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Helicobacter  (H.)  suis  colonizes the stomach of the majority of pigs as well as a minority of humans worldwide. Infection causes chronic inflammation in the stomach of the host, however without an effective clearance of the bacteria. Currently, no information is available about possible mechanisms  H. suis  utilizes to interfere with the host immune response. This study describes the effect on various lymphocytes of the γ-glutamyl transpeptidase (GGT) from  H. suis . Compared to whole cell lysate from wild-type  H. suis , lysate from a  H. suis ggt  mutant strain showed a decrease of the capacity to inhibit Jurkat T cell proliferation. Incubation of Jurkat T cells with recombinantly expressed  H. suis  GGT resulted in an impaired proliferation, and cell death was shown to be involved. A similar but more pronounced inhibitory effect was also seen on primary murine CD4 +  T cells, CD8 +  T cells, and CD19 +  B cells. Supplementation with known GGT substrates was able to modulate the observed effects. Glutamine restored normal proliferation of the cells, whereas supplementation with reduced glutathione strengthened the  H. suis  GGT-mediated inhibition of proliferation.  H. suis  GGT treatment abolished secretion of IL-4 and IL-17 by CD4 +  T cells, without affecting secretion of IFN-γ. Finally,  H. suis  outer membrane vesicles (OMV) were identified as a possible delivery route of  H. suis  GGT to lymphocytes residing in the deeper mucosal layers. Thus far, this study is the first to report that the effects on lymphocytes of this enzyme, not only important for  H. suis  metabolism but also for that of other  Helicobacter  species, depend on the degradation of two specific substrates: glutamine and reduced glutatione. This will provide new insights into the pathogenic mechanisms of  H. suis  infection in particular and infection with gastric helicobacters in general.

plos one

Effects of Helicobacter suis γ- Glutamyl Transpeptidase on Lymphocytes: Modulation by Glutamine and Glutathione Supplementation and Outer Membrane Vesicles as a Putative Delivery Route of the Enzyme