Example sentences for: proinflammatory

How can you use “proinflammatory” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • Treatment with rhIL-11 decreases the production of proinflammatory cytokines, including tumor necrosis factor (TNF)-α and interleukin (IL)-1β, and inhibits NF-κB binding activity [ 2, 3, 4].

  • Several observations support the assertion that a complex interaction between IL-8 and several other growth factors, cytokines, or other proteins is responsible for these tumor-related events [ 5 9 10 11 12 13 ] . Growth regulated protein alpha (GRO-α), beta (GRO-β), and ENA-78 have been reported to be co-induced with IL-8 in A549 cells stimulated with two proinflammatory cytokines, IL-1β and TNF-α [ 14 ] . This result is consistent with the presence of nuclear factor kappa B (NF-κB) consensus binding sites in the promoter regions of all three genes [ 4 15 ] . In addition, GRO-α and -β are also members of the ELR +CXC cytokine family that are reported to be important mediators of tumorigenesis through their angiogenic properties [ 2 16 ] . They both share one of the IL-8 receptors, CXCR2, which has been postulated to regulate the ELR +CXC chemokine-mediated angiogenesis and resulting-tumorigenesis [ 1 ] . These observations suggest that GRO-α and -β may exhibit expression profiles similar to IL-8.

  • Increased serum leptin levels in obesity and metabolic syndrome support the view that these disorders are in fact low-grade systemic inflammatory diseases, characterized by increased concentrations of proinflammatory cytokines like interleukin-6, tumor necrosis factor-α and leptin.

  • Recombinant human interleukin-11 (rhIL-11) is a pleiotropic cytokine that regulates the growth and development of hematopoietic stem cells and decreases the proinflammatory mediators of cytokine and nitric oxide production [ 1].

  • The emerging view is that modified forms of autoantigens generated during cell death might stimulate autoantibody responses if presented to the immune system in a proinflammatory context [ 23 ] . Since the fate of the Golgi complex during cell death has not been extensively explored, we investigated whether the Golgi complex and associated autoantigens are altered during apoptosis and necrosis.


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