Words similar to proinflammatory
Example sentences for: proinflammatory
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Treatment with recombinant IL-10 in CIA, in proteoglycan-induced arthritis, and in experimental autoimmune encephalomyelitis reduced disease severity, and neutralizing IL-10 with antibodies exacerbated disease [ 19 20 22 23 ] . The present data are consistent with previous results and show that a complete absence of IL-10 exacerbates inflammation in CIA [ 37 38 39 ] . The anti-inflammatory properties of IL-10 suggest that endogenous IL-10 may function as a regulator of proinflammatory mediators in vivo [ 39 ] . It is interesting, however, that disease severity inversely correlates with the levels of IFN-γ in IL-10 -/-mice, suggesting that IL-10 may control disease activity via regulating IFN-γ responses.
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.
IL-4 is able to inhibit IL-2 and IFN-γ production by Th1 cells, resulting in suppression of macrophage activation and the production of the proinflammatory cytokines IL-1, IL-6, IL-8, and TNF-α by monocytes and macrophages [ 4, 5, 6, 7, 8, 9].
The proinflammatory cytokines tumor necrosis factor alpha, IL-1, and IL-6 augment osteoclastogenesis [ 9 10 11 ] , while IL-10, IL-12, IL-18, and IFN-γ antagonize osteoclastogenesis in vitro [ 12 13 14 15 ] . It is probable that cytokines play a vital role in the delicate balance of bone remodeling, and that therapies based upon their natural biological function can be designed.
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.