OBJECTIVES: This study aimed to observe the effects of initial periodontal therapy on the level of neutrophil extracellular traps (NETs) in gingival crevicular fluid (GCF) of patients with severe periodontitis and to analyze the factors related to the formation of NETs. METHODS: Thirty-one patients with stage Ⅲ-Ⅳ periodontitis were recruited. Clinical periodontal parameters, including plaque index (PLI), gingival index (GI), probing depth (PD), and clinical atta-chment loss (CAL), were recorded before and 6-8 weeks after initial periodontal therapy. Levels of NETs in GCF were detected by immunofluorescence staining. Quantities of total bacteria, Porphyromonas gingivalis (P. gingivalis), Aggregatibacter actinomycetemcomitans (A. actionomycetemcomitans) and Prevotella intermedia (P. intermedia)in unattached subgingival plaque were determined by real-time quantitative PCR, and levels of tumor necrosis factor-α (TNF-α) and interleukin-8 (IL-8) in GCF were explored by enzyme-linked immunosorbent assay. In addition, the correlations between the level of NETs and the above indicators were analyzed. RESULTS: After initial periodontal therapy, the level of NETs in GCF, PLI, GI, PD, and CAL; quantities of total bacteria, P. gingivalis, A. actinomycetemcomitans, and P. itermedia; and levels of IL-8 and TNF-α significantly decreased (P<0.05). We observed strong positive correlations between the level of NETs and PLI, GI, PD, CAL, the amount of total bacteria, P. gingivalis, TNF-α, and IL-8 (P<0.05). CONCLUSIONS Initial periodontal therapy might decrease the level of NETs in GCF from patients with severe periodontitis, which might be positively correlated with the quantities of P. gingivalis andthe levels of TNF-α and IL-8 in GCF.
Humans ; Gingival Crevicular Fluid ; Extracellular Traps/metabolism* ; Porphyromonas gingivalis/isolation & purification* ; Aggregatibacter actinomycetemcomitans/isolation & purification* ; Periodontitis/metabolism* ; Tumor Necrosis Factor-alpha/analysis* ; Prevotella intermedia/isolation & purification* ; Interleukin-8/analysis* ; Male ; Female ; Middle Aged ; Periodontal Index ; Adult

Chronic gastritis is a kind of chronic gastric mucosal inflammation caused by many factors.Intestinal metaplasia refers to the transformation of gastric mucosal epithelial cells into small/large intestinal mucosal epithelium containing Panette or goblet cells.Chronic gastritis has the highest incidence among stomach diseases,while intestinal metaplasia is the serious manifestation of chronic gastritis.In this experiment,the therapeutic effect of modified Zhengqi Powder on mild intestinal metaplasia in chronic gastritis and on patients' quality of life and inflammatory reaction was investigated to analyze the efficacy and mechanism of traditional Chinese medicine prescription.From April 2016 to April 2017,120 patients of chronic gastritis with mild intestinal metaplasia were selected and divided into two groups according to the envelope method.The control group(60 cases) was treated with famoxetine.After one month of continuous treatment,the total effective rate of treatment in the observation group was 93.3%,which was much higher than 80.0% in the control group.Health questionnaire(SF-36),serum C-reactive protein(CRP),interleukin-8(IL-8) and tumor necrosis factor-α(TNF-α) levels were significantly higher than those in the control group(P<0.05).The results showed that modified Zhengqi Powder has a significant efficacy in treat chronic gastritis with mild intestinal metaplasia,and can obviously alleviate clinical symptoms and intestinal metaplasia,remove inflammatory factors and improve the quality of life of patients,and is worth promotion.
C-Reactive Protein ; analysis ; Drugs, Chinese Herbal ; therapeutic use ; Gastric Mucosa ; drug effects ; Gastritis, Atrophic ; drug therapy ; Humans ; Interleukin-8 ; blood ; Metaplasia ; drug therapy ; Quality of Life ; Tumor Necrosis Factor-alpha ; blood

