Expression of macrophage inflammatory protein-1αin Kupffer cells following liver ischemia or reperfusion injury in rats

AIM： To explore the expression of macrophage inflammatory protein-1α （MIP-1α） in Kupffer cells （KCs） following liver ischemia/reperfusion injury IRI in rats. METHODS： Forty male SD rats were divided randomly into five groups. A model of partial warm ischemia/ reperfusion injury in the rat liver was established. KCs were isolated and incubated one hour, six hours, 12 h, and 24 h after the reperfusion. Tumor necrosis factor alpha （TNF-α） and interleukin-lbeta （IL-1β） in the supernatants were measured by ELISA. MIP-1α in KCs was detected by immunocytochemical and RT-PCR. RESULTS： No or few MIP-1α protein and mRNA were expressed in the KCs of the control group. Its expression in the IRI group had a significant increase after the reperfusion （P 〈 0.05）, which was contrary to the control group. CONCLUSION： The active behavior of the MIP-1α gene in KCs following liver ischemia/reperfusion injury is assumed to be one of the major causes for the hepatic ischemia/reperfusion injury.

Macrophage Inflammatory Protein-1 Beta (MIP-1<i>β</i>) and Platelet Indices as Predictors of Spontaneous Bacterial Peritonitis<br>—MIP, MPV and PDW in SBP

Background/Aims: The objective of this study is to measure macrophage inflammatory protein one beta (MIP-1β), mean platelet volume (MPV) and platelet distribution width (PDW) to evaluate their usefulness in the diagnosis of spontaneous bacterial peritonitis (SBP) in cirrhotic patients. Materials and Methods: This study comprised 41 cirrhotic patients with ascites. MPV, PDW and MIP-1β were measured in serum and ascitic fluid. Results: A significant increase MPV, PDW, C-reactive Protein (CRP) and white blood cell was observed in SBP group compared to non SBP (P ≤ 0.001, P = 0 β was significantly in-creased in ascitic fluid in patients with SBP versus non SBP (P ≤ 0.001). At cutoff value of 8.3 fl MPV had 85.7% sensitivity and 75% specificity (AUC = 0.876) for diagnosis of SBP. At cutoff value of 15.4 PDW had 90.4% sensitivity and 55% specificity (AUC = 0.762). At cutoff value of 121.9 pg/ml MIP-1β in ascitic fluid had 76.1% sensitivity and 100% specificity (AUC = 0.881) for detecting SBP. Conclusion: MIP-1β and platelet indices are useful marker in the diagnosis of SBP in cirrhotic patients. Combined measurement of MIP-1β in serum and ascitic fluid had 100% sensitivity and specificity for diagnosis of SBP.

Expression of Macrophage Inflammatory Protein 1α in the Endothelial Cells Exposed to Diamide

In order to study whether the endothelial cells (ECs) with lipid peroxidation induced by diamide can express and secrete macrophage inflammatory protein 1α (MIP-1α), the expression of MIP-1α protein in the cells was detected by cell enzyme-linked immunosorbent assay (ELISA) and that of MIP-1α mRNA was determined by cell in situ hybridization and nuclease S1 protection assay after the ECs were exposed to different concentrations of diamide for 4 h. The chemotactic activity of MIP-1α was tested by micropore filter method using modified Boyden chambers. Cell ELISA showed that the expression of MIP-1α protein in endothelial cells exposed to 1 μmol/L, 5 μmol/L and 10 μmol/L diamide was 1.9-fold, 2.3-fold and 1.7-fold respectively as much as that in the control cells, which was statistically significant by analysis of variance. In situ hybridization revealed that the mRNA expression of ECs treated with 1 μmol/L, 5 μmol/L and 10 μmol/L diamide was 1 3-fold, 3.0-fold and 1.7-fold as much as that in the control group, which had statistical significance ( F =188.93, P <0.01). The mRNA expression in 5 μmol/L dimide treated ECs, measured by nuclease S1 protection assay, was 3.4-fold as much as that in the control group( t =8 70, P <0 05). Chemotactic response(99.50±4.31 μm) to the culture medium conditioned by 5 μmol/L diamide treated ECs , which was stronger than that(66.47±3.25 μm) conditioned by the ECs ( F =404.31, P <0.05), was significantly decreased ( F =192.25, P <0.05) after adding MIP-1α antibody. It suggests that diamide, a lipid peroxidation inducer, could stimulate ECs to produce high level of MIP-1α, and might play an important role in atherogenesis by promoting the migration of peripheral blood monocytes into arterial intima.

