Adult ; Animals ; Female ; Humans ; Immunoglobulins ; therapeutic use ; Leukemia, Large Granular Lymphocytic ; drug therapy ; Lymphocytes ; metabolism ; Swine ; Thymocytes ; immunology

OBJECTIVEGlucocorticoid is considered as an effective drug for prevention and treatment of brain edema and reducing the blood-brain barrier (BBB) permeability. Intravenous immunoglobulin (IVIG) is frequently used to treat neurological diseases with immune abnormality, its function and potential mechanism on brain edema have not been reported. In this study, the roles of the total hydrosulfide group (TSH), non-protein hydrosulfide group (NPSH) and malondialdehyde (MDA) in etiology of the endotoxin brain edema in infant rats and the interfering effects of dexamethasone (DEX) and IVIG were investigated.

METHODSIn 35 infant rats, 10 mg/kg lipopolysaccharide (LPS) was intraperitoneally injected. The same volume of normal saline was injected to 24 control rats. Ten mg/kg DEX and 400 mg/kg IVIG were intravenously injected respectively to 36 and 24 infant rats instantly following LPS injection. The TSH, NPSH and MDA concentrations and the brain Evans blue contents were detected at different time in the brain tissue. The brain water content was measured by drying method.

RESULTSThe brain water, EB and MDA contents after endotoxin injection were significantly higher than those of control group, while the brain TSH, NPSH content were significantly lower than those of control group (P < 0.05 or P < 0.01); After treatment with DEX or IVIG, the brain EB, MDA and water content significantly decreased with the peak at 6 h (P < 0.05 or P < 0.01), TSH and NPSH significantly increased compared with LPS group. However, the NPSH content in IVIG treatment group did not change significantly (P > 0.05).

CONCLUSIONFree radicals play a role in the brain edema induced by LPS in infant rats. The primary results suggested that DEX and IVIG have therapeutic effect for the endotoxin-induced brain edema by affecting the free radicals.

Animals ; Blood-Brain Barrier ; drug effects ; metabolism ; Brain Edema ; chemically induced ; drug therapy ; metabolism ; Dexamethasone ; therapeutic use ; Endotoxins ; toxicity ; Free Radicals ; analysis ; Glucocorticoids ; therapeutic use ; Immunoglobulins, Intravenous ; administration & dosage ; therapeutic use ; Malondialdehyde ; analysis ; Rats ; Rats, Wistar ; Sulfides ; analysis

Adult ; Aged ; Benzamides ; therapeutic use ; Case-Control Studies ; Female ; Humans ; Imatinib Mesylate ; Immunoglobulins ; metabolism ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; drug therapy ; immunology ; Male ; Middle Aged ; Piperazines ; therapeutic use ; Pyrimidines ; therapeutic use ; T-Lymphocyte Subsets

Kawasaki disease (KD) is a self-limited systemic inflammatory illness, and coronary artery lesions (CALs) are a major complication determining the prognosis of the disease. Epidemiologic studies in Asian children suggest that the etiologic agent(s) of KD may be associated with environmental changes. Laboratory findings are useful for the diagnosis of incomplete KD, and they can guide the next-step in treatment of initial intravenous immunoglobulin non-responders. CALs seem to develop in the early stages of the disease before a peak in inflammation. Therefore early treatment, before the peak in inflammation, is mandatory to reduce the risk of CAL progression and severity of CALs. The immunopathogenesis of KD is more likely that of acute rheumatic fever than scarlet fever. A hypothetical pathogenesis of KD is proposed under the premise of a "protein homeostasis system"; where innate and adaptive immune cells control pathogenic proteins that are toxic to host cells at a molecular level. After an infection of unknown KD pathogen(s), the pathogenic proteins produced from an unknown focus, spread and bind to endothelial cells of coronary arteries as main target cells. To control the action of pathogenic proteins and/or substances from the injured cells, immune cells are activated. Initially, non-specific T cells and non-specific antibodies are involved in this reaction, while hyperactivated immune cells produce various cytokines, leading to a cytokine imbalance associated with further endothelial cell injury. After the emergence of specific T cells and specific antibodies against the pathogenic proteins, tissue injury ceases and a repair reaction begins with the immune cells.
Animals ; Coronary Artery Disease/drug therapy/etiology/metabolism ; Humans ; Immunoglobulins, Intravenous/therapeutic use ; Mucocutaneous Lymph Node Syndrome/complications/*diagnosis/drug therapy/metabolism