BACKGROUND: Empirical evidences for efficacy of hot spring (HS) water in inflammatory skin disorders have not been substantiated with sufficient, immunological “hard evidence”. Mageumsan HS water, characterized by its weakly-alkaline properties and low total dissolved solids content, has been known to alleviate various immune-inflammatory skin diseases, including atopic dermatitis (AD). OBJECTIVE: The trial attempted to quantitatively analyze in vitro expression levels of chemical mediators in cutaneous inflammation from HaCaT cell line treated with Mageumsan HS, and suggest the likely mode of action through which it exerts the apparent anti-inflammatory effects in AD. METHODS: Using membrane-based human antibody array kit, customized to include 30 different, keratinocyte-derived mediator proteins, their expression levels (including interleukin [IL]-1, IL-6, IL-8, thymic stromal lymphopoietin, thymus and activation-regulated chemokine, and granulocyte macrophage colony-stimulating factor) were assessed in vitro. Selected key proteins were further quantified with enzyme-linked immunosorbent assay. RESULTS: There was a clear pattern of overall suppression of the mediators, especially those noted for their pro-inflammatory role in AD (monocyte chemoattractant protein [MCP]-1, regulated on activation, normal T cell expressed and secreted, cutaneous T-cell-attracting chemokine, Eotaxin, and macrophage inflammatory protein-1α, etc.). Also, reduced expression of involucrin and cytokeratin 1 was also reduced in the HS-treated group. CONCLUSION: The present study has shown that Mageumsan HS water may exert its effects on inflammatory skin disorders through regulation of proinflammatory cytokines. These evidences are to be supported with further future investigations to elucidate immunological mechanism behind these beneficial effects of HS water in the chronically inflamed skin of AD.
Cell Line ; Chemokine CCL17 ; Chemokine CCL27 ; Cytokines ; Dermatitis, Atopic ; Enzyme-Linked Immunosorbent Assay ; Granulocytes ; Hot Springs* ; Humans ; In Vitro Techniques* ; Inflammation ; Interleukin-6 ; Interleukin-8 ; Interleukins ; Keratins ; Macrophages ; Protein Array Analysis* ; Skin ; Skin Diseases ; Water

OBJECTIVETo compare the effect between nebulized and intravenous administration of Shenmai Injection () on pulmonary gas exchange function of patients following tourniquet-induced lower limb ischemia-reperfusion.

METHODSThirty-eight patients scheduled for lower extremity surgery were randomized into three groups using the closed envelop method: Shenmai Injection was administered 30 min before tourniquet inflflation by nebulization [0.6 mL/kg in 10 mL normal saline (NS)] in the nebulization group or by intravenous drip (0.6 mL/kg dissolved in 250 mL of 10% glucose) in the intravenous drip group, and equal volume of NS was given intravenously in the NS group; 15 in each group. Arterial blood gases were analyzed, serum levels of malonaldehyde (MDA) and interleukine-6 (IL-6) and interleukine-8 (IL-8) were determined using the method of thiobarbituric acid reaction and enzyme-linked immuno sorbent assay respectively just before tourniquet inflflation (T0), and at 0.5 h (T1), 2 h (T2), 6 h (T3) after tourniquet deflflation.

RESULTSCompared with baselines at T0, MDA levels signifificantly increased at T2, T3 in the NS group and at T3 in the nebulization group, and IL-6 and IL-8 levels were signifificantly increased at T2, T3 in NS, the intravenous drip and the nebulization groups (P <0.05). Arterial pressure of oxygen (PaO) at T3 was decreased, while alveolararterial oxygen tension showed difference (PA-aDO) at T3 in the NS group; RI at T3 in both intravenous drip and the nebulization groups were enhanced (P <0.05). Compared with the NS group, MDA and IL-8 levels at T2, T3, IL-6 at T3 in the intravenous drip group, and IL-8 at T3 in the nebulization group were all remarkably increased (P <0.05). Additionally, MDA level at T3 in the nebulization group was higher than that in the intravenous drip group (P <0.05).

CONCLUSIONSIntravenous administration of Shenmai Injection provided a better protective effect than nebulization in mitigating pulmonary gas exchange dysfunction in patients following tourniquet-induced limb ischemia-reperfusion.

