A change of IL‐2 and IL‐4 production in patients with Helicobactor pylori infection

Abstract

Hellcobacter pylori is the most common cause of gastroduodenal inflammation. However, the exact immune pathogenesis is not fully understood. To look for evidence of the immunological mechanism in H. pylori associated disease, we measured cytokine interleukin-2 (IL-2) and IL-4 levels produced by peripheral blood lymphocytes (PBL) and gastric biopsies in 20 subjects with or without H. pylori infection. H. pylori can stimulate IL-2 and IL-4 production from PBL in H. pylori negative as well as H. pylori positive individuals. The spontaneous IL-2 production by PBL and gastric biopsies was greater (p < 0.0025, <0.001)in H. pylori negative individuals than that in H. pylori infected patients. Increased IL-4 levels from PBL in H. pylori infected patients were found in the presence of H. pylori (p < 0.0025). An increased spontaneous production of IL-4 from gastric biopsies was also observed in H. pylori infected patients (p < 0.025). In conclusion, an enhanced type 2 cytokine production was observed in H. pylori infected patients, which may be responsible for H. pylori chronic infection.

Circulating T‐Cell Response to Helicobacter pylori Infection in Chronic Gastritis

“…This dominant IFN‐γ response has been reported for mucosal cell preparations [6,22] and supports the view that the host response is a polarized Th1 response [9,23]. However, many T‐cell clones derived from the mucosa of subjects infected with H. pylori secrete IL‐4 [8,9], and some studies of PBMNC identify IL‐4 production from both H. pylori –positive and –negative subjects [11]. PBMNC failed to secrete detectable IL‐4 unless an antibody capture assay developed for use with whole‐blood cultures was used (data not shown).…”

“…In other studies, T‐cell proliferation is increased irrespective of disease, antibody, or infection status with H. pylori –associated gastritis when peripheral blood lymphocytes were stimulated with whole killed H. pylori bacteria [15]. Production of IFN‐γ by peripheral blood mononuclear cells (PBMNC) stimulated with H. pylori is lower in H. pylori –positive subjects than in H. pylori –negative subjects [14,16], whereas IL‐4 is lower in the latter [11].…”

“…Many studies of the pathogenesis of H. pylori –associated gastritis have been based on the analysis of T‐cell proliferation and cytokine production in peripheral blood lymphocytes as indicators of the inflammatory response in infected gastric mucosa [10,11]. However, it has been shown that changes in the T‐cell response in peripheral blood do not reflect those in the mucosa [11,12].…”

“…Many studies of the pathogenesis of H. pylori –associated gastritis have been based on the analysis of T‐cell proliferation and cytokine production in peripheral blood lymphocytes as indicators of the inflammatory response in infected gastric mucosa [10,11]. However, it has been shown that changes in the T‐cell response in peripheral blood do not reflect those in the mucosa [11,12]. For instance, in some studies, both H. pylori –positive and –negative subjects have similar levels of T‐cell proliferative response [12,13], whereas in others it is lower in H. pylori –positive subjects [3,14].…”

Antigen-specific lymphocyte proliferation as a marker of immune response in guinea pigs with sustained Helicobacter pylori infection.

“…The T cell proliferation and cytokine production by peripheral blood lymphocytes were considered as markers of the inflammatory responses to H. pylori infection in the milieu of gastric mucosa (Fan et al, 1995;Chmiela et al, 1996). However, it was shown that T cell responses in peripheral blood do not reflect the local processes in the gastric mucosa (Karttunen et al, 1991).…”