A Study of the Relationship_Between Levels of SIgA and IFN-γ in the Female Genital Tract and the Clinical Course of NGU

Objective： To study the relationship of local immunity in the female genital tract with the clinical course of Nongonococcal Urethritis （NGU）. Methods： We collected cervical secretions from patients and examined levels of SIgA and IFN- γ. Results： Levels of SIgA and IFN- γ in the infected group were lower than those in the uninfected group, P1〈0.05 and P2〈0.05. The level of SIgA and IFN- γ in C.t,UU and C.t＋UU infected groups were not significantly different. Comparing the negative-changed group with thenonnegative-changed group, the level of SIgA and IFN-γ was 39.22±20.04mg/L and 103.19±29.94pg/ml, 26.00±10.56mg/I and 88.21±15.10pg/ml, P1〉0.05 and P2〉0.05. Conclusion： SIgA and IFN-γ secreted by genital tractmucosa may help prevent and resist local NGU infection.However, the effect is limited, and is insufficient to eliminate infection completely and prevent reinfection.

Cloning and Sequence Analysis of Interferon γ-2β Full-length cDNA in Cyprinus carpio L.

[Objective] The research aimed to carry out the cloning, identification and sequence analysis of full-length cDNA of carp interferon γ-2β （IFNγ-2β）. [Method] The cDNA library of peripheral blood leucocytes which were separated from carp and stimulated with mitogen was screened by a probe labeled with DIG. The IFNγ- 2β EST sequence was picked out from the constructed cDNA library of peripheral blood leucocyte, and the full length of carp interferon γ-2β was cloned. In addition, the sequence analysis was carried out. [Result] Three positive clones were obtained. Sequence analysis indicated that the sequence had a 119 bp 5’-UTR and a 218 bp 3’-UTR, and the open reading frame （ORF）of this gene was 537 bp which putatively coded 178 amino acids and there were several instable motifs for mRNA （ATTTA） in the 3’-untranslated region. Its homology with IFN from GenBank was up to 97% . Analysis on protein sequence and structure showed that the predicted protein sequence was identified as an IFN family signature. [Conclusion] The research laid the foundation for further studying the expression manner, function characteristic and regulation mechanism of IFNγ-2β in vivo and the action mechanism in the inflammatory reaction, emergency reaction and immune response.

Repression of interferon-γ expression in T cells by Prosperorelated Homeobox protein

Interferon-gamma （IFN-γ） is a major proinflammatory effector and regulatory cytokine produced by activated T cells and NK cells. IFN-γ has been shown to play pivotal roles in fundamental immunological processes such as inflammatory reactions, cell-mediated immunity and autoimmunity. A variety of human disorders have now been linked to irregular IFN-γ expression. In order to achieve proper IFN-γ-mediated immunological effects, IFN-γ expression in T cells is subject to both positive and negative regulation. In this study, we report for the first time the negative regulation of IFN-γ expression by Prospero-related Homeobox （Proxl）. In Jurkat T cells and primary human CD4＋ T cells, Proxl expression decreases quickly upon T cell activation, concurrent with a dramatic increase in IFN-γ expression. Reporter analysis and chromatin immunoprecipitation （CHIP） revealed that Proxl associates with and inhibits the transcription activity of IFN-γ promoter in activated Jurkat T cells. Co-immunoprecipitation and GST pull-down assay demonstrated a direct binding between Proxl and the nuclear receptor peroxisome proliferator-activated receptor gamma （PPARγ）, which is also an IFN-γ repressor in T cells. By introducing deletions and mutations into Proxl, we show that the repression of IFN-γ promoter by Proxl is largely dependent upon the physical interaction between Proxl and PPARγ. Furthermore, PPARγ antagonist treatment removes Proxl from IFN-γ promoter and attenuates repression of IFN-γ expression by Proxl. These findings establish Proxl as a new negative regulator of IFN-γ expression in T cells and will aid in the understanding of IFN-γ transcription regulation mechanisms.

