This could be explained by covalent and irreversible binding of DIDS to its proteins targets (Okubo et al., 1994; Boedtkjer et al., 2012), compared to the reversible nature of binding between S0859 and sodium-bicarbonate cotransporters (Ch’en et al., 2008), which would suggest that concentrations of S0859 at the site of infection may not remain sufficiently high to prevent SLS from disrupting NBCn1. Here, SLC4A7 is linked to infection.