Dynamic Changes of IL-17, occludin, and ZO-1 in Mice with Post-infectious Irritable Bowel Syndrome / 中山大学学报(医学科学版)

[Objective] To observe the dynamic changes of intestinal IL-17,occludin,and ZO-1 in mice with postinfectious irritable bowel syndrome (PI-IBS).[Methods] Forty C57BL/6 mice were randomly divided into 5 groups:control group and infection groups (2 weeks,4 weeks,6 weeks,and 8 weeks after trichinella infection).Infection groups were given by gavaging of 400～500 Trichinella spiralis in 0.2 mL of normal saline.The body weight of mice were recorded at week 2,4,6,and 8 after infection.The visceral sensitivity of mice was measured by the abdominal withdrawal reflex (AWR).The stool was collected continuously for 8 hours to calculate the percentage of fecal water content.Pathological changes of gut were observed by HE staining.The expressions of IL-17,occludin,and ZO-1 in ileocecus and colon were detected by immunohistochemistry and Western blotting.[Results] At week 2 after infection,the acute inflammation of the intestinal tract was observed and the body weight of mice were significantly decreased (P=0.000).Until week 8 after infection,the intestinal inflammation and body weight of mice recovered to normal.When the colorectal dilatation capacity was 0.35 and 0.5 mL,the AWR scores in the infection groups were significantly higher than those in the control group (P＜0.01).The percentages of fecal water content in the infection groups were significantly higher than those in the control group (P＜0.05).Compared with the control group,the expressions of IL-17 were significantly decreased in week 2 group (P＜0.05) and increased in week 8 group (P＜0.05).The expressions of occludin and ZO-1 in the infection groups were significantly lower than those in the control group (P＜0.05).[Conclusion] The dynamic changes of IL-17 and the decrease of Tight junction proteins may be one of the mechanisms of visceral hypersensitivity and increased percentages of fecal water content.They may be involved in the development of PI-IBS.

Roles of cytokines in stress-induced depression / 生理学报

Depression is a very common mental health problem in our modern society. Stress is involved in the provocation of depression. The pathogenesis of depressive disorder is still not well known. The development of neuroendocrine immunology opens a new sight for clarification of mechanism underlying stress-induced depression. Chronic stress activates peripheral and central immune systems accompanied with the release of inflammatory mediators, including cytokines. Activated immune system mediates the process of depression through the interaction with neuron system and neuroendocrine system, including regulating the monoamine neurotransmitter system in synthesis, metabolism and reuptake, inducing the overactivation of hypothalamus-pituitary-adrenal (HPA) axis and its negative feedback regulation, and reducing neurogenesis. This present paper reviews the cytokines mechanisms underlying stress-induced depression.

Studies on sLe~(a/x) and Hematogenous Metastasis of Cancer / 中国生物工程杂志

The expression of sLea/x which correlates with conventional histopathologic parameters serves as a useful indicator for the prognosis of metastatic disease. The bindings between sLea/x and their common ligand E-selectin initiate hematogenous metastasis of cancer. Certain bioactive conformation is crucial for the interaction between sLea/x and their ligands. Thus, a new class of compounds that mimic the structures of sLea/x can potently inhibit not only their functional bindings to selectins, but also the metastasis of cancer. This review is mainly on the sLea/x molecular structure,biosynthesis,distribution, especially the relationship between sLea/x and hematogenous metastasis of cancer and the design of drugs that mimic the structures of sLea/x.