This experiment was conducted to assess the changing patterns and relative values of acute phase proteins and inflammatory cytokines in experimental caprine coccidiosis. Eighteen newborn kids were allocated to 3 equal groups. Two groups, A and B, were inoculated with a single dose of 1x10(3) and 1x10(5) sporulated oocysts of Eimeria arloingi, respectively. The third group, C, received distilled water as the control. Blood samples were collected from the jugular vein of each kid in both groups before inoculation and at days 7, 14, 21, 28, 35, and 42 post-inoculation (PI), and the levels of haptoglobin (Hp), serum amyloid A (SAA), TNF-alpha, and IFN-gamma were measured. For histopathological examinations, 2 kids were selected from each group, euthanized, and necropsied on day 42 PI. Mean Hp concentrations in groups A and B (0.34 and 0.68 g/L) at day 7 PI were 3.2 and 6.3 times higher than the levels before inoculation. The mean SAA concentrations in groups A and B (25.6 and 83.5 microg/ml) at day 7 PI were 4.2 and 13.7 times higher than the levels before inoculation. The magnitude and duration of the Hp and SAA responses correlated well with the inoculation doses and the severity of the clinical signs and diarrhea in kids. These results were consistent with the histopathological features, which showed advanced widespread lesions in group B. In both groups, significant correlations were observed for TNF-alpha and IFN-gamma with SAA and Hp, respectively. In conclusion, Hp and SAA can be useful non-specific diagnostic indicators in caprine coccidiosis.
Acute-Phase Proteins/*analysis ; Animals ; Blood Chemical Analysis ; Coccidiosis/*immunology/*pathology ; Disease Models, Animal ; Eimeria/*pathogenicity ; Goats ; Histocytochemistry ; Inflammation Mediators/*analysis

OBJECTIVETo study the effects of conventional mechanical ventilation (CMV) with low tidal volume on developmental porcine lungs by examining the expression of growth factors and inflammatory mediators.

METHODSTwelve preterm piglets born at 99 days of gestational age, 12 term neonatal piglets and 11 young piglets (4-5-weeks old) were randomly placed on CMV or were not ventilated (control group). The ventilator settings were adjusted to provide a tidal volume of 6-8 mL/kg in order to maintain a normal blood-gas value. After 6 hrs (preterm piglets) or 24 hrs (neonatal and young piglets) of mechanical ventilation, the mRNA expression of growth factors PDGF-B, IGF-I, KGF, HGF, VEGF and TGF-beta1 and proinflammatory cytokines IL-1beta, IL-6, IL-8 and TNF-alpha in the lung tissue was measured using RT-PCR. Growth factor protein expression was measured with immunohistochemistry.

RESULTSIn preterm piglets, the CMV group had increased mRNA expression of PDGF-B (5.11+/-0.10 vs 4.88+/-0.01), IL-1beta (4.95+/-0.27 vs 4.08+/-0.37), IL-6 (4.76+/-0.27 vs 4.00+/-0.28) and IL-8 (5.31+/-0.57 vs 4.15+/-0.46), but decreased IGF-I mRNA expression (3.54+/-0.13 vs 3.80+/-0.11) compared with those in the control group (P<0.05 or 0.01). In term neonatal piglets and young piglets, there were no significant differences in the mRNA expression of growth factors and proinflammatory cytokines between the CMV and control groups.

CONCLUSIONSCMV caused inflammatory injury in immature lungs by increasing the expression of proinflammatory cytokines and PDGF-B and decreasing IGF-I expression. However, CMV had no effects on pulmonary expression of growth factors and inflammatory mediators in term neonatal piglets and young piglets.

Animals ; Bronchoalveolar Lavage Fluid ; chemistry ; Immunohistochemistry ; Inflammation Mediators ; analysis ; Intercellular Signaling Peptides and Proteins ; analysis ; genetics ; Lung ; metabolism ; Peroxidase ; analysis ; Phospholipids ; analysis ; RNA, Messenger ; analysis ; Respiration, Artificial ; Reverse Transcriptase Polymerase Chain Reaction ; Swine ; Tidal Volume ; Vascular Endothelial Growth Factor A ; analysis ; genetics

OBJECTIVETo explore the correlations between serum uric acid (UA) levels and the clinical and cerebrospinal fluid (CSF) parameters of multiple sclerosis (MS).

