About: Viral and bacterial co-infection in severe pneumonia triggers innate immune responses and specifically enhances IP-10: a translational study

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About: Viral and bacterial co-infection in severe pneumonia triggers innate immune responses and specifically enhances IP-10: a translational study Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Viral and bacterial co-infection in severe pneumonia triggers innate immune responses and specifically enhances IP-10: a translational study
Creator	Paranhos-Baccalà, Gláucia Rosa-Calatrava, Manuel Terrier, Olivier Basualdo, Wilma Bénet, Thomas Endtz, Hubert Hoffmann, Jonathan Russomando, Graciela Messaoudi, Mélina Machado, Daniela Picot, Valentina Pouzol, Stephane Espínola, Emilio Guillen, Rosa
Source	Medline; PMC
abstract	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-γ-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 < 0.01). This study demonstrates that viral and bacterial co-infection modulates the JAK-STAT signaling pathway and leads to exacerbated IP-10 expression, which could play a major role in the pathogenesis of pneumonia.
has issue date	2016-12-06(xsd:dateTime)
bibo:doi	10.1038/srep38532
bibo:pmid	27922126
has license	cc-by
sha1sum (hex)	ef3d6cabc804e5eb587b34249b539c1b5efa4cc4
schema:url	https://doi.org/10.1038/srep38532
resource representing a document's title	Viral and bacterial co-infection in severe pneumonia triggers innate immune responses and specifically enhances IP-10: a translational study
has PubMed Central identifier	PMC5138590
has PubMed identifier	27922126
schema:publication	Sci Rep
resource representing a document's body	covid:ef3d6cabc804e5eb587b34249b539c1b5efa4cc4#body_text
is schema:about of	named entity 'OPEN' named entity 'BACTERIAL' named entity 'co-infection' named entity 'play' named entity 'signaling' named entity 'in-vitro' named entity 'patients' named entity 'observed' named entity 'bacterial' named entity 'SEVERE PNEUMONIA' named entity 'TRANSLATIONAL' named entity 'DESCRIBED' named entity '10%' named entity 'MIRNA' named entity 'LEADS' named entity 'CO-INFECTION' named entity 'ASSOCIATED WITH' named entity '28P' named entity 'INFLUENZA VIRUS A' named entity 'COINFECTION' named entity 'IMMUNOPATHOLOGY' named entity 'SUBSEQUENT' named entity 'SERUM' named entity 'MRNA' named entity 'HIGHER' named entity 'IDENTIFIED' named entity 'SAMPLES' named entity 'EXPRESSION' named entity 'KNOWN' named entity 'INTERFERON' named entity 'ENDOGENOUS' named entity 'COMMUNITY-ACQUIRED PNEUMONIA' named entity 'PATIENTS' named entity 'FOLLOWING' named entity 'FOLD' named entity 'PROTEIN' named entity 'HOSPITALIZED' named entity 'IMMUNOMODULATORS' named entity 'REGULATOR' named entity 'BACTERIAL INFECTIONS' named entity 'LEVELS' named entity 'DERIVED' named entity 'IP-10' named entity 'MACROPHAGES' named entity 'HUMAN MONOCYTE' named entity 'CLINICAL' named entity 'MICRORNA' named entity 'VIRAL AND' named entity '10%' named entity 'A MAJOR' named entity 'CXCL10' named entity 'A45' named entity 'SINGLE' named entity 'OLD' named entity 'INFECTED' named entity 'BACTERIAL' named entity 'CO-INFECTION' named entity 'IMMUNE RESPONSES' named entity 'TRIGGERS' named entity 'STUDY' named entity 'IP-10' named entity 'CONDITIONS' named entity 'CHILDREN' named entity 'CYTOKINE' named entity 'VIRAL AND' named entity 'SUPPRESSOR OF CYTOKINE SIGNALING' named entity 'OBSERVED' named entity 'POORLY'

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