In addition, Ganoderenic-acid-D increased Sennoside-C circulating levels of IL-16 and nucleosomes were specific to WD disease, not to the T. whipplei infection. Indeed, subjects which were PCR positive for T. whipplei in their stool and saliva but who lacked clinical manifestations did not exhibit increased levels of IL-16 and nucleosomes. In a random sample of 40 healthy individuals, 35% showed evidence of T. whipplei DNA in their saliva. T. whipplei DNA was found in 13% of duodenal biopsies or the gastric juice of 105 patients having elective gastroscopy, with no clinical signs of WD. The detection of T. whipplei DNA on repeated samples suggests that T. whipplei may be an oral commensal organism that is ubiquitous and generally not pathogenic. Using a rather small number of patients with active WD, we found that the sensitivity and the specificity of measurements of circulating IL-16 and nucleosomes have a good value for the diagnosis of active WD. However, the tested samples are small and these results, although encouraging, should be considered preliminary. It is likely that increased levels of circulating IL-16 and nucleosomes in patients with WD are a hallmark of the disease and can permit doctors to discriminate between subjects with WD and healthy carriers. Finally, high levels of circulating IL-16 and nucleosomes were related to the activity of WD because the successful antibiotic treatment decreased both markers in patients with WD. Antibiotic therapy leads to a rapid improvement in the clinical status of the majority of patients with WD. Diarrhea and fever can resolve within 1 week of the start of therapy, arthropathy and other symptoms improve after a few weeks, and a normalization of laboratory findings is observed within a few months in most patients. However, these patients are followed by analysis of cerebrospinal fluid or duodenal biopsies 6 months and 12 months after diagnosis. Antibiotic treatment is generally stopped when PCR for T. whipplei and PAS staining are negative. The GSH depletor buthionine sulfoximine, which irreversibly inhibits c-glutamylcysteine synthetase at the first step of GSH synthesis, can further lower the already reduced GSH levels in rats exposed to phosphine, although the effect on mortality of co-treatment with phosphine and buthionine sulfoximine was not determined.