Abstract
The failure to eradicate Helicobacter pylori infection with antibiotic therapy has become a major clinical problem, not entirely accounted for by either poor compliance or antibiotic resistance. Recognition that failed eradication is one outcome of the host-parasite relationship focuses attention on impaired host protection as a determinant of nonresponse to antibiotics. A secreted interleukin (IL)-4 whole blood assay was developed to determine whether persistent infection was contributed to by impaired cytokine responses. The blood assay was shown to correlate well with mucosal organ cultures. Significantly lower levels of IL-4 were detected in the whole blood assays in 11 subjects with failed eradication compared with subjects with successful eradication (P<0.05). This latter group underwent a Th1 to Th0 ‘switch’, which appears to be important to successful eradication. Detection of subjects at risk for failing to eradicate infection with standard combination therapy, by virtue of low secreted IL-4 in whole blood cultures, may have clinical value.