P2X7 receptor blockade decreases inflammation, apoptosis, and enteric neuron loss during Clostridioides difficile toxin A-induced ileitis in mice

Figure 6 Scheme of the hypothetical role of the P2X7 receptor during Clostridioides difficile toxin A-induced ileitis. Clostridioides difficile TcdA promotes epithelial damage and the upregulation of the P2X7 receptor in enteric neurons, intestinal epithelial cells, and immune cells. Once activated, the P2X7 receptor promotes the death of enteric neurons and the release of proinflammatory mediators by epithelial/immune cells [interleukin (IL)-1β, IL-6, keratinocyte chemoattractant, and tumor necrosis factor-α]. These proinflammatory mediators induce S100B synthesis by enteric glial cells. Blockade of the P2X7 receptor using a pharmacological approach attenuates these deleterious effects of TcdA. IL: Interleukin; TNF: Tumor necrosis factor; EGC: Enteric glial cell.