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p38 MAPK Regulates Sulfur Mustard‐Induced Cytokines Independent of NF‐κB, and Does Not Regulate Sulfur Mustard‐Induced Cell Death

Cutaneous and ocular injuries caused by sulfur mustard (SM, bis‐(2‐chloroethyl) sulfide) are characterized by severe inflammation and death of exposed cells. Given the known roles of p38 and NF‐κB in inflammatory cytokine production, and the known roles of NF‐κB and p53 in cell fate, these pathways are of particular interest in the study of SM injury. In this study, we utilized inhibitory RNA (RNAi) targeted against p38α, the p50 subunit of NF‐κB, or p53 to elucidate SM‐induced signaling mechanisms in normal human epidermal keratinocytes (NHEK). Analysis of culture supernatant from 200 µM SM‐exposed cells showed that inflammatory cytokine production was inhibited by p38α RNAi but not by NF‐κB p50 RNAi. These findings further support the critical role that p38 plays in SM‐induced inflammatory cytokine production in NHEK and suggest that NF‐κB does not play a role in the SM‐induced inflammatory response of this cell type. Inhibition of NF‐κB by p50 RNAi did, however, partially inhibit SM‐induced cell death, implying a role for NF‐κB in SM‐induced apoptosis or necrosis. Interestingly, inhibition of p53 by RNAi potentiated SM‐induced cell death, indicating that the role of p53 in SM injury is in cell survival and not cell death.