OBJECTIVETo investigate the role of autophagy in acute lung injury (ALI) caused by multiple trauma in rats via pretreat with 3-methyladenine (3-MA).

METHODSForty-five Sprague-Dawley male rats, with age of 4 months and body weight of 250-300 g,were randomly divided into three groups. In the sham group, the rats received sphenotresia only;in the control group, the rats were made model of femur shaft fracture combined with brain injury, and treated with physiological saline by abdominal cavity at 1 hour before making model; in the 3-MA group, the rats were made model of femur shaft fracture combined with brain injury,and treated with 3-MA of 10 mg/kg by abdominal cavity at 1 hour before making model. Histologic changes and the concentration of related inflammatory factors in the damaged lung tissue were examined at 48 h after opteration, at the same time, the effect of 3-MA on the expression of LC-3 II and Beclin-1 was examined through reverse transcriptase polymerase chain reaction technique (RT-PCR).

RESULTSCompared with sham group, LC-3 II and Beclin-1 level in control group at 48 h after operation were obviously increased (P < 0.01). Compared with control group, LC-3 II and Beclin-1 level in 3-MA group at 48 h after operation were obviously decreased (P < 0.01). Compared with sham group, the level of proinflammatory cytokines (TNF-&alpha; and IL-6) in control group obviously enhanced (P < 0.01). Compared with control group, above items in 3-MA group was obviously lower (P < 0.01). Compared with control group,the histopathological damage of lung in 3-MA group obviously reduced (P < 0.01).

CONCLUSIONAutophagy can aggravate the acute lung injury caused by fracture of shaft of femur combined with brain injuries,but 3-MA can reduce tissue damage by inhibiting the autophagy and inflammatory response.

Acute Lung Injury ; prevention & control ; Adenine ; analogs & derivatives ; therapeutic use ; Animals ; Apoptosis Regulatory Proteins ; analysis ; Beclin-1 ; Interleukin-6 ; analysis ; Lung ; chemistry ; immunology ; pathology ; Male ; Multiple Trauma ; complications ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; analysis

OBJECTIVETo explore the effects of body mass index (BMI) and the levels of serum inflammatory cytokines on asthma control in children with asthma.

METHODSOne hundred and sixteen children with asthma were divided into three groups: normal (n=59), thin (n=31), and obesity (n=26) based on their BMI. The levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-&alpha;) were determined using ELISA, and the level of high-sensitivity C-reactive protein (hs-CRP) was measured by immunoturbidimetric assays. Asthma control status in each group was evaluated by the Childhood Asthma Control Test (C-ACT) after 4 weeks of treatment.

RESULTSThe serum levels of IL-6, hs-CRP, and TNF-&alpha; were highest in the obesity group, followed by the thin group and the normal group (P<0.05), while the C-ACT score was highest in the normal group, followed by the thin group and obesity group (P<0.05). The normal group had significantly higher complete controlled and partially controlled rates than the thin and obesity groups (P<0.05); however, there were no significant differences between the thin and obesity groups (P>0.05). The levels of IL-6, hs-CRP, and TNF-&alpha; were negatively correlated with the C-ACT score (P<0.05). There were no significant correlations of BMI with the C-ACT score and levels of IL-6, hs-CRP, and TNF-&alpha; (P>0.05).

CONCLUSIONSWhen BMI is too high or too low, the levels of serum inflammatory cytokines are all increased, which is harmful to asthma control. Maintaining a healthy weight in children with asthma may reduce the levels of serum inflammatory cytokines and improve the asthma control rate.

Asthma ; immunology ; therapy ; Body Mass Index ; C-Reactive Protein ; analysis ; Child ; Child, Preschool ; Cytokines ; blood ; Female ; Humans ; Interleukin-6 ; blood ; Male ; Tumor Necrosis Factor-alpha ; blood