Intravenous immunoglobulin (IVIG) and/or plasmapheresis (PP) are effective in preventing antibody-mediated rejection (AMR) of kidney allografts, but AMR is still a problem. This study reports our experience in living donor renal transplantation in highly sensitized patients. Ten patients with positive crossmatch tests or high levels of panel-reactive antibody (PRA) were included. Eight patients were desensitized with pretransplant PP and low dose IVIG, and two were additionally treated with rituximab. Allograft function, number of acute rejection (AR) episodes, protocol biopsy findings, and the presence of donor-specific antibody (DSA) were evaluated. With PP/IVIG, six out of eight patients showed good graft function without AR episodes. Protocol biopsies revealed no evidence of tissue injury or C4d deposits. Of two patients with AR, one was successfully treated with PP/IVIG, but the other lost graft function due to de novo production of DSA. Thereafter, rituximab was added to PP/IVIG in two cases. Rituximab gradually decreased PRA levels and the percentage of peripheral CD20+ cells. DSA was undetectable and protocol biopsy showed no C4d deposits. The graft function was stable and there were no AR episodes. Conclusively, desensitization using PP/IVIG with or without rituximab increases the likelihood of successful living donor renal transplantation in sensitized recipients.
Adult ; Antibodies, Monoclonal/therapeutic use ; Antigens, CD20/biosynthesis ; Female ; Humans ; Immunoglobulins/metabolism ; Immunophenotyping ; Immunosuppressive Agents/therapeutic use ; Isoantibodies/chemistry ; Kidney Failure, Chronic/therapy ; Kidney Transplantation/*methods ; Lymphocytes/metabolism ; Male ; Middle Aged ; Retrospective Studies

OBJECTIVETo study the effect of Wuhu Decoction (WHD) on the expression of co-stimulation molecule of peripheral dendritic cells (DC), CD80, CD83 and CD86, in infants with asthma, in order to provide practical basis for further elucidate the action mechanism of WHD in preventing and treating infantile asthma.

METHODSSixty infants with asthma of Fei phlegm-heat accumulation syndrome type were randomized into the treatment group treated with WHD and the control group treated with Western medicine (fluticasone propionate oral taking or inhalation). And 10 healthy infants were set as normal control. With Thomas method adopted, the DC were isolated from peripheral blood of all infants subjected. The expressions of surface co-stimulation molecules of DC, CD80, CD83 and CD86, were detected by flow cytometry. Their changes before and after treatment in different groups were analyzed and compared.

RESULTSExpressions of CD80 and CD86 of peripheral blood DC in asthmatic infants were remarkably higher than those in the normal control (P<0.01). In the treated group, CD80 expression lowered from 18.06 +/- 4.53 before treatment to 13.18 +/- 3.02 after treatment and CD86 expression lowered from 38.61 +/- 10.54 to 29.65 +/- 8.55; while in the control group, the two expressions were lowered from 18.40 +/- 3.86 to 15.34 +/- 3.90, and from 38.29 +/- 11.67 to 35.88 +/- 13.85 respectively, the lowering in both groups were statistically significant (P<0.01 and P<0.05), but it was more significant in the treated group (P<0.05). As for CD83, no significant difference existed between groups and no change was found in either group after treatment (P>0.05).

CONCLUSIONWHD can regulate the co-stimulation molecules of dendritic cells in asthma infants to reduce the expressions of CD80 and CD86.

Antigens, CD ; metabolism ; Asthma ; blood ; drug therapy ; B7-1 Antigen ; metabolism ; B7-2 Antigen ; metabolism ; Child, Preschool ; Dendritic Cells ; metabolism ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Immunoglobulins ; metabolism ; Infant ; Male ; Membrane Glycoproteins ; metabolism ; Phytotherapy

OBJECTIVETo observe the clinical efficacy of Compound Xiatianwu tablets in the treatment of active rheumatoid arthritis.

METHODOne hundred and eighty cases with active rheumatoid arthritis were randomly divided into the control group (60 cases) with leflunomide, sulfasalazine, and celecoxib; the treatment group (120 cases) given compound Xiatianwu tablets on the basis of the control group, 2 tablets each time, 3 times/day, with the course of treatment of 3 month. Patients of the two groups were observed for clinical symptoms, erythrocyte sedimentation rate, C-reactive protein, rheumatoid factor, and immunoglobulin changes before and after the treatment.

RESULTThe treatment group showed an overall efficiency of 94. 2% , the Xiatianwu group showed an overall efficiency of 80. 0%, while the control group showed an overall efficiency of 81.7%. The difference among the three groups was statistically significant (P <0. 05 or P <0. 01) , indicating that the treatment group was superior to the Xiatianwu group, while the Xiatianwu group was superior to the control group.

CONCLUSIONCompound Xiatianwu tablets has remarkable effect in the treatment of active rheumatoid arthritis.

Adult ; Arthritis, Rheumatoid ; drug therapy ; immunology ; metabolism ; pathology ; C-Reactive Protein ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Erythrocytes ; drug effects ; Female ; Humans ; Immunoglobulins ; metabolism ; Male ; Middle Aged ; Tablets ; Treatment Outcome ; Young Adult

Anti-Bacterial Agents ; therapeutic use ; Bronchiectasis ; drug therapy ; epidemiology ; etiology ; microbiology ; China ; Ciliary Motility Disorders ; drug therapy ; epidemiology ; etiology ; microbiology ; Connective Tissue ; metabolism ; Humans ; Immunoglobulins ; metabolism ; Pseudomonas aeruginosa ; drug effects ; pathogenicity

OBJECTIVEA great deal of clinical evidence and epidemiologic data suggest that Kawasaki disease (KD) is correlated with an acute regulating imbalance of immunology. Lots of evidences in the past suggested that nuclear transcription factor-kappaB and preinflammation factors were up-regulated significantly in patients with KD. But the causative factors are still unknown. Toll-like receptors (TLRs) is a type I trans-membrane protein which could recognize ligands of pathogen microbes, activate the nuclear transcription factor-kappaB and promote gene transcription of pre-inflammation factors and co-stimulatory molecules on cell surface. Aberrant activation of signal pathway of TLRs could interfere with autoimmune tolerance and cause autoimmune diseases. The study was designed to investigate the role of signal transduction of TLRs on immunological pathogenesis of KD.

