CT-1 administration to DSS-treated mice ameliorated both the clinical course (disease activity index), histological damage, inflammation (colon expression of TNF-α, IL-17, IL-10, INF IFN-γ, and iNOS), and apoptosis.
The arthritis/DSS-treated mice did not demonstrate changes in hind foot volumes or in the concentration of matrix metalloproteinase-3 (MMP-3) in the plasma; however, plasma levels of interleukin-6 (IL-6) and tumor necrosis factor (TNF)-α were increased.
Both gene and protein expression levels of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α are markedly attenuated by WCP treatment in the colon of AOM/DSS-treated mice.
Activation of CRF‑R1 increased the DAI and histological scores of the colons from DSS‑treated mice by promoting M1 macrophage polarization, demonstrated as increased NF‑κB activation, and TNF‑α and IL‑6 release.
Furthermore, 6G and SZ suppresses immunoexpression of tumor necrosis factor alpha, interleukin-1β, inducible nitric oxide synthase, Regulated on activation, normal T cell expressed and secreted (RANTES), and Monocyte chemoattractant protein-1 (MCP-1) in the DSS-treated mice.
In addition, RB supplementation protected the colonic structure (P≤.01), associated with suppressed NF-κB signaling and reduced expression of inflammatory interleukin (IL)-1β, IL-6, IL-17, cyclooxegenase-2, and tumor necrosis factor-α in DSS-treated mice.
The overall findings of the study support the correlation of high-producer TNF-α genotypes combined with low-producer IL-10 haplotypes and IL-12B genotypes in reduced risk of DHF/DSS.
Analysis of the expression of the proinflammatory cytokines interleukin (IL)-1β, tumour necrosis factor (TNF)-α and IL-6 revealed no significant differences between DSS-treated Bcl-3(-/-) and wild-type mice.
The mean TNF-alpha level was highest in those patients with dengue shock syndrome (DSS) or dengue hemorrhagic fever (DHF) grade III (37.44+/-42.0 pg/ml).