METHODSThe medical reports of 47 MS patients admitted to Peking Union Medical College Hospital during 2008 and 2010 were reviewed. And 49 age- and gender-matched cerebral infarction patients were enrolled as control. The mean serum UA level of the MS patients was compared with that of the control group. The correlations between the UA levels and the clinical parameters including gender, disease duration, relapse rate, and disease disabilities as assessed by the Expanded Disability Status Scale score, were explored. Forty-one patients had CSF examinations. The correlations between the UA levels and the CSF parameters reflecting inflammation and tissue damage, including CSF protein, white blood cell count, oligoclonal band, 24-hour IgG index, and myelin basic protein, were also investigated.

RESULTSThe mean serum UA level in the MS patients was lower than that in the control group (247.75±52.59 µmol/L vs. 277.94±74.33 µmol/L, P=0.025) and inversely correlated with the relapse rate (P=0.049). MS patients with lower serum UA levels tended to have higher white blood cell counts and myelin basic protein level. But there was no correlation between CSF protein levels (r=0.165, P=0.273), white blood cell counts (r=-0.051, P=0.732), IgG index (r=0. 045, P=0.802), or myelin basic protein level (r=-0.248, P=0.145) and the serum UA level, respectively.

CONCLUSIONIn MS patients, UA levels might partly reflect the extent of disability and inflammation.

Adolescent ; Adult ; Aged ; Case-Control Studies ; Disease Progression ; Female ; Humans ; Inflammation ; blood ; cerebrospinal fluid ; Inflammation Mediators ; analysis ; cerebrospinal fluid ; metabolism ; Male ; Middle Aged ; Multiple Sclerosis ; blood ; cerebrospinal fluid ; immunology ; metabolism ; Spine ; Uric Acid ; blood ; Young Adult

We report here the use of human inflammation arrays to study the inflammatory gene expression profile of TNF-alpha- treated human SGBS adipocytes. Human preadipocytes (SGBS) were induced to differentiate in primary culture, and adipocyte differentiation was confirmed, using Oil Red O staining. We treated the differentiated adipocytes with TNF-alpha, and RNA from differentiated adipocytes with or without TNF-alpha treatment was hybridized to MWG human inflammation arrays to compare expression profiles. Eleven genes were up- or down-regulated in TNF-alpha-treated adipocytes. As revealed by array analysis, among 6 up-regulated genes, only eotaxin-1, monocyte chemoattractant protein-1 (MCP-1), and vascular cell adhesion molecule 1 isoform a precursor (VCAM1) were confirmed by real-time polymerase chain reaction (PCR). Similarly, among 5 down-regulated genes, only IL-1 family member 5 (IL1F5), a disintegrin and metalloprotease with thrombospondin motifs-1 preproprotein (ADAMTS1), fibronectin 1 isoform 1 preprotein (FN1), and matrix metalloproteinase 15 preprotein (MMP15) were confirmed by real-time PCR. There was a substantial increase (50-fold) in eotaxin-1 in response to TNF-alpha. Taken together, we have identified several inflammatory molecules expressed in SGBS adipocytes and discovered molecular factors explaining the relationship between obesity and atherosclerosis, focusing on inflammatory cytokines expressed in the TNF-alpha-treated SGBS cells. Further investigation into the role of these up- or down-regulated cytokine genes during the pathological processes leading to the development of atherosclerosis is warranted.
Tumor Necrosis Factor-alpha/*pharmacology ; Polymerase Chain Reaction ; Oligonucleotide Array Sequence Analysis ; Inflammation Mediators/*metabolism ; Humans ; Gene Expression Regulation/*drug effects ; Gene Expression Profiling ; Cells, Cultured ; Cell Differentiation ; Adipocytes/cytology/drug effects/*metabolism

INTRODUCTIONThe role of soluble OX40 ligand (sOX40L) in adult bronchial asthma is unclear. This study aims to determine the serum concentrations of sOX40L in adult patients with bronchial asthma, and discussed its relationship with pulmonary function.

MATERIALS AND METHODSWe measured the pulmonary function using the spirometer and detected the serum concentrations of sOX40L by enzyme linked immunosorbent assay (ELISA) in 19 healthy persons in the control group, 58 acute asthmatic adult patients who were grouped according to their disease severity: 18 mild grade, 24 moderate grade, 16 severe grade, and 24 persons in a stable asthmatic group.

