were normalized to β-actin and expressed as fold increase over sham control. Data represents mean and SEM calculated from 3 independent experiments in B and 4 animals in D (* p≤0.05, ANOVA, different from sham).</p>", "links"=>[], "tags"=>["decreases", "irak-1", "alveolar", "macrophages", "mice", "lungs"], "article_id"=>235995, "categories"=>["Virology", "Microbiology", "Immunology"], "users"=>["Benjamin L. Unger", "Andrea N. Faris", "Shyamala Ganesan", "Adam T. Comstock", "Marc B. Hershenson", "Umadevi S. Sajjan"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1002969.g010", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_RV_infection_decreases_IRAK_1_expression_in_alveolar_macrophages_in_vitro_and_in_mice_lungs_in_vivo_/235995", "title"=>"RV infection decreases IRAK-1 expression in alveolar macrophages <i>in vitro</i> and in mice lungs <i>in vivo</i>.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-04 01:39:55"}
  • {"files"=>["https://ndownloader.figshare.com/files/564568"], "description"=>"<p>(A and B) BEAS-2B cells grown to 90% confluence were infected with sham, or RV39, UV-RV39, RV1B, or UV-RV1B at MOI of 1 and incubated at 33°C for 90 min. Infection media was replaced with fresh media, and incubation continued for another 22 h. Cells were then infected with NTHi (10 MOI) or treated with media, incubated for 3 h at 37°C and IL-8 in the media was assayed for IL-8 protein by ELISA. (C and D) Mucociliary-differentiated airway epithelial cells were infected apically with sham, or RV39, UV-RV39, RV1B, or UV-RV1B at MOI and incubated for 24 h. Cells were then infected with NTHi at MOI of 10 and IL-8 in the basolateral medium was determined. (E and F) BEAS-2B cells infected with RV39 or sham were infected with FITC-conjugated NTHi at MOI of 10, incubated for 1 h at 37°C, washed to remove unbound bacteria and analyzed by flow cytometry to determine binding of bacteria to cells. E and F shows representative histograms and mean fluorescence intensity respectively. Data represents mean ± SEM from 2–3 experiments performed in duplicate or triplicates (* p≤0.05, ANOVA, different from sham; #p≤0.05, ANOVA, different from sham/NTHi).</p>", "links"=>[], "tags"=>["alters", "nthi-stimulated", "il-8", "bacterial", "binding", "airway", "epithelial"], "article_id"=>235049, "categories"=>["Virology", "Microbiology", "Immunology"], "users"=>["Benjamin L. Unger", "Andrea N. Faris", "Shyamala Ganesan", "Adam T. Comstock", "Marc B. Hershenson", "Umadevi S. Sajjan"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1002969.g003", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_RV_infection_alters_NTHi_stimulated_IL_8_production_and_bacterial_binding_to_airway_epithelial_cells_/235049", "title"=>"RV infection alters NTHi-stimulated IL-8 production and bacterial binding to airway epithelial cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-04 01:24:09"}
  • {"files"=>["https://ndownloader.figshare.com/files/565048"], "description"=>"<p>BEAS-2B cells were transfected with non-targeting (NT)- or IRAK-1 siRNA and grown for 3 days. (A) Cell lysates were prepared from transfected cells and subjected to Western blot analysis to confirm knockdown of IRAK-1. (B) Transfected cells were infected with NTHi, incubated for 3 h and IL-8 in the media determined. BEAS-2B cells were infected with sham or RV39 in the presence or absence of 5 µM lactacystin and incubated for 24 h. (C and D) Cells were either harvested for determination of IRAK-1 expression by Western blot analysis and band intensities of IRAK-1 were normalized to β-actin. (E) Cells were then infected with NTHi and IL-8 in the media was examined. Western blot images are representative of 3 experiments. Data in B, D and E represents mean±SEM calculated from 3 independent experiments performed in triplicate (* p≤0.05, ANOVA, different from sham; †, p≤0.05, ANOVA different from NT-siRNA transfected cells; # p≤0.05, ANOVA, different from DMSO treated RV/NTHi-infected cells).</p>", "links"=>[], "tags"=>["nthi-stimulated", "il-8"], "article_id"=>235541, "categories"=>["Virology", "Microbiology", "Immunology"], "users"=>["Benjamin L. Unger", "Andrea N. Faris", "Shyamala Ganesan", "Adam T. Comstock", "Marc B. Hershenson", "Umadevi S. Sajjan"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1002969.g007", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_IRAK_1_is_required_for_NTHi_stimulated_IL_8_production_/235541", "title"=>"IRAK-1 is required for NTHi-stimulated IL-8 production.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-04 01:32:21"}