Adult ; Blood Gas Analysis ; Drug Administration Routes ; Drug Combinations ; Drugs, Chinese Herbal ; administration & dosage ; pharmacology ; therapeutic use ; Female ; Humans ; Injections ; Interleukin-6 ; blood ; Interleukin-8 ; blood ; Male ; Malondialdehyde ; blood ; Pulmonary Gas Exchange ; drug effects ; Reperfusion Injury ; blood ; drug therapy ; physiopathology ; Tourniquets ; adverse effects

BACKGROUND: Acne vulgaris is a disease of the pilosebaceous unit characterized by increased sebum production, hyperkeratinization, and immune responses to Propionibacterium acnes (PA). Here, we explore a possible mechanism by which a lipid receptor, G2A, regulates immune responses to a commensal bacterium. OBJECTIVE: To elucidate the inflammatory properties of G2A in monocytes in response to PA stimulation. Furthermore, our study sought to investigate pathways by which lipids modulate immune responses in response to PA. METHODS: Our studies focused on monocytes collected from human peripheral blood mononuclear cells, the monocytic cell line THP-1, and a lab strain of PA. Our studies involved the use of enzyme-linked immunosorbent, Western blot, reverse transcription polymerase chain reaction, small interfering RNA (siRNA), and microarray analysis of human acne lesions in the measurements of inflammatory markers. RESULTS: G2A gene expression is higher in acne lesions compared to normal skin and is inducible by the acne therapeutic, 13-cis-retinoic acid. In vitro, PA induces both the Toll-like receptor 2-dependent expression of G2A as well as the production of the G2A ligand, 9-hydroxyoctadecadienoic acid, from human monocytes. G2A gene knockdown through siRNA enhances PA stimulation of interleukin (IL)-6, IL-8, and IL-1β possibly through increased activation of the ERK1/2 MAP kinase and nuclear factor kappa B p65 pathways. CONCLUSION: G2A may play a role in quelling inflammatory cytokine response to PA, revealing G2A as a potential attenuator of inflammatory response in a disease associated with a commensal bacterium.
Acne Vulgaris ; Blotting, Western ; Cell Line ; Cytokines* ; Gene Expression ; Gene Knockdown Techniques ; Humans* ; In Vitro Techniques ; Interleukin-8 ; Interleukins ; Isotretinoin ; Microarray Analysis ; Monocytes* ; NF-kappa B ; Phosphotransferases ; Polymerase Chain Reaction ; Propionibacterium acnes* ; Propionibacterium* ; Reverse Transcription ; RNA, Small Interfering ; Sebum ; Skin ; Toll-Like Receptors

OBJECTIVETo study the role of triggering receptor expressed on myeloid cells-1(TREM-1) in the pathogenesis of Kawasaki disease (KD).

METHODSBased on color Doppler examination results, 45 children with KD were classified into two groups: coronary artery lesions (CAL group) and no coronary artery lesions (NCAL group). Fifteen children with fever caused by respiratory infection (fever control group) and fifteen healthy children (normal control group) served as controls. Real-time fluorescence quantitative PCR was used to detect the expression of TREM-1 mRNA and DNAX-activating protein 12 (DAP12) mRNA in peripheral blood mononuclear cells (PBMC). ELISA was used to detect the expression of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1), DAP12, monocyte chemoattractant protein-1(MCP-1), interleukin-8 (IL-8) proteins levels.

RESULTSThe mean serum protein concentrations of sTREM-1 and DAP12 and the expression levels of TREM-1 mRNA and DAP12 mRNA in PBMC in 45 children with KD (KD group) were significantly higher than in the two control groups (P<0.05). The levels of sTREM-1 protein and TREM-1 mRNA in the CAL subgroup were significantly higher than in the NCAL subgroup (P<0.05). The serum protein concentrations of MCP-1 and IL-8 in the KD group were significantly higher than in the two control groups (P<0.05). The MCP-1 protein level in the CAL subgroup was significantly higher than in the NCAL subgroup (P<0.05). In children with KD, there was a positive correlation between serum sTREM-1 and MCP-1 levels (r=0.523, P<0.05).

