Encapsulating peritoneal sclerosis is one of the most serious complications of long-term
peritoneal dialysis. The pathogenesis of encapsulating peritoneal sclerosis has not been
elucidated, but several putative factors necessary for the development of peritoneum
fibrosis (PF) have been reported. However, the roles of T helper (Th) cells in the
progression of PF are unknown. The purpose of this study was to clarify the roles of Th1,
Th2, and Th17 cells in the progression of PF. T-bet, GATA-3, and RORγt are Th1, Th2, and
Th17 lineage commitment transcription factors, respectively. We previously generated
Th1-biased (T-bet transgenic (Tg)) mice, Th2-biased (GATA-3 Tg) mice, and Th17-biased
(RORγt Tg) mice. In this study, Th1, Th2, Th17-biased, and wild-type mice were
administered chlorhexidine gluconate (CG) intraperitoneally and analyzed on day 21.
CG-injected GATA-3 Tg mice showed a distended intestinal tract and developed marked
thickening of the submesothelial space compared with the other groups. CG-injected GATA-3
Tg mice also showed significant expression of α-SMA positive cells, macrophages, and
collagen III in the submesothelium. In contrast, CG-injected T-bet Tg mice only developed
mild peritoneal fibrosis. Cytokines analysis in peritoneal fluid showed that IFN-γ was
significantly increased in CG-injected T-bet Tg mice and that IL-13 was significantly
increased in CG-injected GATA-3 Tg mice. Moreover, intraperitoneal administration of IFN-γ
improved PF in GC-injected wild-type mice. Our results suggest that Th2 cells may play
roles in the development of experimental PF and that Th1 cells may alleviate the severity
of experimental PF.