In the present study, we analyzed the role of Ginkgo biloba extract in lipopolysaccharide(LPS)-induced acute lung injury (ALI). ALI was induced in mice by intratracheal instillation of LPS. G. biloba extract (12 and 24 mg·kg(-1)) and dexamethasone (2 mg·kg(-1)), as a positive control, were given by i.p. injection. The cells in the bronchoalveolar lavage fluid (BALF) were counted. The degree of animal lung edema was evaluated by measuring the wet/dry weight ratio. The superoxidase dismutase (SOD) and myeloperoxidase (MPO) activities were assayed by SOD and MPO kits, respectively. The levels of inflammatory mediators, tumor necrosis factor-a, interleukin-1b, and interleukin-6, were assayed by enzyme-linked immunosorbent assay. Pathological changes of lung tissues were observed by H&E staining. The levels of NF-κB p65 and COX-2 expression were detected by Western blotting. Compared to the LPS group, the treatment with the G. biloba extract at 12 and 24 mg·kg(-1) markedly attenuated the inflammatory cell numbers in the BALF, decreased NF-κB p65 and COX-2 expression, and improved SOD activity, and inhibited MPO activity. The histological changes of the lungs were also significantly improved. The results indicated that G. biloba extract has a protective effect on LPS-induced acute lung injury in mice. The protective mechanism of G. biloba extract may be partly attributed to the inhibition of NF-κB p65 and COX-2 activation.
Acute Lung Injury ; chemically induced ; drug therapy ; metabolism ; Animals ; Bronchoalveolar Lavage Fluid ; cytology ; Cell Count ; Cyclooxygenase 2 ; genetics ; metabolism ; Enzyme-Linked Immunosorbent Assay ; Gene Expression ; drug effects ; Ginkgo biloba ; chemistry ; Interleukin-1beta ; analysis ; Interleukin-6 ; analysis ; Lipopolysaccharides ; Lung ; immunology ; pathology ; Male ; Mice ; Mice, Inbred BALB C ; Peroxidase ; metabolism ; Phytotherapy ; Plant Extracts ; pharmacology ; Pulmonary Edema ; Superoxide Dismutase ; metabolism ; Transcription Factor RelA ; genetics ; metabolism ; Tumor Necrosis Factor-alpha ; analysis

Bacterial biofilms have emerged as potential critical triggers in the pathogenesis of bisphosphonate (BP)-related osteonecrosis of the jaw (ONJ) or BRONJ. BRONJ lesions have shown to be heavily colonized by oral bacteria, most of these difficult to cultivate and presents many clinical challenges. The purpose of this study was to characterize the bacterial diversity in BRONJ lesions and to determine host immune response. We examined tissue specimens from three cohorts (n=30); patients with periodontal disease without a history of BP therapy (Control, n=10), patients with periodontal disease having history of BP therapy but without ONJ (BP, n=5) and patients with BRONJ (BRONJ, n=15). Denaturing gradient gel electrophoresis of polymerase chain reaction (PCR)-amplified 16S rRNA gene fragments revealed less bacterial diversity in BRONJ than BP and Control cohorts. Sequence analysis detected six phyla with predominant affiliation to Firmicutes in BRONJ (71.6%), BP (70.3%) and Control (59.1%). Significant differences (P<0.05) in genera were observed, between Control/BP, Control/BRONJ and BP/BRONJ cohorts. Enzyme-linked immunosorbent assay (ELISA) results indicated that the levels of myeloperoxidase were significantly lower, whereas interleukin-6 and tumor necrosis factor-alpha levels were moderately elevated in BRONJ patients as compared to Controls. PCR array showed significant changes in BRONJ patients with downregulation of host genes, such as nucleotide-binding oligomerization domain containing protein 2, and cathepsin G, the key modulators for antibacterial response and upregulation of secretory leukocyte protease inhibitor, proteinase 3 and conserved helix-loop-helix ubiquitous kinase. The results suggest that colonization of unique bacterial communities coupled with deficient innate immune response is likely to impact the pathogenesis of ONJ.
Actinobacteria ; classification ; Bacteria ; classification ; Bacteroidetes ; classification ; Biofilms ; Bisphosphonate-Associated Osteonecrosis of the Jaw ; immunology ; microbiology ; Bone Density Conservation Agents ; therapeutic use ; Cathepsin G ; analysis ; Cohort Studies ; Down-Regulation ; Female ; Fusobacteria ; classification ; Gram-Negative Bacteria ; classification ; Host-Pathogen Interactions ; immunology ; Humans ; I-kappa B Kinase ; analysis ; Immunity, Innate ; immunology ; Interleukin-6 ; analysis ; Male ; Middle Aged ; Mouth ; immunology ; microbiology ; Myeloblastin ; analysis ; antagonists & inhibitors ; Nod2 Signaling Adaptor Protein ; analysis ; Periodontal Diseases ; microbiology ; Peroxidase ; analysis ; Proteobacteria ; classification ; Tumor Necrosis Factor-alpha ; analysis