CONCLUSIONSTREM-1 activation may be involved in the development of KD.

Chemokine CCL2 ; blood ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Interleukin-8 ; blood ; Male ; Membrane Glycoproteins ; blood ; genetics ; physiology ; Mucocutaneous Lymph Node Syndrome ; etiology ; immunology ; RNA, Messenger ; analysis ; Receptors, Immunologic ; blood ; genetics ; physiology ; Triggering Receptor Expressed on Myeloid Cells-1

OBJECTIVETo investigate the correlation of the levels of interleukin-8 (IL-8) and IL-6 in the prostatic fluid with serum levels of serum prostate-specific antigen (PSA) in patients with benign prostatic hyperplasia (BPH) complicated by prostatitis.

METHODSA series of 211 patients undergoing surgery of BPH were divided into BPH group (n=75) and BPH with prostatitis group (n=136) according to the white blood cell count in the prostatic fluid. The clinical and laboratory findings were compared between the two groups, and stepwise regression analysis was used to assess the association of IL-8 and IL-6 with serum PSA level.

RESULTSNo significant differences were found in age, BMI, blood pressure, blood glucose, blood lipids, IPSS score, PSA-Ratio, or prostate volume between the two groups (P<0.05). The patients with prostatitis had significantly increased serum PSA and prostate fluid IL-8 and IL-6 levels compared with those without prostatitis (P<0.001). Multiple linear regression analysis showed that IL-8 and IL-6 levels and white blood cell count in the prostatic fluid were all positively correlated with serum PSA level.

CONCLUSIONProstatitis is an important risk factor for elevated serum PSA level in patients with BPH, and both IL-8 and IL-6 levels in the prostatic fluid are correlated with serum PSA level.

Body Fluids ; chemistry ; Humans ; Interleukin-6 ; chemistry ; Interleukin-8 ; chemistry ; Leukocyte Count ; Male ; Prostate-Specific Antigen ; blood ; Prostatic Hyperplasia ; complications ; diagnosis ; Prostatitis ; complications ; diagnosis ; Regression Analysis ; Risk Factors

OBJECTIVETo study the effects of the change in transient receptor potential vanilloid 1 (TRPV1) channel activity on the degree of airway inflammation in asthmatic mice.

METHODSBALB/c mice were randomly divided into control, asthma, capsaicin (TRPV1 agonist), capsazepine (TRPV1 antagonist), and dexamethasone groups. The asthmatic mouse model was established by intraperitoneal injection of mixed ovalbumin-aluminium hydroxide solution and ultrasonic atomization with OVA for sensitization and challenge. The capsaicin, capsazepine, and dexamethasone groups were given intraperitoneal injection of capsaicin (30 μg/kg), capsazepine (10 μmol/kg), and dexamethasone (2 mg/kg) respectively, at 30 minutes before challenge. Hematoxylin and eosin staining was used to observe the degree of pulmonary inflammation. ELISA was used to measure the content of interleukin-8 (IL-8) and interleukin-13 (IL-13) in bronchoalveolar lavage fluid (BALF). Real-Time PCR was used to measure the relative content of TRPV1 mRNA in lung tissue.

RESULTSCompared with the asthma group, the capsazepine and dexamethasone groups showed reduced pulmonary inflammation, while the capsaicin group showed aggravated pulmonary inflammation. Compared with the control group, the asthma and capsaicin groups showed increases in the content of IL-13 and IL-8 in BALF and the mRNA expression of TRPV1 in lung tissue (P<0.05). Compared with the asthma group, the capsazepine and dexamethasone groups showed reductions in the content of IL-13 and IL-8 in BALF and the mRNA expression of TRPV1 in lung tissue (P<0.05). The capsaicin group showed increases in the content of IL-13 and IL-8 in BALF (P<0.05).

CONCLUSIONSTRPV1 channel agonist and antagonist can influence the degree of airway inflammation in asthmatic mice. Dexamethasone may reduce airway inflammation through regulating TRPV1 level.

