About: Surviving Deadly Lung Infections: Innate Host Tolerance Mechanisms in the Pulmonary System

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Surviving Deadly Lung Infections: Innate Host Tolerance Mechanisms in the Pulmonary System
Creator	Divangahi, Maziar Alcorn, John Crane, Meredith Fitzgerald, Ethan Jamieson, Amanda Krishnamoorthy, Nandini Lee, Kayla
Source	Medline; PMC
abstract	Much research on infectious diseases focuses on clearing the pathogen through the use of antimicrobial drugs, the immune response, or a combination of both. Rapid clearance of pathogens allows for a quick return to a healthy state and increased survival. Pathogen-targeted approaches to combating infection have inherent limitations, including their pathogen-specific nature, the potential for antimicrobial resistance, and poor vaccine efficacy, among others. Another way to survive an infection is to tolerate the alterations to homeostasis that occur during a disease state through a process called host tolerance or resilience, which is independent from pathogen burden. Alterations in homeostasis during infection are numerous and include tissue damage, increased inflammation, metabolic changes, temperature changes, and changes in respiration. Given its importance and sensitivity, the lung is a good system for understanding host tolerance to infectious disease. Pneumonia is the leading cause of death for children under five worldwide. One reason for this is because when the pulmonary system is altered dramatically it greatly impacts the overall health and survival of a patient. Targeting host pathways involved in maintenance of pulmonary host tolerance during infection could provide an alternative therapeutic avenue that may be broadly applicable across a variety of pathologies. In this review, we will summarize recent findings on tolerance to host lung infection. We will focus on the involvement of innate immune responses in tolerance and how an initial viral lung infection may alter tolerance mechanisms in leukocytic, epithelial, and endothelial compartments to a subsequent bacterial infection. By understanding tolerance mechanisms in the lung we can better address treatment options for deadly pulmonary infections.
has issue date	2018-06-22(xsd:dateTime)
bibo:doi	10.3389/fimmu.2018.01421
bibo:pmid	29988424
has license	cc-by
sha1sum (hex)	6191082ec9ddfe582a3ba67622a638c0ed353bde
schema:url	https://doi.org/10.3389/fimmu.2018.01421
resource representing a document's title	Surviving Deadly Lung Infections: Innate Host Tolerance Mechanisms in the Pulmonary System
has PubMed Central identifier	PMC6024012
has PubMed identifier	29988424
schema:publication	Front Immunol
resource representing a document's body	covid:6191082ec9ddfe582a3ba67622a638c0ed353bde#body_text
is schema:about of	named entity 'Mechanisms' named entity 'innate' named entity 'LUNG' named entity 'PULMONARY SYSTEM' named entity 'INFECTIONS' named entity 'HOST' named entity 'TOLERANCE' named entity 'MECHANISMS' named entity 'coinfection' named entity 'viral burden' named entity 'BCR-Abl fusion protein' named entity 'epithelium' named entity 'influenza' named entity 'IL-22' named entity 'lung microbiome' named entity 'infection' named entity 'RSV' named entity 'growth factor' named entity 'endothelial' named entity 'epithelial cells' named entity 'inflammation' named entity 'infection' named entity 'virus' named entity 'lipid' named entity 'E. coli' named entity 'Acinetobacter baumannii' named entity 'lung infections' named entity 'mice' named entity 'respiratory epithelial cell' named entity 'cytokines' named entity 'viral diseases' named entity 'viral infections' named entity 'innate immune response' named entity 'IFN' named entity 'viral infection' named entity 'FGF2' named entity 'autopsy' named entity 'parenchyma' named entity 'NF-κB' named entity 'IAV' named entity 'infection' named entity 'parainfluenza virus' named entity 'tight junctions' named entity 'homeostatic' named entity 'steady state' named entity 'regulatory T cells' named entity 'monocytes' named entity 'tissue repair' named entity 'inflammatory responses' named entity 'infection' named entity 'virus' named entity 'pathology' named entity 'pathology' named entity 'innate immune cells' named entity 'epithelial cell' named entity 'lung disease' named entity 'lung infections' named entity 'pneumonia' named entity 'tissue repair' named entity 'superinfection' named entity 'commensal' named entity 'inflammatory response' named entity 'RSV' named entity 'protein' named entity 'Epstein-Barr virus' named entity 'TGF-β' named entity 'lungs' named entity 'macrophages' named entity 'secretion' named entity 'triage' named entity 'respiratory epithelial cell' named entity 'Streptococcus pneumoniae' named entity 'cAMP' named entity 'viral burden' named entity 'coinfections'

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