UNASSIGNED: Cytokine profiles of peripheral blood and other bodily fluids provide diagnostic indicators for assessing inflammatory processes. Menstrual effluent may provide a noninvasive source of biological material for monitoring cytokine levels in blood and in endometrial tissues. This pilot study investigated the potential of measuring cytokines in menstrual effluent, and compared the cytokine profiles of menstrual versus peripheral blood.
UNASSIGNED: Seven healthy donors (aged ≥18 and ≤45 years) collected menstrual effluent on day 2 of menses. Matched peripheral blood samples were collected by venous blood draw on the same day. Levels of 62 cytokines were measured in all samples by 62-plex Luminex assay.
UNASSIGNED: Peripheral blood and menstrual effluent cytokine profiles were tenuously correlated (r 2 = 0.26, p < 0.0001), with higher levels detected in menstrual effluent for 48/62 cytokines. Thirty five cytokines were significantly elevated in menstrual effluent compared to peripheral blood samples (IL-8, CCL2, CCL4, LIF, IL-1RA, IL-6, IL-1β, HGF, CCL3, FGF-2, TNF-α, VEGF-A, IL-1α, CXCL1, IL-9, IL-10, EGF, CXCL5, CSF3, EOTAXIN, TGF-α, TRAIL, CXCL10, VEGF-D, IL-12P40, CXCL9, IL-18 RESISTIN, IL-22, IL-21, CSF1, IFN-γ, IL-17A, CXCL12, IL-12p70). Two cytokines (LEPTIN, CSF2) were expressed at significantly lower levels in menstrual effluent compared to peripheral blood. Linear regression of individual cytokines found low predictive power (linear regression p > 0.05) for 53/62 cytokines in menstrual effluent versus peripheral blood. Levels of TGF-β (r 2 = 0.87, p = 0.002) and CCL7 (r 2 = 0.63, p = 0.033) were significantly positively correlated between matched menstrual and peripheral blood samples.
UNASSIGNED: In this group of study participants, the cytokine profile of menstrual effluent was quantitatively distinct from peripheral blood, and also characterized by higher levels of inflammatory signaling. This pattern of comparative menstrual blood cytokine profiles points to a need for further studies to evaluate the relationship between peripheral and menstrual blood cytokines in broader populations including both healthy and diseased states.

BACKGROUND: Peritoneal fibrosis is one of the major complications induced by peritoneal dialysis (PD). Damaged integrity and function of peritoneum caused by peritoneal fibrosis not only limits the curative efficacy of PD and but affects the prognosis of patients. However, the detailed mechanisms underlying the process remain unclear and therapeutic strategy targeting TGF-β is deficient. Transforming growth factor-β (TGF-β) signaling participates in the progression of peritoneal fibrosis through enhancing mesothelial-mesenchymal transition of mesothelial cells.
METHODS: The study aims to demonstrate the regulatory role of Sirtuin1 (SIRT1) to the TGF-β signaling mediated peritoneal fibrosis. SIRT1-/- mice were used to establish animal model. Masson\'s staining and peritoneal equilibration assay were performed to evaluate the degree of peritoneal fibrosis. QRT-PCR assays were used to estimate the RNA levels of Sirt1 and matrix genes related to peritoneal fibrosis, and their protein levels were examined by Western blot assays.
RESULTS: SIRT1 significantly decreased in vivo post PD treatment. SIRT1 knockout exacerbated peritoneal fibrosis both in vivo and vitro. Overexpression of SIRT1 efficiently inhibited peritoneal fibrosis by inhibiting the peritoneal inflammation and the activation of TGF-β signaling.
CONCLUSIONS: SIRT1 ameliorated peritoneal fibrosis both in vivo and in vitro through inhibiting the expression of protein matrix induced by TGF-β signaling.