Animals ; Asthma ; etiology ; Female ; Interleukin-13 ; analysis ; Interleukin-8 ; analysis ; Lung ; pathology ; Mice ; Mice, Inbred BALB C ; RNA, Messenger ; analysis ; TRPV Cation Channels ; genetics ; physiology

OBJECTIVEUnder the premise of smoke inhalation injury, to explore the effects of microRNA-146a on Fas-associated factor 2 (FAF-2) and inflammatory factors in human lung adenocarcinoma A549 cells under the stimulation of cigarette smoke extract (CSE).

METHODS(1) The pMIR-FAF-2 recombinant plasmid and the pMIR-FAF-2 recombinant mutated plasmid were constructed. Human embryonic kidney 293 (HEK-293) cells of the third passage were divided into 3 groups according to the random number table, with 5 wells in each group. Cells in plasmid+ microRNA control group were transfected with pMIR-FAF-2 recombinant plasmid, pRL-TK plasmid, and microRNA control; cells in plasmid+ microRNA-146a group were transfected with pMIR-FAF-2 recombinant plasmid, pRL-TK plasmid, and microRNA-146a mimics; cells in mutated plasmid+ microRNA-146a group were transfected with pMIR-FAF-2 recombinant mutated plasmid, pRL-TK plasmid, and microRNA-146a inhibitor. After culture for 24 h, the relative luciferase activity in cells was assessed by dual-luciferase reporter gene assay. (2) Human lung adenocarcinoma A549 cells of the third passage were divided into 3 groups according to the random number table, with 4 wells in each group. Cells in microRNA control group were transfected with microRNA control; cells in microRNA-146a enhancement group were transfected with microRNA-146a mimics; cells in microRNA-146a inhibition group were transfected with microRNA-146a inhibitor. After culture for 24 h, the mRNA expression levels of microRNA-146a and FAF-2 in cells were determined with real-time fluorescent quantitative reverse transcription-PCR. (3) A549 cells of the third passage were stimulated by 0.8% CSE for 24 h after being divided and treated with the same method used in experiment (2). The mRNA expression levels of FAF-2, IL-8, monocyte chemotactic protein-1 (MCP-1), and growth-regulated oncogene-α (GRO-α) in cells were determined with real-time fluorescent quantitative reverse transcription-PCR. The protein expression levels of IL-8, MCP-1, and GRO-α in A549 cell culture supernatant were determined by enzyme-linked immunosorbent assay. The protein expression level of cyclooxygenase 2 (COX-2) of cells was assessed by Western blotting. Data were processed with one-way analysis of variance and LSD test.

RESULTS(1) The pMIR-FAF-2 recombinant plasmid and pMIR-FAF-2 recombinant mutated plasmid were confirmed with successful construction. The relative luciferase activity in HEK-23 cells of plasmid+ microRNA control group was close to that of mutated plasmid+ microRNA-146a group (P>0.05). The relative luciferase activity in HEK-23 cells of plasmid+ microRNA-146a group was significantly lower than that of plasmid+ microRNA control group and mutated plasmid+ microRNA-146a group (with P values below 0.01). (2) The expression level of microRNA-146a in A549 cells of microRNA control group was close to that of microRNA-146a inhibition group (P>0.05), and they were both significantly lower than the expression level of microRNA-146a in A549 cells of microRNA-146a enhancement group (with P values below 0.01). The mRNA expression level of FAF-2 in A549 cells of microRNA control group was close to that of microRNA-146a inhibition group (P>0.05), and they were both significantly higher than the mRNA expression level of FAF-2 in A549 cells of microRNA-146a enhancement group (with P values below 0.05). (3) After stimulation of CSE, the mRNA expression level of FAF-2 in A549 cells of microRNA control group (1.46±0.21) was close to that of microRNA-146a inhibition group (1.43±0.34, P>0.05), which were both significantly higher than the mRNA expression level of FAF-2 in A549 cells of microRNA-146a enhancement group (0.57±0.11, with P values below 0.05). The mRNA expression levels of IL-8, MCP-1, and GRO-α in A549 cells of microRNA-146a enhancement group were significantly lower than those of microRNA control group and microRNA-146a inhibition group (with P values below 0.01). The mRNA expression levels of IL-8, MCP-1, and GRO-α in A549 cells of microRNA-146a inhibition group were significantly higher than those of microRNA control group (with P values below 0.05). The protein expression levels of IL-8, MCP-1, and GRO-α in A549 cell culture supernatant of microRNA-146a enhancement group were significantly lower than those of microRNA control group and microRNA-146a inhibition group (with P values below 0.05). The protein expression level of IL-8 in A549 cell culture supernatant of microRNA-146a inhibition group was close to that of microRNA control group (P>0.05), while the protein expression levels of MCP-1 and GRO-α in A549 cell culture supernatant of microRNA-146a inhibition group were significantly lower than those of microRNA control group (with P values below 0.05). The protein expression level of COX-2 in A549 cells of microRNA-146a enhancement group was significantly lower than the levels of microRNA control group and microRNA-146a inhibition group (with P values below 0.05). The protein expression level of COX-2 in A549 cells of microRNA control group was close to that of microRNA-146a inhibition group (P>0.05).

