Publications by authors named "B Balestrieri"
Severe asthma and sinus disease are consequences of type 2 inflammation (T2I), mediated by interleukin (IL)-33 signaling through its membrane-bound receptor, ST2. Soluble (s)ST2 reduces available IL-33 and limits T2I, but little is known about its regulation. We demonstrate that prostaglandin E (PGE) drives production of sST2 to limit features of lung T2I.
View Article and Find Full Text PDFBackground: Aspirin-exacerbated respiratory disease (AERD) is a severe disease involving dysregulated type 2 inflammation. However, the role other inflammatory pathways play in AERD is poorly understood.
Objective: We sought to broadly define the inflammatory milieu of the upper respiratory tract in AERD and to determine the effects of IL-4Rα inhibition on mediators of nasal inflammation.
Article Synopsis
- Macrophages with group V phospholipase A (Pla2g5) produce linoleic acid (LA), which enhances lung inflammation, particularly during viral infections, but their exact function is not fully understood.
- Researchers created specialized mice and stimulated their macrophages to investigate the effects of Pla2g5 and LA on inflammation, using various immune response triggers.
- Findings revealed that Pla2g5 plays a role in lung inflammation by affecting macrophage activity and recruitment, with LA helping to partially restore inflammation when Pla2g5 is absent.
Increasing evidence points to the involvement of group IIA secreted phospholipase A (sPLA-IIA) in pathologies characterized by abnormal osteoclast bone-resorption activity. Here, the role of this moonlighting protein has been deepened in the osteoclastogenesis process driven by the RANKL cytokine in RAW264.7 macrophages and bone-marrow derived precursor cells from BALB/cJ mice.
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