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The role of interleukin-1 and interleukin-18 in pro-inflammatory and anti-viral responses to rhinovirus in primary bronchial epithelial cells. | LitMetric

AI Article Synopsis

  • Human Rhinovirus (HRV) exacerbates chronic respiratory diseases and sparks immune responses in healthy individuals that help clear the infection.
  • Key cytokines like IL-1α, IL-1β, and IL-18 are released during HRV infection in human epithelial cells, playing a major role in causing inflammation, particularly neutrophilic inflammation in the airways.
  • Blocking IL-1 signaling reduces pro-inflammatory mediator production and neutrophil attraction, but doesn’t impact the body’s direct antiviral responses, indicating IL-1's role is more about inflammation than directly fighting the virus.

Article Abstract

Human Rhinovirus (HRV) is associated with acute exacerbations of chronic respiratory disease. In healthy individuals, innate viral recognition pathways trigger release of molecules with direct anti-viral activities and pro-inflammatory mediators which recruit immune cells to support viral clearance. Interleukin-1alpha (IL-1α), interleukin-1beta (IL-1β) and interleukin-18 (IL-18) have critical roles in the establishment of neutrophilic inflammation, which is commonly seen in airways viral infection and thought to be detrimental in respiratory disease. We therefore investigated the roles of these molecules in HRV infection of primary human epithelial cells. We found that all three cytokines were released from infected epithelia. Release of these cytokines was not dependent on cell death, and only IL-1β and IL-18 release was dependent on caspase-1 catalytic activity. Blockade of IL-1 but not IL-18 signaling inhibited up-regulation of pro-inflammatory mediators and neutrophil chemoattractants but had no effect on virus induced production of interferons and interferon-inducible genes, measured at both mRNA and protein level. Similar level of virus mRNA was detected with and without IL-1RI blockade. Hence IL-1 signaling, potentially involving both IL-1β and IL-1α, downstream of viral recognition plays a key role in induction of pro-inflammatory signals and potentially in recruitment and activation of immune cells in response to viral infection instigated by the epithelial cells, whilst not participating in direct anti-viral responses.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665753PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0063365PLOS

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