RESULTSThe serum concentrations of sOX40L in asthmatic adult patients (6.80 ± 4.95 ng/L) were distinctly higher than those in the control group (3.98 ± 2.83 ng/L, P <0.05), and they were negatively correlated with pulmonary function indexes (FEV1%, FVC%, FEV1/FVC) (r = -0.754, P <0.01, r = -0.557, P <0.01, r = -0.457, P <0.01, respectively). Moreover, the serum concentrations of sOX40L showed obvious differences among control, mild, moderate, and severe groups (3.98 ± 2.83, 4.87 ± 1.89, 6.97 ± 5.91, 8.71 ± 5.18 ng/L, respectively; P <0.01). The concentrations of sOX40L decreased to the same extent as the control group after therapeutic treatments were provided to the asthmatic adult patients.

CONCLUSIONThe concentrations of sOX40L were found to be high in adult asthmatic patients and were associated with the severity of the disease. Therefore, sOX40L could be a potential inflammatory mediator in the pathogenesis of asthma.

Adult ; Analysis of Variance ; Asthma ; blood ; etiology ; physiopathology ; Case-Control Studies ; Enzyme-Linked Immunosorbent Assay ; Female ; Forced Expiratory Volume ; Humans ; Inflammation Mediators ; blood ; Lung ; physiopathology ; Male ; Middle Aged ; OX40 Ligand ; blood ; Severity of Illness Index ; Spirometry

OBJECTIVES: Eosinophils play an important role in asthmatic airway inflammation collaborately with other inflammatory cells. The present study was aimed to determine whether the eosinophil activation markers in induced sputum reflect the clinical status in asthmatics. METHODS: The clinical severity and FEV1 were measured. Hypertonic saline induced sputum was obtained from 25 asthmatics and ten control subjects. We processed freshly expectorated sputum separated from saliva by treatment with an equal volume of dithiothreitol 0.1+ACU-, cytospins for cell count and special stain, and a collection of the supernatant for biochemical assay. We used a fluoroimmunoassay to detect eosinophil cationic protein (ECP), and a sandwich ELISA to detect interleukin (IL)-5. RESULTS: Asthmatics, compared with control subjects, had a significantly higher proportion of eosinophils (25.6 4.6+ACU- vs 1.7 0.2+ACU-, p +ADw- 0.01) and higher levels of ECP (1117.8 213.9 micrograms/L vs 154.6 47.4 micrograms/L, p +ADw- 0.01) in their sputum. IL-5 was detected more frequently in asthmatics than in control subjects +AFs-11/25 (44+ACU-) vs 1/10 (10+ACU-), p +ADw- 0.05+AF0-. Moderate to severe asthmatics had a significantly higher proportion of eosinophils, higher levels of ECP and IL-5 compared to mild asthmatics. FEV1, FEV1/FVC were significantly correlated with the proportion of eosinophils and the levels of ECP and IL-5. Significant positive correlations were noted between the proportion of eosinophils and the level of ECP and IL-5. Sputum ECP level showed a significant positive correlation with IL-5 level. CONCLUSION: These findings demonstrate that eosinophils and the eosinophil activation markers, such as ECP and IL-5 in induced sputum, are closely related to the clinical status in asthmatics. Induced sputum study may thus be useful in clinically measuring indices of airway inflammation in asthma.
Adult ; Asthma/physiopathology ; Asthma/classification+ACo- ; Biological Markers/analysis ; Blood Proteins/analysis+ACo- ; Bronchoalveolar Lavage ; Enzyme-Linked Immunosorbent Assay ; Female ; Fluoroimmunoassay ; Human ; Inflammation Mediators/analysis+ACo- ; Interleukin-5/analysis+ACo- ; Male ; Middle Age ; Prognosis ; Respiratory Function Tests ; Sensitivity and Specificity ; Severity of Illness Index ; Sputum/cytology+ACo-

