Alkylamides, key active compounds in Echinacea, work by inhibiting the cyclooxygenase (COX) and lipoxygenase (LOX) pathways in epithelial and immune cells. These pathways are crucial for the biosynthesis of inflammatory prostaglandins like PGE2. By blocking these pathways, alkylamides prevent the production of these prostaglandins. This inhibition then allows Natural Killer (NK) cells—the body’s own killer cells—to act more freely. NK cells identify abnormal, dying, or microbial cells and eliminate them by releasing toxic substances.

Meanwhile, Echinacea also contains oligomeric compounds called polysaccharides. Among these, arabinogalactan directly binds to Pattern Recognition Receptors (PRRs) on innate immune cells like macrophages. This binding activates these cells, prompting them to produce inflammatory cytokines such as IL-1 and TNFα. These cytokines not only recruit various immune cells to the site of inflammation but also activate phagocytic cells (cells that “eat” pathogens) and further stimulate NK cells.

Additionally, a type of active compound in Echinacea called alkylamide has been shown to directly bind to certain surface receptors on T lymphocytes, such as CB2. The activation of these receptors, through several intracellular pathways like the cAMP pathway, MAPKs pathway, and calcineurin pathway, ultimately leads to the activation of the nuclear transcription factor NF-kB. This activation of NF-kB then initiates the transcription of genes encoding cytokines like IL-3, IL-4, IL-5, IL-10, and TNFα.

If the T lymphocyte is activated simultaneously by both the CB2 receptor and the TCR receptor, the production of inflammatory cytokines decreases, while cytotoxic T lymphocytes become activated. However, if the T lymphocyte is stimulated simultaneously by the CB2 receptor and the CD28 receptor, then cytokine production increases. This increase in cytokines, in turn, activates various types of T lymphocytes and phagocytic cells.