IL-33 Protects Mice against DSS-Induced Chronic Colitis by Increasing Both Regulatory B Cell and Regulatory T Cell Responses as Well as Decreasing Th17 Cell Response.

BACKGROUND: Previously, we have reported that IL-33 functioned as a protective modulator in dextran sulfate sodium- (DSS-) induced chronic colitis by suppressing Th17 cell response in colon lamina propria and IL-33 induced both regulatory B cells (Bregs) and regulatory T cells (Tregs) in mesenteric lymph nodes (MLNs) of mice with DSS-induced acute colitis. Moreover, we speculated that IL-33 would promote the Treg or Breg responses leading to the attenuation of DSS-induced chronic colitis. So, we investigated the role of IL-33 on Bregs and Tregs in the MLN of DSS-induced chronic colitis mice. METHODS: IL-33 was administered by intraperitoneal injection to mice with DSS-induced chronic colitis. Clinical symptoms, colon length, and histological changes were determined. The production of cytokines was measured by ELISA. The T and B cell subsets were measured by flow cytometry. The expression of mRNA of transcription factors was measured by quantitative real-time PCR. RESULTS: We show that IL-33 treatment increases both Breg and Treg responses in the MLN of mice with DSS-induced chronic colitis. Moreover, IL-33 treatment also decreases Th17 cell response in the MLN of mice with DSS-induced chronic colitis. CONCLUSION: Our data provide clear evidence that IL-33 plays a protective role in DSS-induced chronic colitis, which is closely related to increasing Breg and Treg responses in the MLN of mice as well as suppressing Th17 cell responses.

Dense RGB-D SLAM with Multiple Cameras.

A multi-camera dense RGB-D SLAM (simultaneous localization and mapping) system has the potential both to speed up scene reconstruction and to improve localization accuracy, thanks to multiple mounted sensors and an enlarged effective field of view. To effectively tap the potential of the system, two issues must be understood: first, how to calibrate the system where sensors usually shares small or no common field of view to maximally increase the effective field of view; second, how to fuse the location information from different sensors. In this work, a three-Kinect system is reported. For system calibration, two kinds of calibration methods are proposed, one is suitable for system with inertial measurement unit (IMU) using an improved hand⁻eye calibration method, the other for pure visual SLAM without any other auxiliary sensors. In the RGB-D SLAM stage, we extend and improve a state-of-art single RGB-D SLAM method to multi-camera system. We track the multiple cameras' poses independently and select the one with the pose minimal-error as the reference pose at each moment to correct other cameras' poses. To optimize the initial estimated pose, we improve the deformation graph by adding an attribute of device number to distinguish surfels built by different cameras and do deformations according to the device number. We verify the accuracy of our extrinsic calibration methods in the experiment section and show the satisfactory reconstructed models by our multi-camera dense RGB-D SLAM. The RMSE (root-mean-square error) of the lengths measured in our reconstructed mode is 1.55 cm (similar to the state-of-art single camera RGB-D SLAM systems).

IL-33 induces both regulatory B cells and regulatory T cells in dextran sulfate sodium-induced colitis.

Interleukin (IL)-33 is a member of the IL-1 family. Serum levels of IL-33 are increased in inflammatory bowel diseases (IBD), suggesting that IL-33 is involved in the pathogenesis of IBD, although its role is not clear. In this study, we investigated the role of IL-33 in the regulation of T-helper (Th) cell and B cell responses in mesenteric lymph nodes (MLN) in mice with dextran sulfate sodium (DSS)-induced colitis. Here, we showed that IL-33-treated mice were susceptible to DSS-induced colitis as compared with PBS-treated mice. The production of spontaneous inflammatory cytokines production by macrophages or dendritic cells (DC) in MLN significantly increased, and the responses of Th2, regulatory T cells (Treg) and regulatory B cells (Breg) were markedly upregulated, while Th1 responses were significantly downregulated in MLN of IL-33-treated mice with DSS-induced colitis. Our results demonstrate that IL-33 contributes to the pathogenesis of DSS-induced colitis in mice by promoting Th2 responses, but suppressing Th1 responses, in MLN. Moreover, IL-33 treatment increased Breg and Treg responses in MLN in mice with DSS-induced colitis. Therefore, modulation of IL-33/ST2 signaling is implicated as a novel biological therapy for inflammatory diseases associated with Th1 responses.