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Objective To clear the intestinal commensal microbiota by using antibiotics in order to investigate the effect of commensal microbiota on atherosclerosis in ApoE -/- mice with different diets. Methods The ApoE -/- mice were fed with normal chow diet and high-fat diet respectively, and antibiotics (vancomycin+metronidazole+neomycin sulfate+ampicillin) were used to intervene for 14 weeks. The formation of atherosclerotic plaques in the aorta of mice was evaluated by oil red O staining. The serum lipid metabolism and the levels of IL-1β, TNF- α and LPS were detected by ELISA. The expressions of inflammatory factors and tight junction proteins in the ileal and colonic epithelial cells of mice were also measured by Western blot and immunohistochemical staining. Results With normal chow diet, the atherosclerotic plaques of mice increased significantly in the antibiotic intervention group (P=0.016). The levels of serum IL-1β and TNF- α in antibiotics group mice were significantly increased (P=0.005，P= 0.021). The expressions of inflammatory factors IL-1β and TNF-α in ileal tissue of mice were significantly increased (P=0.003，P=0.007), and the expression of tight junction protein in intestinal tissue was significantly decreased (P<0.050). With high-fat diet, the formation of atherosclerotic plaque of the mice in the antibiotic group were decreased (P=0.040)； the serum total cholesterol level was decreased (P< 0.001), and the serum LPS level was also decreased (P=0.003). The expressions of inflammatory factors TNF-α(ileum：P=0.030，colon：P=0.029), IL-6(ileum：P=0.040，colon：P=0.001) and IL-1β(ileum：P= 0.004, colon：P=0.017) in intestinal tissue were significantly decreased, while the expression of tight junction protein in intestinal epithelial cells didn’t change. Conclusion The lack of intestinal commensal microbiota increases the level of systemic inflammation in ApoE -/- mice and promotes the formation of atherosclerotic plaque, which suggests that normal intestinal commensal bacteria may have a protective effect on atherosclerosis in ApoE -/- mice. [ABSTRACT FROM AUTHOR]

Objective To explore the effect of 6-hydroxydopamine blockade of sympathetic nerves on systemic inflammation in an imiquimod(IMQ)-induced psoriasis-like mouse model. Methods Twenty-four SPF C57BL/6J mice were randomly divided into psoriasis-like dermatitis model group (model group), Candida albicans infected group, blank control group, psoriasis-like dermatitis model with vehicle treatment group (vehicle model group), 6-hydroxydopamine (6-OHDA) treated group, vehicle control group, with 4 mice in each group. The changes of lesion in each group were observed every day. Local inflammation in the dorsal and ear lesions of mice was detected by HE staining, q-PCR and Western blotting of interleukin 17A(IL-17A). Spleens of mice were taken to detect inflammatory cells by flow cytometry, and the level of interleukin 6(IL-6) and interleukin 1β(IL-1β) were detected by q-PCR and Western blotting for the systemic inflammation. Results Epidermal thickening, hypokeratosis, basal keratinocyte proliferation, inflammatory cell infiltration and IL-17A increasing were observed on the dorsal lesions of mice in the Candida albicans infection group and the psoriasis-like model group. Compared with the Candida albicans infected group, there were a large number of skin scale production and spleen enlargement, and splenic inflammatory cells increased, the level of IL-6, IL-1β increased in the psoriasis-like model group. Compared with the solvent model group, the spleen in the 6-OHDA treated group was smaller, the number of macrophages derived from neutrophils and monocytes in the spleen was significantly decrease, and the levels of IL-6 and IL-1β in the spleen were significantly lower. Conclusions IMQ-induced psoriasis-like mouse model lead to systemic inflammation, which can be caused by excessive sympathetic activation.

The intestinal microbiota plays a vital role in regulating host immunity and energy metabolism, and is related to the occurrence of obesity, diabetes, and cardiovascular diseases. At present, various animal models and human studies have proved that Akkermansia muciniphila (Akkermansia muciniphila/A. muciniphila) levels are negatively correlated with the occurrence of metabolic diseases such as obesity, diabetes, obese liver disease, and atherosclerosis. A. muciniphila has broad prospects in the treatment of metabolic disorders by increasing the thickness of the intestinal mucus layer, reducing systemic inflammation, improving glucose tolerance and insulin resistance, and is considered to be a new generation of therapeutic drugs. This article systematically reviews the basic mechanism of the interaction between A. muciniphila and metabolic diseases and hosts. [ABSTRACT FROM AUTHOR]

