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IL-33 priming amplifies ATP-mediated mast cell cytokine production. | LitMetric

AI Article Synopsis

  • - Inflammatory responses are crucial for preventing infections but can also cause hypersensitivity and chronic inflammation; barrier tissues release signals like IL-33 and ATP to help detect pathogens.
  • - Mouse mast cells showed a significant increase in cytokine production when pre-treated with IL-33 before exposure to ATP, particularly at low ATP concentrations and with brief IL-33 exposure.
  • - The study identified the P2X7 receptor and the calcineurin/NFAT pathway as key components in this enhanced response, suggesting that alarmins work together to trigger an inflammatory response by promoting the recruitment of immune cells like eosinophils and macrophages.

Article Abstract

Inflammatory responses are required to block pathogen infection but can also lead to hypersensitivity and chronic inflammation. Barrier tissues actively release IL-33, ATP, and other alarmins during cell stress, helping identify pathogenic stimuli. However, it is unclear how these signals are integrated. Mast cells are critical initiators of allergic inflammation and respond to IL-33 and ATP. We found that mouse mast cells had a 3-6-fold increase in ATP-induced cytokine production when pre-treated with IL-33. This effect was observed at ATP concentrations < 100 µM and required < 30-minute IL-33 exposure. ATP-induced degranulation was not enhanced by pretreatment nor was the response to several pathogen molecules. Mechanistic studies implicated the P2X7 receptor and calcineurin/NFAT pathway in the enhanced ATP response. Finally, we found that IL-33 + ATP co-stimulation enhanced peritoneal eosinophil and macrophage recruitment. These results support the hypothesis that alarmins collaborate to surpass a threshold necessary to initiate an inflammatory response.

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Source
http://dx.doi.org/10.1016/j.cellimm.2021.104470DOI Listing

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