Excessive production of nitric oxide (NO) and proinflammatory cytokines from activated microglia play an important role in human neurodegenerative disorders. Here, we investigated whether celastrol, which has been used as a potent anti-inflammatory and anti-oxidative agent in Chinese medicine, attenuates excessive production of NO and proinflammatory cytokines such as TNF-alpha and IL-1beta in LPS-stimulated BV-2 cells, a mouse microglial cell line. We report here that the LPS-elicited excessive production of NO, TNF-alpha, and IL-1beta in BV-2 cells was largely inhibited in the presence of celastrol, and the attenuation of inducible iNOS and these cytokines resulted from the reduced expression of mRNAs of iNOS and these cytokines, respectively. The molecular mechanisms that underlie celastrol-mediated attenuation were the inhibition of LPS-induced phosphorylation of MAPK/ERK1/2 and the DNA binding activity of NF-kappaB in BV-2 cells. The results indicate that celastrol effectively attenuated NO and proinflammatory cytokine production via the inhibition of ERK1/2 phosphorylation and NF-kappaB activation in LPS-activated microglia. Thus, celastrol may be an effective therapeutic candidate for use in the treatment of neurodegenerative human brain disorders.
Animals ; Cell Line ; Cytokines/*biosynthesis/drug effects ; Gene Expression Regulation, Enzymologic/drug effects/immunology ; Inflammation/immunology ; Inflammation Mediators/immunology ; Mice ; Microglia/*drug effects/immunology ; Mitogen-Activated Protein Kinases/*physiology ; NF-kappa B/metabolism/*physiology ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase Type II/biosynthesis/drug effects ; RNA, Messenger/analysis ; Signal Transduction/*drug effects/physiology ; Transcription, Genetic/drug effects/immunology ; Triterpenes/*pharmacology

OBJECTIVESTo investigate the effect of Shenfu Injection (, SFI) on inflammatory factors in patients with acute myocardial infarction complicated by cardiogenic shock (CS) treated with and intra-aortic balloon pump (IABP).

METHODSThis study enrolled 60 patients with ST-segment elevation myocardial infarction (STEMI) complicated by CS. Patients underwent IABP and emergency percutaneous coronary intervention (PCI) were randomly divided into two groups by random number table with 30 cases in each group, one given Sfitreatment (100 mL/24 h), one not. The two groups were then compared in a clinical setting for left ventricular function, biochemical indicators and Inflammatory factors, including C-reactive proteins (CRP), interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-α). Major adverse cardiac and cerebrovascular events (MACCE) events were compared between patients of the two groups both in-hospital and in follow-ups.

RESULTSThe IABP support treatment times of patients in the IABP+Sfigroup were signifificantly shorter than the IABP group (52.87±28.84 vs. 87.45±87.31, P=0.047). In the patients of the IABP+Sfigroup, the CRP peak appeared in 24 h after PCI operation. The CRP peak in the patients of the IABP+Sfigroup was signifificantly lower than that in the IABP group (31.27±3.93 vs. 34.62±3.47, P=0.001). The increases in range of TNF-α in the patients of the IABP+Sfigroup were signifificantly lower than those of the IABP group (182.29±22.79 vs. 195.54±12.02, P=0.007). The increases in range of IL-1 in the patients of the IABP+Sfigroup were signifificantly lower than those of the IABP group (214.98±29.22 vs. 228.60±7.03, P=0.019). The amplitude elevated TNF-α 72 h after admission was an independent risk factor of in-hospital MACCE events (OR 0.973, 95% CI 0.890-0.987, P=0.014) in patients with STEMI and CS.

CONCLUSIONPatients with STEMI complicated by CS treated by IABP and Sfihad a reduced inflammatory reaction, a reduced dependence of CS on IABP and shortened the course of disease.

Drugs, Chinese Herbal ; administration & dosage ; adverse effects ; therapeutic use ; Enzyme-Linked Immunosorbent Assay ; Female ; Follow-Up Studies ; Hospital Mortality ; Humans ; Inflammation ; blood ; complications ; drug therapy ; Inflammation Mediators ; metabolism ; Injections ; Logistic Models ; Male ; Middle Aged ; Multivariate Analysis ; Myocardial Infarction ; blood ; complications ; drug therapy ; mortality ; Shock, Cardiogenic ; complications ; drug therapy ; Treatment Outcome

OBJECTIVEBuckwheat has been considered as a potential source of nutraceutical components on the world market of probiotic foodstuffs. The purpose of this study was to evaluate the effects of tartary buckwheat (Fagopyrum tataricum) sprouts on oxidation and pro-inflammatory mediators.