Effect of pharmacological intervention on MIP-1α,MIP-1β and MCP-1 expression in patients with psoriasis vulgaris

Objective:To detect the expression level of macrophage inflammatory protein-1(MIP-1)α,MIP-1βand monocyte chemoattractant protein-1(MCP-1)in with psoriasis vulgaris and explore the role in the pathogenesis of psoriasis vulgaris.Methods:The level of MIP-1α,MIP-1βand MCP-1 in peripheral blood from 50 patients with psoriasis vulgaris and 50 normal controls were measured by enzyme linked immunosorbent assay.The correlation with psoriasis area and severity index(PASI)was analyzed.The level of MIP-1α,MIP-1βand MCP-1 was compared between psoriasis vulgaris patients at active stage and resting stage.And the change in MIP-1α,MIP-1βand MCP-1 before and after therapy was also observed.Results:The content of MIP-1α,MIP-1βand MCP-1 in patients with psoriasis vulgaris was(1342.78±210.30),(175.28±28.18)and(266.86±32.75)ng/L,respectively,significantly higher than those in control group(P<0.05).The expression level of MIP-1α,MIP-1βand MCP-1 in peripheral blood of patients with psoriasis vulgaris was positively correlated wilh PASI(P<0.01).After acitretin therapy,expression level of MIP-1α,MIP-1βand MCP-1 in peripheral blood of patients with psoriasis vulgaris was significantly decreased.Conclusions:Chemokine factor MIP-1α,MIP-1βand MCP-1 may be involved in the pathogenesis of psoriasis vulgaris.

Effect of glucocorticoid on MIP-1α and NF-кb expressing in the lung of rats undergoing mechanical ventilation with a high tidal volume

BACKGROUND： Ventilator induced lung injury （VILI） is a serious complication in the treatment of mechanical ventilating patients, and it is also the main cause that results in exacerbation or death of patients. In this study, we produced VILI models by using glucocorticoid in rats with high tidal volume mechanical ventilation, and observed the content of macrophage inflammatory protein-1α （MIP-1α） in plasma and bronchoalveolar lavage fluid （BALF） and the expression of MIP-1α mRNA and nuclear factor-kappa B （NF-кB） p65 mRNA in the lung so as to explore the role of glucocorticoid in mechanical ventilation.METHODS： Thirty-two healthy Wistar rats were randomly divided into a control group, a ventilator induced lung injury （VILI） group, a dexamethasone （DEX） group and a budesonide （BUD） group. The content of MIP-1a in plasma and BALF was measured with ELISA and the level of MIP-1α mRNA and NF-кBp65 mRNA expressing in the lung of rats were detected by RT-PCR. The data were expressed as mean±SD and were compared between the groups.RESULTS： The content of MIP-1α in plasma and BALF and the level of MIP-1α mRNA and NF-кBp65 mRNA in the lung in the DEX and BUD groups were signifi cantly lower than those in the VILI group （P〈0.001）. Although the content of MIP-1α in plasma and BALF and the level of MIP-1α mRNA and NF-кBp65 mRNA in the lung in the BUD group were higher than those in the DEX group, there were no signifi cant differences between them （P〉0.05）.CONCLUSIONS： Glucocorticoid could down-regulate the expression of MIP-1α by inhibiting the activity of NF-кB in the lung and may exert preventive and therapeutic effects on VILI to some extent. The effect of local use of glucocorticoid against VILI is similar to that of systemic use, but there is lesser adverse reaction.

The clinical significance of dynamic changes of MIP-1α, MIP-1βand MCP-1 levels in patients with acute pancreatitis