METHODSSixteen children with KD and 16 age-matched health children were studied. Reverse-transcription PCR (RT-PCR) and real-time PCR were used to evaluate the levels of TLRs 1 - 10, MD-2, MyD88, IL-1beta, IL-6 and IL-8 mRNA expressions in peripheral blood mononuclear cells, and expressions of TLRs 2, 4 and co-stimulatory molecules such as CD80 and CD86 in monocyte/macrophage were analyzed by flow cytometry.

RESULTS(1) Compared with control group, the protein and mRNA levels of TLR4 in KD group were up-regulated significantly [(Real-time PCR: 325.22 +/- 50.34 vs. 2.20 +/- 0.23, P < 0.01); (flow cytometry: 15.96% +/- 5.94% vs. 3.21% +/- 0.62%, P < 0.01)], the difference being not significant as to other TLRs. (2) Transcriptional levels of MD-2 and Myd88 were significantly up-regulated in acute phase of KD (P < 0.01), and down-regulated after the treatment with intravenous gamma globulin therapy. (3) Expressions of co-stimulatory molecules and cytokines in monocyte/macrophage during acute phase of KD were higher than those of control group (P < 0.01).

CONCLUSIONExpressions of TLRs 4, MD-2 and Myd88 were up-regulated during acute phase in KD, suggesting that aberrant activation of TLRs 4 might be one of the initiating factors of immune aberrance in KD.

Case-Control Studies ; Child, Preschool ; Female ; Flow Cytometry ; Humans ; Immunoglobulins, Intravenous ; immunology ; therapeutic use ; Immunologic Factors ; immunology ; therapeutic use ; Infant ; Leukocytes, Mononuclear ; drug effects ; immunology ; metabolism ; Male ; Mucocutaneous Lymph Node Syndrome ; drug therapy ; immunology ; Myeloid Differentiation Factor 88 ; genetics ; metabolism ; RNA, Messenger ; Reverse Transcriptase Polymerase Chain Reaction ; Toll-Like Receptor 4 ; genetics ; metabolism ; Toll-Like Receptors ; genetics ; metabolism ; Up-Regulation ; drug effects

OBJECTIVETo observe the clinical effect of Shengxueling (SXL) on idiopathic thrombocytopenic purpura (ITP), and study the possible mechanism.

METHODSEighty-six cases of ITP were randomly divided into two groups. The SXL group, 56 patients treated with SXL, a traditinal Chinese medicine and 30 patients administered with prednisone were taken as control. Each group took drugs for 3 months and was under follow-up observation.

RESULTSIn the SXL group, the total effective rate was 85.71%, similar to prednisone 83.33% (P > 0.05) for 3 months, but the total effective rate of SXL (91.07%) were obviously better than that of the control group (53.33%) (P < 0.01) for 6 months and had no obvious adverse reaction. The patients bleeding was alleviated or stopped, the general condition was improved. At the same time, blood platelet count (PLT) was increased, platelet associated immunoglobulin (PAIg) and interleukin-4 (IL-4) were markedly dropped, the level of natural killers cells activity (NKa) increased, the rate of T lymphocyte subsets gradually returned to normal level. Megakaryocyte tended to maturation on bone marrow smear after treatment. All differences above were statistically significant.

CONCLUSIONSXL is an effective and safe medicine for ITP. Its mechanism could regulate cytoimmune, inhibit platelet antibody to reduce the destruction of platelet, increase the number of platelet, promote the division and maturation of megakaryocyte, facilitate the production and release of platelet, lower the fragility of capillary, prevent and cure hemorrhagic tendency.

Adolescent ; Adult ; Blood Platelets ; metabolism ; Bone Marrow ; pathology ; Female ; Glucocorticoids ; therapeutic use ; Hemorrhage ; etiology ; physiopathology ; Humans ; Immunoglobulins ; blood ; Interleukin-4 ; blood ; Killer Cells, Natural ; pathology ; Lymphocyte Count ; Male ; Medicine, Chinese Traditional ; Middle Aged ; Phytotherapy ; adverse effects ; Plant Preparations ; adverse effects ; therapeutic use ; Platelet Count ; Prednisone ; therapeutic use ; Purpura, Thrombocytopenic, Idiopathic ; blood ; complications ; pathology ; therapy ; T-Lymphocyte Subsets ; pathology ; Treatment Outcome