Objective The effects of endotoxin, cytokines, nitric oxide were reviewed in the development of hyperdynamic circulatory syndrome in portal hypertension. Methods Liceratures of overseas main studies in hyperdynamic circulatory syndrome of portal hypertension in recent 10 years were reviewed. Results The hyperdynamic circulatory syndrome was found in 30%-50% of patients with cirrhosis and in all animal models of portal hypertension. The research results of the effects of endotoxin, cytokines, nitric oxide in the development of hyperdynamic circulatory syndrome were different. Conclusion Hyperdynamic circulatory syndrome contribute to the maintenance and aggregation of portal hypertension. Endotoxin, cytokines, nitric oxide may play a role in the development of hyperdynamic circulatory syndrome. Nitric oxide is a more important factor. The effect of other factors is probably mediated by nitric oxide.
Objective To investigate the values of cytokines in evaluating the severity and prognosis of patients with coronavirus disease 2019 (COVID-19). Methods A total of 205 COVID-19 patients in Wuhan Leishenshan Hospital were retrospectively analyzed. According to the severity of the disease, patients were divided into common group (n=117), severe group (n=69) and critical group (n=19). The patients’ basic condition and cytokine related parameters were collected, the differences between the three groups were compared and their values in assessing the severity and prognosis of COVID-19 patients were analyzed. Results There were statistically significant differences in the age, severe acute respiratory syndrome coronavirus 2 nucleic acid test results, interleukin (IL)-6, IL-10, IL-2 receptor, IL-8, and tumor necrosis factor-α among the three groups of patients (P<0.05). Correlation analysis showed that the age, severe acute respiratory syndrome coronavirus 2 nucleic acid test continued to be positive for 20 days, IL-6 level, IL-10 level, IL-2 receptors level, IL-8 level and tumor necrosis factor-α level were related to the classification of COVID-19. The correlation coefficient rs was 0.354, 0.187, 0.366, 0.327, 0.329, 0.273 and 0.157, respectively (P<0.05). The levels of IL-6, IL-10, IL-2 receptor, IL-8, and tumor necrosis factor-α in dead patients with COVID-19 were higher than those in surviving patients (P<0.05). Multivariate analysis showed that age [odds ratio (OR)=1.034, 95% confidence interval (CI) (1.006, 1.063), P=0.016], IL-6 level [OR=1.030, 95%CI (1.006, 1.055), P=0.015], IL-10 level [OR=1.088, 95%CI (1.003, 1.179), P=0.042] and IL-2 receptor level [OR=1.003, 95%CI (1.001, 1.005), P=0.001] were independent risk factors for common COVID-19 to become severe or critical. Conclusion The levels of cytokines in COVID-19 patients are closely related to the severity and prognosis of the disease.
ObjectiveTo determine the nuclear factor kappa B (NFkB) activity in peripheral blood mononuclear cells (PBMC) in patients with acute cholangitis of severe type (ACST) and correlate the degree of NFkB activation with severity of biliary tract infection and clinical outcome.MethodsTwenty patients with ACST were divided into survivor group (14 cases) and nonsurvivor group (6 cases). Other 10 patients undergoing elective gastrectomy or inguinal hernia repair were selected as control group. Peripheral blood samples were taken 24 hours after operation, PBMC was separated and nuclear proteins were isolated from PBMC, and NFkB was determined with electrophoretic mobility shift assay (EMSA). The levels of TNFα, IL6 and IL10 in plasma were determined by using an enzymelinked immunoassay (ELISA). ResultsThe NFkB activity was 5.02±1.03, 2.98±0.51 and 1.02±0.34 respectively in three groups. It was increased in all patients with ACST, versus the control group (P＜0.05), and the patients of nonsurvivor group had higher levels of NFkB activation than those of survivor group (P＜0.05). The levels of TNFα and IL6 were (496.28±52.35) ng/L and (578.13±67.72) ng/L in nonsurvivor group; (284.47±39.41) ng/L and (318.67±34.92) ng/L in survivor group; (89.43±10.39) ng/L and (101.27±13.47) ng/L in control group. All patients with ACST had increased levels of TNFα and IL6, which were many fold greater than that of control group, and there was an evidence of significantly higher levels in nonsurvivor group than in survivor group (P＜0.05). All patients had also increased levels of IL10 as compared to control group (P＜0.05), but the IL10 concentrations in plasma were not significantly higher in nonsurvivors than that of in those survivors (Pgt;0.05). ConclusionNFkB activation in PBMCs in patients with ACST
ObjectiveTo investigate the expression of CD4+CD25highCD127lowTreg (Treg) and related cytokines in peripheral blood of COPD patients with pulmonary hypertension and explore its clinical significance.