Adeno-associated virus mediated interferon-gamma inhibits the progression of hepatic fibrosis in vitro and in vivo

AIM:To investigate the effects of adeno-associated virus (AAV) mediated expression of human interferon-γ for gene therapy in experimental hepatic fibrosis in vitro and in vivo. METHODS: We constructed the recombinant AAV encoding human INF-γ (rAAV- INF-γ) and took the primary rat hepatic stellate cells and carbon tetrachloride induced rats as the experimental hepatic fibrosis model in vitro and in vivo. Immunocytochemistry analysis was used to reveal the expression of α-SMA, the marker protein expressed in hepatic stellate cells. The mRNA expression of TGF-β, TIMP-1, and MMP-13 were analyzed by RT-PCR method. In vivo study, the hydroxyproline content in liver and serum AST, ALT were also detected. RESULTS: In vitro study, AAV vector could mediated efficient expression of human INF-γ, which inhibit the activation of hepatic stellate cells, decrease the expression of α-SMA and mRNA of TIMP-1, TGF-β, with the MMP-13 unchanged. In vivo study, the histological examination revealed that rAAV- INF-γ could inhibit the progression of the hepatic fibrosis. In the rAAV-INF-γ induced group, the hydroxyproline content and serum AST, ALT level were decreased to 177±28 μg/g wet liver, 668.5±140.0, 458.4±123.5 U/L, compare with the fibrosis control group 236±31 μg/g wet liver, 1 019.1±276.3, 770.5±154.3 U/L, respectively (P<0.01). mRNA expression of TIMP-1 in the rAAV-INF-γ induced rat liver was decreased while no significant change was observed in TGF-β and MMP-13. CONCLUSION: All these results indicated that rAAV-INF-γ has potential effects for gene therapy of hepatic fibrosis, which could inhibit the progression of hepatic fibrosis.

Inhibition of hepatitis B virus DNA replicative intermediate forms by recombinant interferon-γ

AIM: To evaluate the in vitro anti-HBV activity of recombinant human IFN-γ, alone and in combination with lamivudine. METHODS: A recombinant baculovirus-HBV/HepG2 culture system was developed which could support productive HBV infection in vitro. Expression of HBsAg and HBeAg in infected HepG2 culture medium was detected by commercial enzyme immunoassays. HBV DNA replication intermediates were detected in infected cells by Southern hybridization and viral DNA load was determined by dot hybridization. RESULTS: IFN-γat 0.1 to 5μg/L efficiently down regulated HBsAg expression in transduced HepG2 cells. At 5μg/L, IFN-γalso suppressed HBV DNA replication in these cells. While treatment with a combination of lamivudine and IFN-γshowed no additive effect, sequential treatment first with lamivudine and then IFN-γwas found to be promising. In this culture system the best HBV suppression was observed with a pulse of 2μmol/L lamivudine for two days, followed by 1μg/L IFN-γfor another four days. Compared to treatment with lamivudine alone, the sequential use of 0.2μmol/L lamivudine for two days, followed by 5μg/L IFN-γfor six days showed a 72% reduction in HBV cccDNA pool. CONCLUSION: This in vitro study warrants further evaluation of a combination of IFN-γand lamivudine, especially in IFN-αnon-responder chronic hepatitis B patients. A reduced duration of lamivudine treatment would also restrict the emergence of drug-resistant HBV mutants.