Body fat is an important source of adipokine, which is associated with energy balance and inflammatory and immune responses. However, the role of adipokines in coronary artery complications in Kawasaki disease (KD) has not yet been fully explained. We investigated whether serum adipokine level can be a useful marker for patients with KD who are at higher risk of developing coronary artery lesion (CAL). We measured adipokine levels and other inflammatory parameters in 40 patients with KD, 32 febrile controls, and 15 afebrile controls. Interleukin (IL)-6, tumor necrosis factor (TNF)-alpha and other laboratory parameters were also measured before and after intravenous immunoglobulin therapy, and in the convalescent phase. At admission, the serum resistin levels in KD children were significantly higher than those in controls (177.56 ng/mL in KD children, 76.48 ng/mL in febrile controls, and 17.95 ng/mL in afebrile controls). In patients with KD, resistin levels were significantly associated with decreased hemoglobin levels (P=0.049) and increased IL-6 levels (P=0.014). The serum IL-6 levels were significantly higher and body mass index was significantly lower in the group of KD with CALs than those without CALs (228.26 ng/mL vs. 39.18 ng/mL and 15.09 vs. 16.60, respectively). In conclusion, resistin is significantly elevated in KD patients, although it has no prognostic value of predicting coronary artery lesion in the acute stage.
Biological Markers/*blood ; Child ; Child, Preschool ; Coronary Vessels/pathology ; Echocardiography ; Female ; Hemoglobins/analysis ; Humans ; Immunoglobulins, Intravenous/therapeutic use ; Inflammation/blood/immunology ; Interleukin-6/*blood ; Male ; Mucocutaneous Lymph Node Syndrome/*blood/pathology ; Resistin/*blood ; Tumor Necrosis Factor-alpha/*blood

OBJECTIVETo explore the effects of sacral canal injection on nerve root local inflammatory factors in rat model with lumbar disc herniation, in order to identify its mechanism of treatment.

METHODSForty-eight male SD rats were randomly divided into sham operation group(group A), model group (group B), Chinese medicine group(group C) and western medicine group(group D). There were 12 rats in each group. The model of lumbar disc herniation was established using compression and inflammatory stimulation in group B, C, D. All rats were given epidural catheterization and group A and B with physiological saline (1 ml/kg), group C with mixed liquor of 2% lidocaine and compound Danshen injections and physiological saline (2:2: 16) and group D with mixed liquor of 2% lidocaine and triamcinolone acetonide injection and physiological saline (2:2:16), once a week for a total of three treatments. Four rats were killed every 1 week after injection for once, and the inflammatory factors of tumor necrosis factor (TNF-alpha), prostaglandin E2 (PGE2), interleukin-l (IL-1) and interleukin-6 (IL-6) were detected by ELISA method.

RESULTSThe levels of TNF-alpha, PGE2, IL-1 and IL-6 in compressed nerve tissues in group B were increased than those of group A (P < 0.01). The levels of PGE2, IL-1 and IL-6 in group C and D were decreased than those of group B, and group D was much less(P<0.05). There was no significant difference in level of TNF-alpha among group B, C, D (P > 0.05).

CONCLUSIONCompound compression with inflammatory stimulation can lead to massive release of inflammatory mediators, such as TNF-alpha, PGE2, IL-1 and IL-6. Both injection with compound Danshen injections and triamcinolone acetonide injections by sacral canal can reduce the levels of part inflammatory mediators (PGE2, IL-1 and IL-6), and the effect of Glucocorticoid is better than Danshen (P < 0.05).