Objective:To observe dynamic changes of MIP-1α, MIP-1β and MCP-1 in Acute pancreatitis patients, and to evaluate the value of MIP-1α, MIP-1β and MCP-1 in acute pancreatitis severity assessment.Methods: A total of 112 cases of acute pancreatitis were divided into mild pancreatitis (MAP group, 44 cases), moderate severe acute pancreatitis group (MSAP group, 36 cases) and severe acute pancreatitis group (SAP group, 32 cases). Serum MIP-1α, MIP-1βand MCP-1 levels were detected by enzyme-linked immunosorbent assay in patients at 1st, 4th day, 7th days.Results:(1) In 1st day, Serum concentrations of MIP-1α, MIP-1β and MCP-1 were significantly increased in three Groups, There were significant differences between the control group, MAP, MSAP and SAP group. (2) Serum concentrations of MIP-1α, MIP-1β and MCP-1 reached the peak level on 4th day in MAP group and were significantly higher than the level of those on 1st day. In the MSAP and SAP group, serum concentration of MIP-1α, MIP-1β and MCP-1 reached the peak level on 1st day, and significantly higher than the level of those on the 4th day and 7th day. There was a significant difference between MSAP group and MAP group, SAP group and MSAP group in the serum concentration of MIP-1α, MIP-1β and MCP-1 at each monitoring time.Conclusions:MIP-1α, MIP-1β and MCP-1 levels have the rule of dynamic change in Patients with acute pancreatitis, which are useful in evaluating the severity of the patients with acute pancreatitis.

Predictors of Spontaneous Bacterial Peritonitis (SBP) in Liver Cirrhosis: Current Knowledge and Future Frontiers

Spontaneous bacterial peritonitis (SBP) in patients with cirrhotic liver disease is a serious complication that contributes to the high morbidity and mortality rate seen in this population. Currently, there is a lack of consensus amongst the research community on the clinical predictors of SBP as well as the risks and benefits of prophylactic antibiotic therapy in these patients. Pharmacological gastric acid suppression (namely with PPIs and H2RAs) are frequently prescribed for these patients, many times without a clear indication, and may contribute to gut bacterial overflow and SBP development. However, this remains controversial as there are conflicting findings in SBP prevalence between PPI/H2RA-users and non-users. In addition, studies show recent antibiotic use, whether for SBP prophylaxis or for another infectious process, appear to be associated with higher rates of SBP and drug-resistant organisms. Other researchers have also explored the link between zinc, platelet indices (MPV), and macrophage inflammatory protein-1 β (MIP-1β) levels in liver cirrhosis, all of which appear to be promising markers for classifying SBP risk and diagnosis. This literature review was limited by the number and quality of studies available as most are retrospective in nature. Thus, more ongoing, prospective studies and trials are needed to judge the true value of the findings in the studies reviewed in hopes that they can guide appropriate prevention, diagnosis, and management of SBP.

Glomerular chemokine expression and the effect of steroid and cyclophosphamide pulse therapy in human crescentic glomerulonephritis

OBJECTIVE: To study glomerular expression of C-C chemokines, monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1alpha and beta (MIP-1alpha, MIP-1beta) and the effect of steroid and cyclophosphamide (CTX) intermittent intravenous pulse therapy on expression in patients with crescentic glomerulonephritis (CGN) to further investigate the underlying mechanism of the treatment. METHODS: Twelve patients with initial biopsy-proven CGN(2), 6 with lupus nephritis (lupus-CGN, LN-CGN) and 6 with vasculitis, (vasculitis-CGN, V-CGN) were enrolled in this study. They underwent an initial biopsy before steroid and CTX intermittent intravenous pulse therapy and were biopsied again one to three months later. Expression of MCP-1, MIP-1alpha, MIP-1beta, and CD68 in glomeruli with cellular and fibrocellular crescents were examined by immunohistochemical analysis in serial sections of renal biopsies. The effect of the pulse therapy on histopathological changes was also observed. RESULTS: Although steroid and CTX intermittent intravenous pulse therapy markedly reduced the degree of glomerular crescent formation both in LN-CGN and V-CGN, the effect of the therapy on glomerular chemokine expression was significantly different between LN-CGN and V-CGN. It was found that steroid and CTX intermittent intravenous pulse therapy reduced the expression of CD68, MCP-1, and MIP-1alpha, but had no effect on MIP-1beta in glomeruli with cellular crescents of patients with LN-CGN. In patients with V-CGN, the therapy also reduced the expression of CD68, but had no effect on MCP-1, MIP-1alpha, and MIP-1beta in glomeruli with cellular crescents. It was noted that the degree of glomerulosclerosis and tubular interstitial fibrosis increased more significantly at the second biopsy in V-CGN as compared to LN-CGN. CONCLUSIONS: The efficacy of steroid and CTX intermittent intravenous pulse therapy in CGN might be affected by reduction of glomerular chemokine expression. The different changes in glomerular expression of MCP-1 and MIP-1alpha in patients with LN-CGN and V-CGN after pulse therapy may correlate to different responses to treatment and prognosis.