IFN-γ increases efficiency of DNA vaccine in protecting ducks against infection

AIM： To detect the effects of DNA vaccines in combination with duck IFN-γ gene on the protection of ducks against duck hepatitis B virus （DHBV） infection. METHODS： DuIFN-γ cDNA was cloned and expressed in COS-γ cells, and the antiviral activity of DuIFN-γ was detected and neutralized by specific antibodies, Ducks were vaccinated with DHBpreS/S DNA alone or coimmunized with plasmid expressing DuIFN-γ. DuIFN-γ mRNA in peripheral blood mononuclear cells （PBMCs） from immunized ducks was detected by semi-quantitative competitive RT-PCR. Anti-DHBpreS was titrated by enzyme-linked immunosorbent assay （EUSA）. DHBV DNA in sera and liver was detected by Southern blot hybridization, after ducks were challenged with high doses of DHBV. RESULTS： DuIFN-γ expressed by COS-γ was able to protect duck fibroblasts against vesicular stomatitis virus （VSV） infection in a dose-dependent fashion, and anti DuIFN-γ antibodies neutralized the antiviral effects. DuIFN-γ in the supernatant also inhibited the release of DHBV DNA from LMH-D2 cells. When ducks were co-immunized with DNA vaccine expressing DHBpreS/S and DuIFN-γ gene as an adjuvant, the level of DuIFN-γ mRNA in PBMCs was higher than that in ducks vaccinated with DHBpreS/S DNA alone. However, the titer of anti-DHBpreS elicited by DHBpreS/S DNA alone was higher than that co-immunized with DuIFN-γ gene and DHBpreS/S DNA. After being challenged with DHBV at high doses, the load of DHBV in sera dropped faster, and the amount of total DNA and cccDNA in the liver decreased more significantly in the group of ducks co-immunized with DuIFN-γ gene and DHBpreS/S DNA than in other groups.

Enhancing effect of tazarotene on the HLA-DR expression of cultured human keratinocytes induced by interferon-gamma

Objective: To investigate the effect of tazarotene on the expression of HLA-DR induced by IFN-γ. Methods: (1) Keratinocytes from normal human skin were cultured in vitro;(2) Tazarotene, IFN-γ and the combination of the two compounds were incubated with the keratinocytes in medium, respectively. The expression of HLA-DR in keratinocytes was determined using immunocytochemistry techniques at 24h after incubation. Results: (1) There was rare expression of HLA-DR in normal human keratinocytes; (2) 10 -6mol/L tazarotene failed to induce the expression of HLA-DR in keratinocytes at 24h after incubation; (3) 500 U/ml IFN-γ obviously induced the HLA-DR expression in keratinocytes at 24h after treatment; (4) After 24h, 10 -7-10 -5 mol/L tazarotene had a significantly enhancing effect on the expression of HLA-DR induced by IFN-γ (P<0.005). Conclusion: Tazarotene up-regulates the expression of HLA-DR in keratinocytes cultured in vitro when combined with IFN-γ . Therefore, the reduction of HLA-DR positive keratinocytes in psoriatic lesions may be attributed to not direct interaction of tazarotene in combination with IFN-γ but other pathways.

IgE PRODUCTION IS INVOLVED IN BUTYRATE- ENHANCED NK CELL ACTIVITY IN VIVO

It has been demonstrated that patients with asthma have a large number of NK cells and show a stronger NK activity. These results indicate that NK cell activity may be related to total IgE level in serum in healthy subjects. Previously,we have found that sodium butyrate (NaBu) markedly enhanced the IL- 4- induced IgE production in the LPS- stimulated murine splenocytes in vitro, and inductive rat IgE production in vivo, and enhanced the NK cell activity ex vivo .We hypothesized that the IgE production might be involved in butyrate- enhanced NK cell activity in vivo. Mice were intraperitoneally treated/immunized with NaBu or/and Ascaris suum extract (ASC),and the spleen NK cell activity was evaluated. Furthermore, the effect of serum (NAS) on IL- 2- or IFN-γ- induced spleen NK cell activity was determined. The spleen NK cell activity and IL- 2- or IFN-γ- induced spleen NK cell activity of mice treated/immunized with NaBu or/and ASC were stronger than those of untreated/unimmunized mice. Although IL- 4 blocked IL- 2 (100 U/ml)- or IFN-γ (100 U/ml)- induced increase in NK cell activity,these NK cell activities in mice treated/immunized with NaBu/ASC were not inhibited. IgE production showed a tendency to rise in NaBu- treated mice serum, and a synergistic effect was observed with treatment of NaBu and ASC. Moreover, the NAS significantly increased IL- 2(25 U/ml)- or IFN-γ (25 U/ml)- induced NK cell activity, and its effect was inhibited by anti- mouse IgE mAb. These data show that IgE plays an important role in NAS- enhanced IL- 2/IFN-γ- induced NK cell activity, and IL- 4 does not inhibit IgE and IL- 2/IFN-γ- induced NK cell activity in mice.