MethodsPeripheral blood lymphocytes and serum were collected from 65 COPD patients with chronic pulmonary hypertension (the CPH group) and 20 COPD patients with normal pulmonary artery pressure (the control group). Flow cytometry was used to detect the Treg/CD4+ T cells and calculate its ratio, enzyme-linked immunosorbent assay was used to detect the serum contents of interleukin (IL)-6,IL-10 and tumor necrosis factor α (TNF-α).
ResultsTreg can be detected in the peripheral blood of patients of COPD with or without PH, however, the Treg ratio in the CPH group was significantly lower than that in the control group [(7.41±1.12)% vs. (9.04±2.11)%, P<0.05]. Compared with the control group, the IL-10 level was significantly lower [(4.47±0.88)pg/mL vs. (5.18±0.26)pg/mL], while IL-6and TNF-α contents were significantly higher in the CPH group [(7.49±0.95)pg/mL vs. (6.76±0.35)pg/mL, (28.61±9.16)pg/mL vs. (19.64±4.85)pg/mL, P<0.05]. There was a positive correlation between Treg ratio and serum IL-10 level (r=0.41, P<0.05), and negative correlation between Treg ratio and TNF-α or IL-6 contents (r=0.45 or 0.37,P<0.05). The Treg ratio of the patients with severe pulmonary hypertension was lower than that in the patients with mild pulmonary hypertension [(7.42±1.03)% vs. (10.47±2.55)%,P<0.05).
ConclusionsContents of Treg and IL-10 decrease while IL-6 and TNF-α increase in peripheral blood of COPD patients with pulmonary hypertension. It suggests that Treg cells and related cytokines may involve in the pathogenesis and progression of CPH. Treg may becomea potential biological prognosis indicator and treatment target of CPH in the future.
The aim of this study was to investigate the role of tumor necrosis factor (TNF), interleukin-6(IL-6), C-reactive protein (CRP) in pancreatitis and its systemic complications. Thirty six patients with acute pancreatitis were studied, 12 with mild disease, and 24 severe disease, of whom 9 developed systemic complications. TNF, IL-6, CRP in these patients with pancreatitis was assessed during the first, 4th, 8th days of admission. The serum concentration of TNF, IL-6, CRP were significantly increased, and significantly higher in complicated group than in mild group and severe group. These findings suggest that proinflammatory cytokines play a central role in the pathophysiology of the disease, the host systemic response to pancreatic inflammation and the level of the response did relate to the development of organ dysfunction.
ObjectiveTo monitor the airway inflammatory factors in exhaled breath condensate(EBC) of severe stable COPD patients during salmeterol/fluticasone (50/500μg, bid) treatment, and explore their clinical significance.
MethodsTwenty-four sever stable COPD patients and 18 healthy controls were included in the study. EBC was collected from COPD patients before treatment (day 0) and 14 days, 28 days, 90 days after treatment. Meanwhile lung function test and SGRQ score were measured.Concentrations of IL-6 and IL-10 were measured by liquid chip and 8-isoprostane by enzyme-linked immunosorbent assay.
ResultsLevels of 8-isoprostane, IL-6 and IL-10 in EBC were significantly higher in the sever stable COPD patients before treatment compared with the healthy controls. 8-isoprostane was decreased significantly at day 14 compared with day 0[(11.59±4.12) pg/mL vs. (14.17±4.66) pg/mL, P < 0.05], and kept in low level till day 90 (P > 0.05). IL-6 was significantly decreased at day 28 compared with day 0[(1.46±0.19) pg/mL vs. (1.59±0.19) pg/mL, P < 0.05], but did not change significantly till day 90. IL-10 was in low level but showed increase at day 90 compared with day 28[(1.72±0.19) pg/mL vs. (1.62±0.12) pg/mL, P < 0.05]. FEV1 and FEV1/FVC were improved and SGRQ score was decreased after 90 days treatment (P < 0.05). FEV1 was not correlated with 8-isoprostane, IL-6 or IL-10 level.
ConclusionsDynamic observation of EBC 8-isoprostane level in severe COPD patients can help in evaluating drug efficacy. IL-10 may play a role in airway anti-inflammation.
The serum activities of 3 cytokines (TNF,IL-1 and IL-6) were observed in 23 patients admitted within 4 days of onset of acute pancreatitis (AP). The results showed that the serum level of 3 cytokines raised in all of the AP patients, significant difference between TNF and IL-1 was abserved at admission and IL-6 did after one week of admission, suggesting that proper cytokine criteria are useful in predicting severity of the disease but the relationship between cytokines and MOF had not established.