METHODSThe anti-oxidant effects of buckwheat extract (BWE) and rutin were evaluated by using 1,1-diphenyl-2-picrylhydrazyl (DPPH)- and nitric oxide (NO)-scavenging activities, serum peroxidation and chelating assays. Lipopolysaccharide (LPS)-stimulated RAW264.7 cells were used to evaluate anti-inflammatory activities of buckwheat and rutin. NO production in LPS-stimulated RAW264.7 cells was determined by using Griess reagent. The expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor-kappa B (NF-κB) p65 subunit in cytosolic and nuclear portions were determined by Western blot analysis. Also, the production of inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) was determined by enzyme-linked immunosorbent assay.

RESULTSInhibitory concentration 50 values for DPPH- and NO-scavenging activities of BWE were 24.97 and 72.54 μg/mL respectively. BWE inhibited serum oxidation and possessed chelating activity. Furthermore, BWE inhibited IL-6 and TNF-α production in LPS-stimulated RAW264.7 cells. Also, BWE inhibited iNOS and COX-2 expression and NF-κB p65 translocation.

CONCLUSIONBuckwheat sprouts possessed strong antioxidant activity and inhibited production of pro-inflammatory mediators in the applied model systems. Thus, buckwheat can be suggested to be beneficial in inflammatory diseases by inhibiting the free radicals and inflammatory mediators.

Animals ; Cells, Cultured ; Cyclooxygenase 2 ; analysis ; Fagopyrum ; Free Radical Scavengers ; pharmacology ; Inflammation Mediators ; antagonists & inhibitors ; Interleukin-6 ; biosynthesis ; Lipopolysaccharides ; pharmacology ; Macrophages ; drug effects ; metabolism ; Mice ; NF-kappa B ; metabolism ; Nitric Oxide ; biosynthesis ; Nitric Oxide Synthase Type II ; analysis ; Plant Extracts ; pharmacology ; Tumor Necrosis Factor-alpha ; biosynthesis

To explore the therapeutic effect of honokiol on particulate matter 2.5 (PM2.5)-induced lung injury in asthmatic mice and the possible mechanisms.
 Methods: A total of 32 BALB/C mice were randomly divided into four groups: a normal saline group, a model group, a PM2.5 group and a honokiol group (n=8 in each group). The asthma mouse model was established by ovalbumin treatment. The mice were treated with physiological saline, ovalbumin, PM2.5 and honokiol, respectively. Lung tissues and serum were collected. The pathological changes of lung tissues were evaluated. The levels of inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and serum were measured and the expressions of Toll like receptor 4 (TLR4), nuclear factor kappa B (NF-κB), retinoid-related orphan receptor gamma-t (RORγt) and forkhead box protein 3 (Foxp3) in lung tissues were detected.
 Results: 1) The lung tissues of mice in the asthma group showed obvious pathological changes and inflammatory state, suggesting that the asthma model was established successfully. PM2.5 could aggravate the pathological condition of inflammatory injury in lung tissues in asthmatic mice. 2) Compared to the PM2.5 group, the pathological symptoms in the lung tissues were alleviated in the honokiol group and the percentage of inflammatory cells in BALF and the levels of inflammatory cytokines in BALF and serum were significantly reduced (all P<0.05). 3) Compared to the PM2.5 group, the expressions of TLR4, NF-κB (p-p65) and RORγt in lung tissues were significantly decreased, while the expression of Foxp3 was increased; the ratio of RORγt/Foxp3 was also decreased in the honokiol group (all P<0.05).
 Conclusion: Honokiol can resist lung injury induced by PM2.5 in asthmatic mice. These effects are through inhibiting TLR4-NF-κB pathway-mediated inflammatory response or regulating the balance of Th17/Treg cells.
Animals ; Asthma ; chemically induced ; complications ; Biphenyl Compounds ; pharmacology ; Bronchoalveolar Lavage Fluid ; chemistry ; Cytokines ; analysis ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; Inflammation Mediators ; analysis ; Lignans ; pharmacology ; Lung ; metabolism ; pathology ; Lung Injury ; drug therapy ; etiology ; metabolism ; pathology ; Mice ; Mice, Inbred BALB C ; NF-kappa B ; metabolism ; Ovalbumin ; Particulate Matter ; toxicity ; Random Allocation ; Toll-Like Receptor 4 ; metabolism