Interferon-γ mRNA attenuates its own translation by activating PKR： A molecular basis for the therapeutic effect of interferon-β in multiple sclerosis

PKR, the interferon （IFN）-inducible protein kinase activated by double-stranded RNA, inhibits translation by phosphorylating the initiation factor eIF2α chain. Uniquely, human IFN-γ mRNA uses local activation of PKR in the cell to control its own translation yield. IFN-γ mRNA activates PKR through a structure in its 5＇- region harboring a pseudoknot which is critical for PKR activation. Mutations that impair pseudoknot stability reduce the ability of IFN-γ mRNA to activate PKR and strongly increase its translation efficiency. The cis-acting RNA element in IFN-γ mRNA functions as a biological sensor of intracellular PKR levels. During an immune response, as IFN-γ and other inflammatory cytokines build up in the cell＇s microenvironment, they act to induce higher levels of PKR in the cell, resulting in a more extensive activation of PKR by IFN-γ mRNA. With the resulting phosphorylation of eIF2α, a negative feedback loop is created and the production of IFN-γ is progressively attenuated. We propose that the therapeutic effect of IFN-β in multiple sclerosis may rest, at least in part, on its exquisite ability to induce high levels of PKR in the cell and thereby to limit IFN-γ mRNA translation through this negative feedback loop, blocking the excessive IFN-γ gene expression that precedes clinical attacks.

Effect of expression of TGF-beta and TNF-alpha with Qidan granule treatment in rats by bleomycin-induced pulmonary fibrosis

Objective: To evaluate the therapeutic effects and mechanisms of Qidan granule in blemycinA5-induced pulmonary interstitial fibrosis (PIF)in rats. Methods: PIF models were established by blemycinA5-induced in rats. They were treated by Qidan granule and Hydrocortisone respectively. The pathological changes and collagen protein disposition were observed, and the expression of TGF-β, TNF-α proteins were measured by immunohistochemical technique. Results: The pulmonary alveolitis and fibrosis were alleviated remarkably in Qidan granule group compared with those in the model control group and hydrocortisone group (P<0.01). The expression of TGF-β and TNF-α protein were higher in Qidan granule group than those in normal group ,and were significantly less than those in the model control group and in hydrocortisone group (P<0.01). Conclusion: Qidan granule would ameliorate the pulmonary alveolitis and fibrosis. TGF-β and TNF-α might play an important role in the development of alveolitis and fibrosis in rats.

Interferon-γ inhibits in situ expression of PDGF-β mRNA by smooth muscle cells in injured rabbit arteries after transluminal balloon angioplasty

Objective To elucidate the mechanism of interferon-gamma (IFN-γ) to inhibit the restenosis after successful percutaneous transluminal angioplasty (PTA).Methods A rabbit vascular restenotic model was constructed and the proliferation of intimal smooth muscle cells (SMCs) were observed by monitoring their expression of proliferating cell nuclear antigen (PCNA) and platelet-derived growth factor β chain mRNA (PDGF-β mRNA) at the indicated time points. Results IFN-γ could significantly inhibit the expression of PCNA by intimal SMCs one week after denudation, when counting 200 intimal cells for PCNA-positive reactions with an inhibitory rate of 88.50% (P<0.001). IFN-γ could downregulate in situ expression of PDGF-β mRNA by these cells as we calculated the average number of PDGF-β mRNA positive cells per square millimetre area at ×400 magnification with reduced rates of 86.85% in 1 week group (P<0.001), of 93.66% in 2 week group (P<0.001) and of 52.92% in 4 week group (0.02<P<0.05), respectively. Conclusions The local production of PDGF-β by vascular intimal SMCs via an autocrine mechanism may be responsible for continuous proliferation of these cells and the formation of neointima after injury. This could be inhibited by IFN-γ through downregulating the expression of PDGF-β mRNA. These results provide an in vivo basis for IFN-γ to be used clinically for the management of restenosis after percutaneous transluminal angioplasty.

