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51, 74, 75, 76, 77, 78 The molecular mechanisms that underlie the cytotoxic potential of cytoplasmic CDDP are poorly understood, yet may involve: (i) the accumulation of reactive oxygen species (ROS) and nitric oxide (NO), which not only exacerbate CDDP genotoxicity but also exert direct cytotoxic effects by favoring the opening of the so-called permeability transition pore complex (PTPC)

Notably, these alterations occur prior to the onset of inflammation and induce the upregulation of epithelial-derived cytokines such as thymic stromal lymphopoietin (TSLP) and interleukin-33 (IL-33), which subsequently activate the Th2 immune axis in a sustained manner (Jo et al., 2018