  • {"files"=>["https://ndownloader.figshare.com/files/565175"], "description"=>"<p>BEAS-2B cells were transfected with NT, TLR2, TLR4, TLR5, TLR7 or TLR8 siRNA and grown for 2 days. (A and B) Cells were infected with sham, UV-RV39 or RV39 and incubated for 24 h. mRNA and protein levels of IL-8 was determined by qPCR and ELISA respectively. (C) Knockdown of TLRs was confirmed by qPCR. Data is normalized to GAPDH and is representative of three independent experiments. (D) Cells transfected with NT-, TLR2 or TLR8 siRNA were infected with sham or RV39 as above and cell lysates subjected to Western blot analysis with IRAK-1 antibody. (E) Band intensities of IRAK-1 were normalized to β-actin and expressed as fold increase over respective NT/sham control. Image in D is representative of 3 independent experiments. Data in A, B and E represents mean±SEM calculated from 3 independent experiments performed in triplicate (* p≤0.05, ANOVA, different from sham; # p≤0.05, ANOVA, different from NT-siRNA transfected cells).</p>", "links"=>[], "tags"=>["irak-1", "tlr2"], "article_id"=>235668, "categories"=>["Virology", "Microbiology", "Immunology"], "users"=>["Benjamin L. Unger", "Andrea N. Faris", "Shyamala Ganesan", "Adam T. Comstock", "Marc B. Hershenson", "Umadevi S. Sajjan"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1002969.g008", "stats"=>{"downloads"=>1, "page_views"=>7, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_RV_decreases_IRAK_1_protein_via_TLR2_activation_/235668", "title"=>"RV-decreases IRAK-1 protein via TLR2 activation.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-04 01:34:28"}
  • {"files"=>["https://ndownloader.figshare.com/files/564906"], "description"=>"<p>(A and B) BEAS-2B cells were infected with sham, RV39, or UV-RV39, incubated for 24 h and the cells were lysed in RIPA buffer. The cell lysates containing equal amounts of protein was subjected to Western blot analysis with IRAK-1 antibody. (C and D) BEAS-2B cells were infected with sham or RV39 and cells were lysed at 4, 12 and 24 h post-infection and the lysates subjected to Western blot analysis with IRAK-1 antibody. (E and F) BEAS-2B cells infected with sham, UV-RV1B or RV1B were examined for IRAK-1 levels 24 h post- infection by Western blot analysis. (G and H) Mucociliary differentiated cells were infected apically with sham, RV39 or RV1B and IRAK-1 levels were determined 24 h later by Western blot analysis. Images are representative of 2–4 independent experiments. (B, D, F and H) Band intensities of IRAK-1 were normalized to β-actin and expressed as fold change over respective sham control. Data represents mean ± SEM calculated from 3 to 4 independent experiments (* p≤0.05, ANOVA, different from sham).</p>", "links"=>[], "tags"=>["decreases", "irak-1", "levels", "beas-2b", "airway", "epithelial"], "article_id"=>235394, "categories"=>["Virology", "Microbiology", "Immunology"], "users"=>["Benjamin L. Unger", "Andrea N. Faris", "Shyamala Ganesan", "Adam T. Comstock", "Marc B. Hershenson", "Umadevi S. Sajjan"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1002969.g006", "stats"=>{"downloads"=>1, "page_views"=>6, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_RV_infection_decreases_IRAK_1_protein_levels_in_both_BEAS_2B_and_primary_airway_epithelial_cells_/235394", "title"=>"RV infection decreases IRAK-1 protein levels in both BEAS-2B and primary airway epithelial cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-04 01:29:54"}
  • {"files"=>["https://ndownloader.figshare.com/files/564443"], "description"=>"<p>Mice were infected with sham or RV followed by NTHi as described in <a href=\"http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1002969#ppat-1002969-g001\" target=\"_blank\">Figure 1</a>. (A and B) Hematoxylin and eosin stained lung sections from Sham/NTHi-infected mice at 1 and 3 days post NTHi infection respectively. (C to E) Hematoxylin and eosin stained lung sections from RV1B/NTHi-infected mice at 1, 3 and 7 days post NTHi infection respectively. Inserts in the top left corners of A, C and D are magnified view of area marked in respective panels showing neutrophils. (Fand G) Chemokine levels in lung homogenate supernatants were determined by ELISA. Images in A to E are representative of 3 to 4 animals per group. Data in F and G represent mean±SD (n = 4–9, * p≤0.05, two-way ANOVA, different from sham; # p≤0.05, two-way f ANOVA, different from sham/NTHi infected animals).</p>", "links"=>[], "tags"=>["prolongs", "inflammation", "caused", "nthi", "suppresses", "chemokine"], "article_id"=>234928, "categories"=>["Virology", "Microbiology", "Immunology"], "users"=>["Benjamin L. Unger", "Andrea N. Faris", "Shyamala Ganesan", "Adam T. Comstock", "Marc B. Hershenson", "Umadevi S. Sajjan"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1002969.g002", "stats"=>{"downloads"=>1, "page_views"=>8, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_RV_infection_prolongs_lung_inflammation_caused_by_NTHi_and_suppresses_initial_chemokine_response_/234928", "title"=>"RV infection prolongs lung inflammation caused by NTHi and suppresses initial chemokine response.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-04 01:22:08"}