Up-regulated intragraft gene expression, ICAM-1 and IL-2R molecules, and apoptotic epithelial cells during rejection of rat small intestine allografts

Objective To investigate the kinetics and the magnitude of intragraft gene expression of interleukin-2(IL-2), interferon-gamma (IFN-y), perforin and granzyme B, and intragraft expression of interieukin-2receptor (IL-2R) and intercellular adhesion molecule-1 ( ICAM-1 ) during acute rejection episodes, and to analyze the changes in apoptosis in small intestinal allograft rejection.Methods Heterotopic small intestine transplantation was performed with inbred rats F344/N (RT11) and Wistar/A (RT1-Ak, RT1-Ed). All recipients were divided into four groups: group 1 : Wistar, native control;group 2: Wistar→Wistar; group 3: F344→Wistar and group 4: F344→Wistar + cyclosporine A (6 mg·kg-1 ·d-1 I.M. ). The grafts were harvested on postoperative days (PODs) 3, 5 and 7. All samples were examined pathologically. Intragraft mRNA expression of IL-2, IFN-γ, perforin and granzyme B were detected with reverse transcriptase polymerase chain reaction (RT-PCR) and intragraft expression of IL-2R and ICAM-1 were stained using immunohistochemistry. We also analyzed the change in apoptosis rejection with terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL).Results Mild acute rejection occurred on POD 3 in the ailograft group, moderate acute rejection on POD 5, and severe acute rejection on POD 7, while none of the isografts had histological evidence of acute rejection. Cyclosporine A could effectively control rejection. Gene expression was virtually negative in the native control. Only on POD 5 was IL-2 mRNA expression of ailografts significantly higher than that of isografts ( P ＜ 0.05). IFN-γ mRNA expression was significantly higher than that of the control groups ( P ＜0.01 ) on PODs 3, 5 and 7, and the level of perforin and granzyme B mRNA expression reached significantly higher levels than in the other two control groups on POD 5 and POD 7. Intragraft IL-2Rexpression of the allograft was significantly higher than that of the other three control groups. Only on POD 3 was intragraft ICAM-1 expression of allografts significantly higher than isografts. The number of apoptotic cells per crypt of allografts was significantly higher than that of the other three control groups on POD 3 and POD 5 ( P ＜ 0.01 ).Conclusion Transcription of IL-2, IFN-γ, perforin and granzyme B, and expression of IL-2R and ICAM-1as well as apoptosis of epithelial cells of the grafts play an important role in small intestine allograft rejection.Intragraft gene expression of IFN-γ and intragraft expression of IL-2R as well as apoptotic epithelial cells may become a specific and sensitive diagnostic method of clinical value. Furthermore, therapeutic strategies to alter these molecules in small intestine transplantation may improve the outcome of current antirejection therapy.

Interferon-γ regulates cell malignant growth via the c-Abl/HDAC2 signaling pathway in mammary epithelial cells

