ArticleThe Annals of thoracic surgery2008
Alveolar macrophage secretory products effect type 2 pneumocytes undergoing hypoxia-reoxygenation.
Article in The Annals of thoracic surgery, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Gut microbiome-derived propionate reprograms alveolar macrophages metabolically and regulates lung injury responses in mice.Gut microbes · 2026Article
- Article
- Association of MMP-2 and MMP-9 expression with recurrences in primary spontaneous pneumothorax.The Kaohsiung journal of medical sciences · 2017Article
- Mixed serum-deprived and normal adipose-derived mesenchymal stem cells against acute lung ischemia-reperfusion injury in rats.American journal of translational research · 2015Article
- Primary graft dysfunction.Seminars in respiratory and critical care medicine · 2013Review
- Temporal expression of hypoxia-regulated genes is associated with early changes in redox status in irradiated lung.Free radical biology & medicine · 2012Article
- Autologous transplantation of adipose-derived mesenchymal stem cells markedly reduced acute ischemia-reperfusion lung injury in a rodent model.Journal of translational medicine · 2011Article
- Acute hypoxia decreases E. coli LPS-induced cytokine production and NF-kappaB activation in alveolar macrophages.Respiratory physiology & neurobiology · 2010Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundActivation of the alveolar macrophage is centrally important to the development of lung ischemia reperfusion injury. Alveolar macrophages and type 2 pneumocytes secrete a variety of proinflammatory mediators in response to oxidative stress. The manner in which they interact and how the macrophage may influence pneumocyte responses in lung ischemia reperfusion injury is unknown. Utilizing an in vitro model of hypoxia and reoxygenation, we sought to determine if the proinflammatory response of type 2 pneumocytes to oxidative stress would be amplified by alveolar macrophage secretory products.
methodsCultured pneumocytes were exposed to control media or media from cultured macrophages exposed to hypoxia and reoxygenation. Pneumocytes were subsequently subjected to hypoxia and reoxygenation and assessed for both nuclear translocation of nuclear factor kappa B and inflammatory cytokine and chemokine secretion. To examine for any reciprocal interactions, we reversed the experiment, exposing macrophages to conditioned pneumocyte media.
resultsIn the presence of media from stimulated macrophages, production of proinflammatory mediators by type 2 pneumocytes was dramatically enhanced. In contrast, exposure of the macrophage to conditioned pneumocyte media had an inhibitory effect on macrophage responses subsequently exposed to hypoxia and reoxygenation.
conclusionsThe alveolar macrophage drives the development of lung reperfusion injury in part through amplification of the inflammatory response of type 2 pneumocytes subjected to hypoxia and reoxygenation.
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