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The last-minute redemption of inflammatory cells in lung repair
Senin, 18 Apr 2022 16:21:49

Paula Martín-Vicente, Cecilia López-Martínez, Guillermo M. Albaiceta

European Respiratory Journal 2022 59: 2103000; DOI: 10.1183/13993003.03000-2021


Inflammatory cells play a central role in the pathogenesis of acute lung injury. Danger signals within the alveolar structures trigger a stereotypical response that results in the activation of an inflammatory response within alveoli and the interstitium. In addition to resident cells, the release of proinflammatory mediators, including chemoattractants, results in the recruitment of inflammatory cells from the circulation. Activated macrophages and neutrophils participate in the early phase of acute injury, mainly by promoting tissue disruption [1]. This acute response aims to remove pathogens and damaged cells in an expedited way and, if the severity of injury is mild or moderate, may result in effective repair or even regeneration. However, in case of severe damage, the intra-alveolar inflammatory response may impair lung function, worsening gas exchange and respiratory mechanics.

Tweetable abstract @ERSpublications

Inflammatory cells play a key role in lung repair after acute injury. These cells switch to a pro-repair phenotype over time in response to extracellular signals. Among these, VEGF-C promotes neutrophil clearance (efferocytosis) in macrophages.


  • Conflict of interest: The authors have nothing to disclose.

  • Support statement: Supported by Instituto de Salud Carlos III (PI20/01360, FEDER funds). P. Martín-Vicente is the recipient of a grant from Instituto de Salud Carlos III (FI21/00168). C. López-Martínez is the recipient of a grant from Ministerio de Ciencia, Innovación y Universidades (FPU18/02965). Instituto Universitario de Oncología del Principado de Asturias is supported by Fundación Liberbank. Funding information for this article has been deposited with the Crossref Funder Registry.

  • Received November 23, 2021.
  • Accepted January 10, 2022.