Animals ; Dinoprostone ; analysis ; Disease Models, Animal ; Injections ; Interleukin-1 ; analysis ; Interleukin-6 ; analysis ; Intervertebral Disc Displacement ; drug therapy ; immunology ; Lumbar Vertebrae ; Male ; Rats ; Rats, Sprague-Dawley ; Salvia miltiorrhiza ; Spinal Nerve Roots ; immunology ; Triamcinolone Acetonide ; administration & dosage ; Tumor Necrosis Factor-alpha ; analysis

This study investigated the effect of breast-feeding in protection against protozoan infection in infants with persistent diarrhea. Infants were classified into 2 groups; 161 breast-fed infants and the same number of non-breast-fed infants. Microscopic examinations of stool were done for detection of parasites and measuring the intensity of infection. Moreover, serum levels of IgE and TNF-alpha were measured by ELISA. Cryptosporidium spp., Entamoeba histolytica/Entamoeba dispar, Giardia lamblia, and Blastocystis sp. were demonstrated in infants with persistent diarrhea. The percentage of protozoan infections was significantly lower in breast-fed infants than that in the non-breast-fed infants. The levels of IgE and TNF-alpha were significantly lower in the breast-fed group than in the non-breast-fed group. There were significant positive associations between the serum levels of IgE and TNF-alpha and the intensity of parasite infection in the breast-fed group. It is suggested that breast-feeding has an attenuating effect on the rate and intensity of parasite infection.
Antigens, Protozoan/analysis/*immunology ; Diarrhea, Infantile/*diagnosis/parasitology ; Entamoeba ; Entamoeba histolytica/*isolation & purification ; Entamoebiasis/*diagnosis/parasitology ; Enzyme-Linked Immunosorbent Assay ; Feces/parasitology ; Female ; Giardia lamblia ; Giardiasis/*diagnosis/parasitology ; Humans ; Infant ; Intestines/parasitology ; Protozoan Infections/*diagnosis/parasitology ; Tumor Necrosis Factor-alpha/metabolism

OBJECTIVETo investigate the regulating effect of Ginkgo biloba extract 50 (GBE50) on pre-inflammatory factors interleukin-1 beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and anti-inflammatory factors interleukin-4 (IL-4), interleukin-10 (IL-10) of hippocampus in senile rats, in order to explore the protective mechanism of GBE50 on central nervous system of senile animals.

METHODSD rats were randomly divided into four groups: the normal group, the model group, the GBE50 group and the EGB761 group. Rats were intraperitoneally injected with 100 mg x kg(-1) D-galactose every day for 42 days to establish the senile rat model. At the 21st day, the GBE50 group and the EGB761 group were orally administered with 60 mg x kg(-1) for 21 days. IL-1beta mRNA and TNF-alpha mRNA expressions were detected by real-time fluorescence quantitative PCR assay, IL-1beta and TNF-alpha protein expressions were detected by immunohistochemistry, IL-4 and IL-10 protein contents were detected by ELISA.

RESULTD-galactose caused imbalance between pre-inflammatory factors and anti-inflammatory factors of hippocampus in senile rats, GBE50 and EGB761 reduced IL-1beta mRNA expression (P < 0.05) and TNF-alpha and IL-1beta protein level (P < 0.01) and up-regulated IL-10 protein content (P < 0.01, P < 0.05).

CONCLUSIONThe mechanism of GBE50 in protecting central nervous system is probably related to its effect in mitigating inflammatory of central nervous system.

Animals ; Ginkgo biloba ; Hippocampus ; drug effects ; immunology ; Interleukin-1beta ; analysis ; Male ; Plant Extracts ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; analysis

OBJECTIVETo explore the effects of Pilose antler polypeptide on apoptosis of chondrocyte and related cytokines in experimental knee osteoarthritis.

METHODSTotally 64 New Zealand White rabbits of 6 months old were randomly divided into 2 groups:normal group(n=8)and model group (n=56). Model group was surgically induced into knee osteoarthritis model by method of Hulth. After successful modeling,the rabbits of model group were further divided into 2 groups: Pilose antler polypeptide-treatment group (n=24) and control group (n=24). Pilose antler polypeptide-treatment group received 0.5 ml intraarticular injection of Pilose antler polypeptide dilution liquid once per 2 days for 30 days while control group received 0.5 ml intra-articular injection of physiological saline. On days 7, 15 and 30 after intervention, articular cartilage samples and synovial fluid were collected respectively. The morphological changes of articular cartilage under optical microscope and the structural change of chondrocyte were observed by transmission electron microscopy. The levels of interleukin-1beta and tumor necrosis factor-alpha in synovial fluid was detected by Enzyme-linked Immunosorbent Assay.