Objective To observe the expression and investigate the significance of suppressor of cytokine signaling (SOCS) in peripheral blood mononuclear cells (PBMC) of experimental autoimmune uveitis (EAU). Methods 100 Lewis rats were immunized with interphotoreceptor retinoid-binding protein (IRBP) to induce EAU animal model, and they were divided into control group and treatment group randomly. The treatment group was administered cyclosporine A 20mg/（kgmiddot;d）after 1 to 28 days of immunization; the control group received saline buffer at equal quantity. All eyes were evaluated by slit-lamp microscopy before and after 7, 14, 21, 28 days of immunization; IL-4，IL-12，IFN-gamma; in the serum were measured by enzyme linked immunosorbent assay(ELISA); the SOCS mRNA and protein level in PBMC were measured by quantitative polymerase chain reaction (q-PCR) and western blot. Results The inflammation was most obvious at 14 days after immunization. The control group showed obvious iridocyclitis; the treatment group showed mild anterior chamber inflammation but no posterior synechia and hypopyon. The highest level of IL-12 and IFN-gamma; were observed at 14 days after immunization, followed by decline to the baseline at 28 days after immunization in control group; the highest level of IL-12 and IFN-gamma; were found at 14 days after immunization in treatment group, but the level was lower than control group obviously. Compared with the level before immunization, there are no differences at other time-point. The concentration of IL-4 decreased indistinctly in control group but increased in treatment group. SOCS1、Both of SOCS1 and SOCS5 increased to the highest level at 14 days after immunization, as 4.05 and 383 times of preimmunization in control group respectively, as 1.15 and 1.16 times in treatment group respectively. The CIS and SOCS3 mRNA increased lightly in two groups and treatment group milder than control group. Marked increased expression of SOCS1 and SOCS5 protein was detected at 7, 14, 21days than preimmunization, both of CIS and SOCS3 protein were significantly increased on 14, 21 days in control group; only SOCS1 protein was significantly increased on 14 days in treatment group and there are no differences at other time-point compared to pre-immunization. Conclusion Up-regulation of SOCS1 and SOCS5 expression maybe related to intensive response of Th1 in the development of EAU. Mild up-regulation of CIS and SOCS3 maybe associated with intensive response of Th2 which against the reaction of Th1 to carry out the dynamic immune balance.
Objective To observe the inhibitory effects of gene transfer of canstatin on retinal neovascularization in mice. Methods Fifty-six 7-day-old C57BL/6J mice were randomly divided into control group,oxygen-induced retinopathy (OIR) group, empty vector group and treated group,14 mices in each group. Except for the control group,the mice in the other groups were exposed to (75plusmn;2)% oxygen for 5 days and then back to the normal air to establish the model of OIR. On postnatal 12 day, the treated group was received intravitreal injection of canstatin pCMV-HA, while the empty vector group was received the same volume of empty plasmid.The changes of retinal vessels were observed by Evans blue angiography on postnatal 17 day. With parafin section which stained by hematoxylin and eosin, then the number of endotheliocyte nuclei breaking throuhgh the internal limiting membrane（ILM） was observed and counted by optical microscope.Results Retinal blood vessels distributed regularly in treated group compared with OIR group and empty vector group.The differences of the number of endotheliocyte nuclei breaking throuhgh ILM in treated group was significant compared with the other two groups（F=39.006，Plt;0.001).Conclusion The canstatin pCMV-HA can effectively inhibit the retinalneovascularization in OIR.
ObjectiveTo study the cytokine changes in the cerebrospinal fluid (CSF) of mesial temporal lobe epilepsy (MTLE) patients, and the mechanism of the development of hippocampal sclerosis.
MethodsFifty MTLE patients who sought treatment from January 2013 to March 2014 were included in the study. Clinical features were investigated. All CSF samples of the 59 patients along with 19 samples of the control group were tested for 12 common cytokines using a chemokine magnetic bead panel. Data were statistically analyzed.
ResultsClinical features showed no significant difference between hippocampal sclerosis and non-hippocampal sclerosis patients. Interleukin (IL)-1 receptor antagonist (RA), IL-4 and IL-9 expression decreased, and tumor necrosis factor (TNF)-α, IL-3 and IL-5 expression increased. Up-regulation of TNF-α was significantly different between hippocampal sclerosis and non-hippocampal sclerosis patients.
ConclusionIL-1RA, IL-3, IL-4, IL-5 and IL-9 changes may be non-specific seizure-related cytokine regulation. TNF-α is associated with hippocampal sclerosis pathology. TNF-α is a possible pathological element in hippocampal sclerosis development.
