Figure 12.

Model of a possible mechanism by which 1-heptanol inhibits FcεRI-mediated mast cell activation. FcεRI signaling in control and 1-heptanol-treated cells are shown on the top and bottom, respectively. The initial steps in FcεRI signaling, including FcεRI and PLCγ1 phosphorylation and release of Ca²⁺ from the endoplasmic reticulum (ER) stores, are similar in control and 1-heptanol-treated cells. However, ORAI1-STIM1 coupling is decreased in 1-heptanol-treated cells activated with antigen, suggesting that the resulting membrane hyperfluidization disrupts CRAC channels. The reduced influx of Ca²⁺ ions from extracellular space is associated with impaired degranulation and ROS production. In addition, exposure to 1-heptanol leads to overexpression of HSP70 and inhibition of IκB-α and SAPK/JNK phosphorylation, contributing to the inhibition of cytokine production.