Figures index

From

The Irreversible Inhibition of the MAPKp38 Pathway Downregulates LPS-augmented Release of Interleukin-Related Inflammatory Cytokines (IL-1β, IL-6): Immune Surveillance Unraveling IκB-α/NF-κB Phosphorylation State-independent Mechanism in vitro

John J Haddad

American Journal of Medical and Biological Research. 2015, 3(5), 133-138 doi:10.12691/ajmbr-3-5-3
  • Figure 1. Histogram analysis of the cell culture supernatant levels of pro-inflammatory cytokines with selective MAPKp38 inhibition. (A) The levels of IL-1β in the presence or absence of LPS/SB203580. (B) The levels of IL-6 in the presence or absence of LPS/SB203580. (C) The levels of TNF-α in the presence or absence of LPS/SB203580, shown here for comparison purposes with interleukins, mainly IL-1β and IL-6 . The number of experimental observations is n = 3 – 5, for separate and independently prepared cell cultures of alveolar epithelial cells with or without pre-treatments with LPS/SB203580. * P < 0.05, ** P < 0.01, *** P < 0.001, as compared with LPS. ϕ P < 0.001 (LPS), as compared with control baseline
  • Figure 2. Electrophoretic typical gel analysis for the effect of LPS/SB203580 on IκB-α cytosolic phosphorylation. (A) Cell cultures were pretreated with ascending concentrations of SB203580 for 1h, followed by incubation with LPS for 24h. The phosphorylated (pIκB-α) and non-phosphorylated forms of IκB-α were subsequently determined. Semi-quantitative loading per lane is verified by the consistent expression of the constitutive form of β-actin (B) Histogram analysis of the relative levels of pIκB-α and IκB-α with selective MAPKp38 inhibition. The number of experimental observations is n = 3 – 5, for separate and independently prepared cell cultures of alveolar epithelial cells with or without pre-treatments with LPS/SB203580
  • Figure 3. Hypothetical putative pathways depicting the intertwined signaling crosstalk between the MAPKp38 and NF-κB pathways. The involvement of upstream and downstream kinases in regulating either pathway is also shown. In addition, the selective inhibition of the MAPKp38 pathway attenuated the release of pro-inflammatory cytokines, however, it contributes to phosphorylation of IκB-α and subsequent NF-κB activation (see Results section for further details)