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Broad Institute Inc gene set enrichment analysis java applet
Cd promotes mouse lung myeloid cell responses to H1N1 infection. Inflammatory lung tissue cell counts (7 cell types, Fig. 2), leading edge gene intensities (293 leading edge genes selected by <t>GSEA)</t> and lung tissue metabolites measured by untargeted LC-MS (total of 2956 metabolic features) were correlated using sparse PLS regression implemented by xMWAS (n = 5/group). (A) Networks were constructed of variables with inter-dataset absolute association score >0.88 at p < 0.05 (n = 5) for H1N1 or Cd+H1N1 groups. Symbols depict metabolic features (orange rectangle), gene transcripts (green circle) or cell counts (blue triangle), and lines indicate relationship between symbols (red, positive correlation; blue, negative correlation). The blue triangles have been enlarged for easier viewing. Abbreviations for cells are as follows: Monocytes, ‘Mono’; neutrophils, ‘PMN’; CD11b+ dendritic cells, ‘CD11b+ DC’; CD103+ dendritic cells, ‘CD103+ DC’; plasmacytoid dendritic cells, ‘pDC’; CD4 T lymphocytes, ‘CD4+’; and CD8 T lymphocytes, ‘CD8+’. Note, CD103+ DC is not found in the Cd+H1N1 network. (B) The absolute value of difference in eigenvector centrality (Delta Centrality) of each immune cell type was contrasted between the networks of Cd+H1N1 and H1N1 networks. Pearson’s correlation (r) was analyzed for the abundance of lung IFNγ protein and lung monocytes (C), CD11b+ DCs (D) and neutrophils (E). Open circles, H1N1 alone; closed circles, Cd+H1N1. The resulting statistics of correlation (r) and significance (p) were as follows: C, monocytes (Cd+H1N1 r = 0.97, p = 3×10−7; H1N1, r = 0.21, p = 0.49); D, CD11b+ DCs (Cd+H1N1, r = 0.92, p = 2×10−5; H1N1, r = −0.05, p = 0.86); E, neutrophils (Cd+H1N1, r = 0.89, p = 9×10−5; H1N1, r = 0.22, p = 0.48). n = 12-13.
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1) Product Images from "Low-dose cadmium potentiates lung inflammatory response to 2009 pandemic H1N1 influenza virus in mice"

Article Title: Low-dose cadmium potentiates lung inflammatory response to 2009 pandemic H1N1 influenza virus in mice

Journal: Environment international

doi: 10.1016/j.envint.2019.03.054

Cd promotes mouse lung myeloid cell responses to H1N1 infection. Inflammatory lung tissue cell counts (7 cell types, Fig. 2), leading edge gene intensities (293 leading edge genes selected by GSEA) and lung tissue metabolites measured by untargeted LC-MS (total of 2956 metabolic features) were correlated using sparse PLS regression implemented by xMWAS (n = 5/group). (A) Networks were constructed of variables with inter-dataset absolute association score >0.88 at p < 0.05 (n = 5) for H1N1 or Cd+H1N1 groups. Symbols depict metabolic features (orange rectangle), gene transcripts (green circle) or cell counts (blue triangle), and lines indicate relationship between symbols (red, positive correlation; blue, negative correlation). The blue triangles have been enlarged for easier viewing. Abbreviations for cells are as follows: Monocytes, ‘Mono’; neutrophils, ‘PMN’; CD11b+ dendritic cells, ‘CD11b+ DC’; CD103+ dendritic cells, ‘CD103+ DC’; plasmacytoid dendritic cells, ‘pDC’; CD4 T lymphocytes, ‘CD4+’; and CD8 T lymphocytes, ‘CD8+’. Note, CD103+ DC is not found in the Cd+H1N1 network. (B) The absolute value of difference in eigenvector centrality (Delta Centrality) of each immune cell type was contrasted between the networks of Cd+H1N1 and H1N1 networks. Pearson’s correlation (r) was analyzed for the abundance of lung IFNγ protein and lung monocytes (C), CD11b+ DCs (D) and neutrophils (E). Open circles, H1N1 alone; closed circles, Cd+H1N1. The resulting statistics of correlation (r) and significance (p) were as follows: C, monocytes (Cd+H1N1 r = 0.97, p = 3×10−7; H1N1, r = 0.21, p = 0.49); D, CD11b+ DCs (Cd+H1N1, r = 0.92, p = 2×10−5; H1N1, r = −0.05, p = 0.86); E, neutrophils (Cd+H1N1, r = 0.89, p = 9×10−5; H1N1, r = 0.22, p = 0.48). n = 12-13.
Figure Legend Snippet: Cd promotes mouse lung myeloid cell responses to H1N1 infection. Inflammatory lung tissue cell counts (7 cell types, Fig. 2), leading edge gene intensities (293 leading edge genes selected by GSEA) and lung tissue metabolites measured by untargeted LC-MS (total of 2956 metabolic features) were correlated using sparse PLS regression implemented by xMWAS (n = 5/group). (A) Networks were constructed of variables with inter-dataset absolute association score >0.88 at p < 0.05 (n = 5) for H1N1 or Cd+H1N1 groups. Symbols depict metabolic features (orange rectangle), gene transcripts (green circle) or cell counts (blue triangle), and lines indicate relationship between symbols (red, positive correlation; blue, negative correlation). The blue triangles have been enlarged for easier viewing. Abbreviations for cells are as follows: Monocytes, ‘Mono’; neutrophils, ‘PMN’; CD11b+ dendritic cells, ‘CD11b+ DC’; CD103+ dendritic cells, ‘CD103+ DC’; plasmacytoid dendritic cells, ‘pDC’; CD4 T lymphocytes, ‘CD4+’; and CD8 T lymphocytes, ‘CD8+’. Note, CD103+ DC is not found in the Cd+H1N1 network. (B) The absolute value of difference in eigenvector centrality (Delta Centrality) of each immune cell type was contrasted between the networks of Cd+H1N1 and H1N1 networks. Pearson’s correlation (r) was analyzed for the abundance of lung IFNγ protein and lung monocytes (C), CD11b+ DCs (D) and neutrophils (E). Open circles, H1N1 alone; closed circles, Cd+H1N1. The resulting statistics of correlation (r) and significance (p) were as follows: C, monocytes (Cd+H1N1 r = 0.97, p = 3×10−7; H1N1, r = 0.21, p = 0.49); D, CD11b+ DCs (Cd+H1N1, r = 0.92, p = 2×10−5; H1N1, r = −0.05, p = 0.86); E, neutrophils (Cd+H1N1, r = 0.89, p = 9×10−5; H1N1, r = 0.22, p = 0.48). n = 12-13.

Techniques Used: Infection, Liquid Chromatography with Mass Spectroscopy, Construct



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