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10.1038/srep38532

http://scihub22266oqcxt.onion/10.1038/srep38532
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suck abstract from ncbi


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pmid27922126
      Sci+Rep 2016 ; 6 (ä): 38532
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  • Viral and bacterial co-infection in severe pneumonia triggers innate immune responses and specifically enhances IP-10: a translational study #MMPMID27922126
  • Hoffmann J ; Machado D ; Terrier O ; Pouzol S ; Messaoudi M ; Basualdo W ; Espínola EE ; Guillen RM ; Rosa-Calatrava M ; Picot V ; Bénet T ; Endtz H ; Russomando G ; Paranhos-Baccalà G
  • Sci Rep 2016[Dec]; 6 (ä): 38532 PMID27922126 show ga
  • Mixed viral and bacterial infections are widely described in community-acquired pneumonia; however, the clinical implications of co-infection on the associated immunopathology remain poorly studied. In this study, microRNA, mRNA and cytokine/chemokine secretion profiling were investigated for human monocyte-derived macrophages infected in-vitro with Influenza virus A/H1N1 and/or Streptococcus pneumoniae. We observed that the in-vitro co-infection synergistically increased interferon-?-induced protein-10 (CXCL10, IP-10) expression compared to the singly-infected cells conditions. We demonstrated that endogenous miRNA-200a-3p, whose expression was synergistically induced following co-infection, indirectly regulates CXCL10 expression by targeting suppressor of cytokine signaling-6 (SOCS-6), a well-known regulator of the JAK-STAT signaling pathway. Additionally, in a subsequent clinical pilot study, immunomodulators levels were evaluated in samples from 74 children (?5 years-old) hospitalized with viral and/or bacterial community-acquired pneumonia. Clinically, among the 74 cases of pneumonia, patients with identified mixed-detection had significantly higher (3.6-fold) serum IP-10 levels than those with a single detection (P?=?0.03), and were significantly associated with severe pneumonia (P?
  • |*Immunity, Innate/genetics [MESH]
  • |Adult [MESH]
  • |Aged [MESH]
  • |Bacterial Infections/*immunology/microbiology/virology [MESH]
  • |Base Sequence [MESH]
  • |Chemokine CXCL10/*metabolism [MESH]
  • |Coinfection/immunology/*microbiology/*virology [MESH]
  • |Female [MESH]
  • |Gene Expression Profiling [MESH]
  • |Humans [MESH]
  • |Infant [MESH]
  • |Influenza A Virus, H1N1 Subtype [MESH]
  • |Macrophages/immunology/microbiology/virology [MESH]
  • |Male [MESH]
  • |MicroRNAs/genetics/metabolism [MESH]
  • |Middle Aged [MESH]
  • |Models, Biological [MESH]
  • |Pneumonia/*immunology/*microbiology/virology [MESH]
  • |RNA, Messenger/genetics/metabolism [MESH]
  • |Streptococcus pneumoniae [MESH]
  • |Suppressor of Cytokine Signaling Proteins/metabolism [MESH]
  • |Translational Research, Biomedical [MESH]
  • |Virus Diseases/*immunology [MESH]


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