CONCLUSIONSIn A549 cells, after being transfected with microRNA-146a and stimulated by CSE, microRNA-146a can decrease the expression of FAF-2 through integrating with the 3'-untranslated region of target gene FAF-2, thereby decrease the expression of inflammatory factors.

Adenocarcinoma ; chemically induced ; Blotting, Western ; Chemokine CCL2 ; metabolism ; Enzyme-Linked Immunosorbent Assay ; HEK293 Cells ; Humans ; Interleukin-8 ; Lung ; drug effects ; metabolism ; Lung Neoplasms ; chemically induced ; MicroRNAs ; analysis ; Plasmids ; RNA, Messenger ; Smoke ; adverse effects ; Smoking ; Transfection

OBJECTIVETo study the effect of oral administration of dimethyl dimethoxy biphenyl dicarboxylate (DDB) on adjusting angiogeneic/inflammatory mediators and ameliorating the pathology of bones in rats with collagen-induced arthritis (CIA).

METHODSWistar rat model of CIA was set up using bovine collagen type II. Fifty rats were divided into five groups randomly: normal, CIA model, DDB treatment, methotrexate (MTX) treatment, and combined DDB+MTX treatment. Ankle joints of rats were imaged with digital X-ray machine to show the destruction of joints. Fore and hind paw and knee joints were removed above the ankle joint then processed for haematoxylin and eosin staining. Plasma levels of vascular endothelial growth factor (VEGF), platelet derived growth factor, interleukin-8 (IL-8), IL-4, tumor necrosis factor α (TNF-α), and cyclooxygenase-2 (COX-2) were quantified by enzyme-linked immunosorbent assay. Nitric oxide levels were detected by Griess reagent.

RESULTSCompared with the CIA model group, a remarkable reduction in various angiogenic (VEGF and IL-8) and inflammatory mediators (TNF-α, IL-4 and COX-2) after treatment with DDB either alone or combined with MTX P<0.05 or P<0.01). Histopathological and X-ray findings were confirmatory to the observed DDB anti-arthritic effect. The DDB-treated group showed amelioration in signs of arthritis which appeared essentially similar to normal.

CONCLUSIONOur data shed light on the therapeutic efficacy of DDB in experimental rheumatoid arthritis (RA) compared with a choice drug (MTX) and it may be offered as a second-line drug in the treatment of RA.

Animals ; Arthritis, Experimental ; chemically induced ; diagnostic imaging ; drug therapy ; pathology ; Arthritis, Rheumatoid ; diagnostic imaging ; drug therapy ; pathology ; Collagen ; Cyclooxygenase 2 ; blood ; Dioxoles ; therapeutic use ; Enzyme-Linked Immunosorbent Assay ; Female ; Interleukin-4 ; blood ; Interleukin-8 ; blood ; Methotrexate ; therapeutic use ; Nitric Oxide ; biosynthesis ; Platelet-Derived Growth Factor ; analysis ; Radiography ; Rats ; Rats, Wistar ; Tumor Necrosis Factor-alpha ; blood ; Vascular Endothelial Growth Factor A ; blood