ObjectiveTo explore the expression and clinical significance ofaquaporin (AQP) 1 and AQP 4 in human pulmonary adenocarcinoma H1299 cell line.MethodsH1299 cell line in human pulmonary adenocarcinoma(pulmonary adenocarcinoma group) were obtained,the expressions of AQP1 and AQP4 in mRNA level and their locations were determined in H1299 cell line respectively by semiquantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis.The migration of tumor cells were observed by Matrigel invasion assay.Then normal tissues adjacent of pulmonary adenocarcinoma (above cancer line 3 cm,no tumor cell with pathological proven) were as control group.ResultsThe results of RT-PCR showed that AQP1,AQP4 mRNA was 1.030 ± 0.070 and 1.140 ± 0.190 in conlrol group,which were lower than those in pulmonary adenocarcinoma group (2.021 ± 0.250 and 2.180 ±0.180)(P＜0.05 ).The results of Western blot showed AQP1,AQP4 located on the membrane of H1299 cell.Both AQPI and AQP4 mRNA expressed very high in pulmonary adenocarcinoma group,while expressed very low in control group (P＜0.05).Matrigel invasion assay showed that the invasion was positively related to AQP1,AQP4(r =0.351,P ＜ 0.05 ).ConclusionAQP1,AQP4 significantly over express in H1299 cell line,both of them phy important roles in the growth of tumor tissue and cell migration.

Objective: To establish a quantitative assay of serum Golgi protein 73 (GP73) using xMAP technology and evaluate its performance. Methods: Monoclonal antibodies against GP73 were prepared and purified, and antibody pair screening was performed by double-antibody sandwich enzyme-linked immunosorbent assay. The screened antibodies were used to construct a Luminex liquid chip detection system, and the analysis performance of the detection system was evaluated. The serum levels of GP73 were detected in 90 clinical samples from healthy controls and patients with chronic hepatitis B infection (CHB) and hepatocellular carcinoma (HCC). Results: Five anti-GP73 monoclonal antibodies were prepared and purified, and 5 antibody pairs were successfully screened. The Luminex liquid chip detection system of GP73 was successfully constructed using 8F10D1 and 10B9F11 antibody pairs. The analytical performance evaluation showed that the sensitivity of this system was 0.25 ng/ml and the dynamic range was 0.25-100 ng/ml. No cross reactivity was observed. The intra- and inter-assay variation for GP73 was <8% and <11%, respectively. The recovery was 83%-92%. The linear regression equation was y=1.141x+ 6.436 (r²=0.998 4, P<0.001). The GP73 concentrations in the serum samples of healthy control, CHB group, and HCC group were 42.8 (38.68, 55.90) ng/ml, 61.49 (43.59, 81) ng/ml, and 122.78 (49.36 liter, 264.55) ng/ml, respectively. The levels of GP73 in HCC group were significantly higher than those in CHB group and healthy controls (P<0.05). Moreover, the levels of GP73 in CHB group were significantly higher than those in healthy controls (P<0.05). Conclusions A liquid chip detection system of GP73 was successfully constructed. It provides a powerful tool for the clinical application of GP73 in the future.

Interactions between gut microbiome and host immune system are fundamental to maintaining the intestinal mucosal barrier and homeostasis. At the host-gut microbiome interface, cell wall-derived molecules from gut commensal bacteria have been reported to play a pivotal role in training and remodeling host immune responses. In this article, we review gut bacterial cell wall-derived molecules with characterized chemical structures, including peptidoglycan and lipid-related molecules that impact host health and disease processes via regulating innate and adaptive immunity. Also, we aim to discuss the structures, immune responses, and underlying mechanisms of these immunogenic molecules. Based on current advances, we propose cell wall-derived components as important sources of medicinal agents for the treatment of infection and immune diseases.
Gastrointestinal Microbiome ; Intestinal Mucosa ; Bacteria ; Immune System ; Symbiosis ; Immunity, Mucosal ; Immunity, Innate