Objective Obstructive sleep apnea-hypopnea syndrome (OSAHS), which is characterized by chronic intermittent hypoxia (CIH). CIH destroys the balance between oxidation and antioxidation, resulting in the occurrence of oxidative stress. OSAHS also affects systemic inflammation by activating inflammatory cells and increasing levels of circulating inflammatory mediators and pro-inflammatory cytokines. Erectile dysfunction (ED) is common among male OSAHS patients. The aim of this study was to investigate the relationship between sex hormone level and oxidative stress, systemic inflammation in OSAHS patients with erectile dysfunction. Methods Forty-eight male patients with OSAHS, confirmed by polysomnography (PSG) study, were enrolled in the study. The patients were divided into mild-moderate groups and severe groups. Twenty male subjects who were confirmed as not having OSAHS served as the controls. The international index of erectile function-5 (IIEF-5) scale was used to evaluate the erectile function. Blood samples were collected from all subjects for measurement of testosterone, luteinizing hormone(LH), total antioxidant capacity(TAOC), reactive oxygen species (ROS), inflammatory cytokines including tumor necrosis factor-⓰(TNF-⓰)and interleukin-6 (IL-6). Results There was significant difference in IIEF-5 score between OSAHS patients and the control group (P＜ 0.05). The IIEF-5 score of the mild-moderate group was (16.67±4.2), and the severe group was(12.15±4.1), the difference between the mild-moderate group and the severe group was statistically significant (P<0.05). The incidence of ED in OSAHS patients was significantly higher than that of the control group(P< 0.05). The incidence of ED was higher in severe group than that in the mild-moderate group. The serum levels of testosterone, LH, TAOC were also decreased significantly in the OSAHS group as compared to those in the control group(P<0.05). The serum level of ROS, IL-6 and TNF-⓰were increased in the OSAHS group compared with those in the control group (P<0.05). There were no significant differences in the levels of testosterone, LH, TAOC, ROS, IL-6 and TNF-⓰between the mild-moderate OSAHS group and the severe OSAHS group(P>0.05). There were significant differences in AHI, testosterone and LH levels between the mild-moderate ED group and severe ED group (P<0.05). Correlation analysis showed that the testosterone was positively correlated with TAOC, and negatively correlated with ROS, RDI and ODI. LH was negatively correlated with RDI, ODI and positively correlated with LSpO2. IIEF-5 score was negatively correlated AHI, ROS, IL-6 and TNF-⓰in the OSAHS group (P<0.05). Conclusion The imbalance of oxidation and antioxidation and the enhancement of systemic inflammatory were found in OSAHS patients. Oxidative stress was related to the decrease of testosterone level, and then involved in the occurrence of erectile dysfunction. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis is a common systematic inflammation disease in adults. The increasing mortality rate of RA patients was mainly caused by cardiovascular diseases (CVD). Possible mechanisms involved in RA progress could be lipid metabolism disorders, and elevated lipoprotein (a), called as Lp-a, was identified as an independent risk factor for CVD. Many papers have reported that Lp-a was related with C VD complications and the inflammation reaction in RA patients. Lp-a gene shows a highly polymorphism and relates with Lp-a synthesis, subtypes and function. Besides, Lp-a levels in serum remain fairly stable, not related with the different gene types in individuals. Alos Lp-a are not influenced by diet or treatment for lipid metabolisms. In recent years, the relationship between Lp-a and CVD was reported in chronic inflammatory diseases, such as RA, and an elevated Lp-a level might be correlated with C VD development and systemic inflammation. So Lp-a could be useful for evaluating CVD risk in RA patients. [ABSTRACT FROM AUTHOR]

Periodontitis and diabetes mellitus are both chronic diseases with a rather high prevalence and they are closely associated with each other. On one hand, diabetes mellitus poses as a risk factor for periodontitis. On the other hand, periodontitis has a negative impact on glucose control in diabetic patients. The two-way relationship has aroused a lot of research interest in recent years. Herein, approaching the issue by looking at the effect of periodontitis on diabetes, we summarized the mechanism of the traditional periodontal pocket-blood circulation pathway and reviewed the role of the oral-gut axis in the mechanism, which has been proposed in recent years. In addition, regarding the impact of diabetes on periodontitis, we summarized new findings concerning changes in oral microbiota, abnormal levels of cytokines and adipokines, oxidative stress, unbalanced osteogenic and osteoclastic activities, and the accumulation of advanced glycation end-products. We hope this paper will be helpful for further studies on the mechanism of association between periodontitis and diabetes., (Copyright© by Editorial Board of Journal of Sichuan University (Medical Sciences).)

Chronic kidney disease (CKD) can result in alteration of intestinal flora and damage of intestinal barrier function. Intestinal dysbios is contributes to the generation of colon-derived uremic solutes and the translocation of bacteria and endotoxins from gut lumen into the bloodstream, subsequently increasing uremic toxicity and triggering systemic inflammation, which is related to CKD progression and many complications. Studies have revealed that dietary fiber can reduce uremic toxin levels and systemic inflammation in CKD through targeting the "gut-kidney axis". Dietary fiber seems to be a promising measure for CKD treatment.

Objective: To investigate the association of sleep quality with the levels of systemic inflammatory markers in patients with chronic obstructive pulmonary disease(COPD) and the correlations between the frequency of acute exacerbation of COPD (AECOPD) and Pittsburgh sleep quality index (PSQI). Methods: A total of 198 COPD patients admitted in our hospital from October, 2016 to June, 2017 were screened, and 124 patients were eligible for the study. On the first day of hospitalization, the serum samples and clinical data were collected, including white blood cells, lymphocytes, platelet count, CRP and PSQI. Poor sleep quality was defined as PSQI score >5. Results: The percentage of COPD patients with poor sleep quality was about 68%. Poor sleep quality was positively correlated with the frequency of acute exacerbation in COPD patients. The ratio of neutrophil to lymphocyte (NLR), ratio of platelet to lymphocyte (PLR) and levels of CRP were higher in patients with poor sleep quality than those in the control group. NLR, PLR and CRP in peripheral blood of the patients with poor sleep quality were positively correlated with PSQI score. The CRP levels and PSQI score in COPD patients with poor sleep quality group were positively correlated with the frequency of exacerbations in the past year ( r =0.437, r =0.430). Conclusion: A high percentage of COPD patients had poor sleep quality, which was positively correlated with the levels of systemic inflammation as well as the frequency of AECOPD.