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. 2023 Nov 23;8(12):506. doi: 10.3390/tropicalmed8120506

Figure 1.

Figure 1

This schematic illustrates the host’s immune response during C. difficile infection and its impact on the infection’s outcomes. C. difficile toxins A and B lead to epithelial damage, triggering immune-cell activation and the release of cytokines and chemokines from both immune cells and the damaged epithelium. These signaling molecules, in turn, activate innate lymphoid cells (ILCs) and promote the recruitment of neutrophils to the site of injury. Activated ILC1 and ILC3 release Interferon IFNγ and IL-22, conferring protection against C. difficile. Neutrophils, though known for their protective function, may also have the potential to cause epithelial damage and have a detrimental impact on the outcome of CDI. Specific cytokines, such as IL-25 and IL-33, induce a type 2 immune response, enhancing host defense by increasing eosinophil infiltration and activation at the site of damage. Abbreviations: ILC1 (Innate Lymphoid Cell 1), ILC2 (Innate Lymphoid Cell 2), ILC3 (Innate Lymphoid Cell 3), TcdA (C. difficile Toxin A), TcdB (C. difficile Toxin B).