  • {"files"=>["https://ndownloader.figshare.com/files/564786"], "description"=>"<p>(A and B) BEAS-2B cells were infected with sham, RV39 or UV-RV39 as described under <a href=\"http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1002969#ppat-1002969-g002\" target=\"_blank\">Figure 2</a>. Aliquots of total cell lysates corresponding to equal amount of protein from were subjected to Western blot analysis with IRAK-M antibody. (A) Representative blot showing IRAK-M expression. (B) Band intensities were quantified by NIH image and levels of IRAK-M was normalized to β-actin and expressed as fold increase over sham infected cells. (C) BEAS-2B cells were transfected with non-targeting (NT)- or IRAK-M siRNA and knockdown of IRAK-M was confirmed by Western blot analysis. (D) Similarly transfected cells were infected with sham or RV followed by NTHi as described in <a href=\"http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1002969#ppat-1002969-g003\" target=\"_blank\">Figure 3</a> and IL-8 determined in the media. Data represents mean±SEM calculated from 3 independent experiments performed in triplicate (* p≤0.05, ANOVA, different from sham; #p≤0.05, ANOVA, different from sham/NTHi).</p>", "links"=>[], "tags"=>["rv-induced", "suppression", "nthi-stimulated", "il-8", "airway", "epithelial"], "article_id"=>235275, "categories"=>["Virology", "Microbiology", "Immunology"], "users"=>["Benjamin L. Unger", "Andrea N. Faris", "Shyamala Ganesan", "Adam T. Comstock", "Marc B. Hershenson", "Umadevi S. Sajjan"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1002969.g005", "stats"=>{"downloads"=>0, "page_views"=>3, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_IRAK_M_is_not_responsible_for_RV_induced_suppression_of_NTHi_stimulated_IL_8_in_airway_epithelial_cells_/235275", "title"=>"IRAK-M is not responsible for RV-induced suppression of NTHi-stimulated IL-8 in airway epithelial cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-04 01:27:55"}
  • {"files"=>["https://ndownloader.figshare.com/files/564301"], "description"=>"<p>BALB/C mice were infected with RV1B or sham by intranasal route. Two days later, mice were infected with NTHi or treated with PBS via intratracheal route and sacrificed at 6 h, 1 day, 3 days or 7 days post-NTHi infection. (A) Mice were sacrificed and lungs collected aseptically, homogenized in sterile PBS and 10 fold serial dilutions of lung homogenates were plated to determine bacterial density. (B) Cytospins of BAL cells and (C) lung digests enriched for leukocytes were prepared, stained with Diffquick and number of neutrophils were counted. Data in A represent mean and range and in B and C, mean±SD (n = 4–9, * p≤0.05, two-way ANOVA, different from sham; # p≤0.05, two-way ANOVA, different from sham/NTHi infected animals).</p>", "links"=>[], "tags"=>["bacterial", "persistence", "decreases", "neutrophil", "infiltration"], "article_id"=>234786, "categories"=>["Virology", "Microbiology", "Immunology"], "users"=>["Benjamin L. Unger", "Andrea N. Faris", "Shyamala Ganesan", "Adam T. Comstock", "Marc B. Hershenson", "Umadevi S. Sajjan"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1002969.g001", "stats"=>{"downloads"=>0, "page_views"=>3, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_RV_infection_promotes_bacterial_persistence_and_decreases_neutrophil_infiltration_to_subsequent_bacterial_challenge_in_vivo_/234786", "title"=>"RV infection promotes bacterial persistence and decreases neutrophil infiltration to subsequent bacterial challenge <i>in vivo</i>.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-04 01:19:46"}
  • {"files"=>["https://ndownloader.figshare.com/files/565323"], "description"=>"<p>MH-S cells were infected with sham, RV1B or UV-RV1B. Cells were then challenged with (A to C) NTHi, (D to F) Pam3CSK4 or (G to I) flagellin and protein levels of KC, MIP-2 and TNF-α in the medium was measured after 3 (for TNF-α) or 6 h (for KC and MIP-2) post challenge by ELISA. Data represent mean±SEM calculated from 3 independent experiments performed in duplicates (* p≤0.05, ANOVA, different from sham; # p≤0.05, ANOVA, different from sham/NTHi infected cells).</p>", "links"=>[], "tags"=>["suppresses", "nthi-", "tlr-stimulated", "chemokine", "cytokine", "responses", "alveolar"], "article_id"=>235809, "categories"=>["Virology", "Microbiology", "Immunology"], "users"=>["Benjamin L. Unger", "Andrea N. Faris", "Shyamala Ganesan", "Adam T. Comstock", "Marc B. Hershenson", "Umadevi S. Sajjan"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.1002969.g009", "stats"=>{"downloads"=>1, "page_views"=>8, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_RV_infection_suppresses_NTHi_and_TLR_stimulated_chemokine_and_cytokine_responses_in_alveolar_macrophage_/235809", "title"=>"RV infection suppresses NTHi- and TLR-stimulated chemokine and cytokine responses in alveolar macrophage.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-10-04 01:36:49"}

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Relative Metric

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