In human monocyte-derived macrophages, T. whipplei stimulates the release of interleukin that is critical for Cefetamet pivoxil HCl bacterial replication, and induces macrophage apoptosis. Through its interaction with CD4, IL-16 acts as a chemoattractant for CD4 + immune cells including Tcells, monocytes and eosinophils. IL-16-expressing cells include mononuclear phagocytes, CD4 + and CD8 + Tcells, eosinophils and mast cells. In preliminary Liranaftate experiments, we have shown that circulating levels of IL-16 are increased in some patients with WD. In this study, we examined whether IL-16 and apoptosis markers were increased in patients with WD. Increased circulating levels of IL-16 and nucleosomes were present in patients with WD before the beginning of their treatment. Antibiotic treatment decreased the levels of both circulating IL-16 and nucleosomes, whereas patients who relapsed exhibited similar levels of IL-16 and nucleosomes to those of untreated patients. We suggest that IL-16 and nucleosomes may be useful to assess the prognosis for and the response to treatment in patients with WD. We show here that systemic IL-16 is related to WD. While increased IL-16 has been reported in local lesions of chronic immune diseases, including allergen-induced bronchial asthma and rheumatoid arthritis and in the mucosa of patients with inflammatory bowel disease, including ulcerative colitis and Crohn��s disease, the systemic role of IL-16 is a new finding. Indeed, circulating levels of IL-16 were not increased in patients with ulcerative colitis or Crohn��s disease even though IL16 is expressed in tissue lesions. Conversely, circulating IL-16 was increased in patients with WD and is produced by macrophages isolated from blood, but the expression of IL-16 is not increased in macrophages infiltrating intestinal lesions of one patient with WD, suggesting that IL-16 is associated with the systemic phase of WD. The presence of high circulating levels of IL-16 in WD could not be explained by the production of IL-16 by human macrophages stimulated by T. whipplei but evoked other cell types as a source for IL-16.