RESULTSAlong with the extending of time, articular cartilage degenerated gradually and chondrocytes apoptosis increased significantly. On days 7,15 and 30 after intervention, the chondrocyte apoptosis index of the Pilose antler polypeptide-treatment group were (20.30 +/- 1.23), (28.60 +/- 2.37), (37.10 +/- 1.82) and those of control group were (31.50 +/- 2.44), (34.40 +/- 1.77), (42.30 +/- 2.33). There were significant differences between them (P<0.05). At the same time, the chondrocyte apoptosis index of the Pilose antler polypeptide-treatment group were lower than those of control group,which had a statistical significance (P<0.05). On days 7,15 and 30 after intervention, the levels of interleukin-1beta in synovia fluid of Pilose antler polypeptide-treatment group were (15.81 +/- 1.26), (12.59 +/- 1.42), (9.57 +/- 0.92) microg/L and the level of tumor necrosis factor-alpha were (48.47 +/- 2.64), (43.46 +/- 1.33), (40.96 +/- 1.05) microg/L, with statistical differences(P<0.05). The levels of interleukin-1beta in synovia fluid of control group were (18.92 +/- 1.83), (20.25 +/- 2.76), (22.13 +/- 2.24) microg/L and the levels of tumor necrosis factor-alpha were (57.92 +/- 2.12), (60.25 +/- 1.48), (63.35 +/- 2.15) microg/L. At the same period,the levels of interleukin-1beta and tumor necrosis factor-alpha were lower than those of the control group,which had a statistical significance (P<0.05).

CONCLUSIONPilose antler polypeptide can inhibit chondrocytes apoptosis, decrease the levels of interleukin-1beta and tumor necrosis factor-alpha and delay the degeneration of articular cartilage to some extent.

Animals ; Antlers ; chemistry ; Apoptosis ; drug effects ; Chondrocytes ; drug effects ; pathology ; Female ; Interleukin-1beta ; analysis ; Male ; Osteoarthritis, Knee ; drug therapy ; immunology ; pathology ; Peptides ; pharmacology ; Rabbits ; Tumor Necrosis Factor-alpha ; analysis

OBJECTIVETo investigate the immunoregulation effects of umbilical cord mesenchymal stem cells (UC-MSCs) on the rats with collagen II induced arthritis (CIA).

METHODSThe rats were first immunized by intradermal injection of chicken collagen type II emulsified with complete Freund's adjuvant (CFA) to monitor their swelling of foot, hair color and action state. After injected UC-MSC by caudal vein, the rats were scored with the arthritis index (AI) once a week. Then, the concentration of interleukin (IL-6), tumor necrosis factor-&alpha; (TNF-&alpha;) in serum and D-dimer (D-D), antithrombin-III (AT-III), thrombomodulin (TM) in plasma were detected by ELISA.

RESULTSObvious swellings of the feet were found in the experiment group compared with normal one. ELISA analysis showed that the concentrations of IL-6, TNF-&alpha;, D-D and TM in plasma of the experiment group as of (200.48 ± 15.04) ng/L, (450.25 ± 45.39) ng/L, (274.26 ± 67.93) ng/L and (9.18 ± 0.84) µg/L, respectively were higher than of(167.62 ± 0.97) ng/L, (371.44 ± 21.26) ng/L, (193.95 ± 8.22) ng/L and (6.30 ± 0.32) µg/L respectively in normal group (P < 0.05), but the concentration of AT-III \[(89.57 ± 6.40) ng/L\] was lower than normal group \[(112.82 ± 1.74) ng/L\] (P < 0.05). The levels of cytokines through the UC-MSCs treatment were significantly different from the model group (P < 0.05). After 9 weeks, these cytokines in the UC-MSCs group were mostly the same as the normal group.

CONCLUSIONThe thrombophilia status of the CIA rats was caused by immune injury. The UC-MSCs reduced the production of inflammatory cytokines and regulated and repaired the balance of coagulation and anticoagulation system of the body to cure the immune-related thrombophilia.

Animals ; Antithrombins ; blood ; Arthritis, Experimental ; immunology ; physiopathology ; prevention & control ; Female ; Fibrin Fibrinogen Degradation Products ; analysis ; Inflammation ; Interleukin-6 ; blood ; Mesenchymal Stem Cell Transplantation ; Rats ; Rats, Sprague-Dawley ; Thrombosis ; prevention & control ; Tumor Necrosis Factor-alpha ; blood ; Umbilical Cord ; cytology