Interferon-γ(IFN-γ) has been used to control cancers in clinical treatment. However, an increasing number of reports have suggested that in some cases effectiveness declines after a long treatment period, the reason being unclear. We have reported previously that long-term IFN-γ treatment induces malignant transformation of healthy lactating bovine mammary epithelial cells(BMECs) in vitro. In this study, we investigated the mechanisms underlying pthe malignant proliferation of BMECs under IFN-γ treatment. The primary BMECs used in this study were stimulated by IFN-γ(10 ng/mL) for a long term to promote malignancy. We observed that IFN-γ could promote malignant cell proliferation, increase the expression of cyclin D1/cyclin-dependent kinase 4(CDK4), decrease the expression of p21, and upregulate the expression of cellular-abelsongene(c-Abl) and histone deacetylase 2(HDAC2). The HDAC2 inhibitor, valproate(VPA) and the c-Abl inhibitor, imatinib, lowered the expression level of cyclin D1/CDK4, and increased the expression level of p21, leading to an inhibitory effect on IFN-γ-induced malignant cell growth. When c-Abl was downregulated, the HDAC2 level was also decreased by promoted proteasome degradation. These data suggest that IFN-γ promotes the growth of malignant BMECs through the c-Abl/HDAC2 signaling pathway. Our findings suggest that long-term application of IFN-γ may be closely associated with the promotion of cell growth and even the carcinogenesis of breast cancer.

Ran binding protein 9(RanBPM) binds IFN-λR1 in the IFN-λsignaling pathway

Like the type I interferons(IFNs),the recently discovered cytokine IFN-λ displays antiviral,antiproliferative,and proapoptotic activities,mediated by a heterodimeric IFN-λ receptor complex composed of a unique IFN-λR1 chain and the IL-10R2 chain.However,the molecular mechanism of the IFN-λ-regulated pathway remains unclear.In this study,we newly identified RAN-binding protein M(RanBPM) as a binding partner of IFN-λR1.The interaction between RanBPM and IFN-λRl was identified with a glutathione S-transferase pull-down assay and coimmunoprecipitation experiments.IFN-λ1 stimulates this interaction and affects the cellular distribution of RanBPM.However,the interaction between RanBPM and IFN-λR1 does not correlate with their conserved TRAF6-binding sites.Furthermore,we also found that RanBPM is a scaffolding protein with a modulatory function that regulates the activities of IFN-stimulated response elements.Therefore,RanBPM plays a novel role in the IFN-λ-regulated signaling pathway.

T helper cells in patients with chronic hepatitis B virus infection

OBJECTIVE: To investigate the compositions of Th1/Th2/Th3 cells in chronic hepatitis B virus (HBV)-infected individuals by determining the expression of interleukin-4 (IL-4), inetrferon-gamma (IFN-gamma), and transform growth factor-beta (TGF-beta) in single CD4(+) T cells isolated from peripheral blood mononuclear cells (PBMCs) and the role of polarized Th cell populations in chronic HBV-infection was discussed. METHODS: PBMCs from chronically infected HBV individuals were isolated, stimulated by PMA/Ionomycin/Monensin, and IL-4, IFN-gamma and TGF-beta production by CD4(+) T cells was determined by using fluorescence activated cell sorter (FACS) analysis. RESULTS: The percentage of IFN-gamma-producing T cells, IL-4-producing T cells and TGF-beta-producing T cells ranged from 2.3% - 18.6%, 1.1% - 8.7% and 0.7% - 7.1% respectively in CD4(+) T cells from non-infected individuals. Most of CD4(+) T cells from PBMCs in chronically infected HBV individuals were Th0 cells. The proportion of Th1 cells increased significantly with hepatic inflammatory activity, and in the active period of chronic hepatitis B infection were higher than those in the non-active period (P 0.05), but were higher than that from controls (P

Regulatory effect of moxibustion for rats with ulcerative colitis on the macrophage functional phenotype protein of lung tissueRegulatory effect of moxibustion for rats with ulcerative colitis on the macrophage functional phenotype protein of lung tissue

Objective： To observe the regulatory effect of moxibustion on the expression of CD86 and CD163, which are the important functional phenotypes of macrophage differentiation in lung tissue of ulcerative colitis（UC） rats. The mechanism of the regulatory effect of moxibustion for macrophage differentiation based on the key cytokine interferon-gamma（IFN-γ）, tumor necrosis death factor-alpha（TNF-α）, interleukin- 4（IL-4） and interleukin-13（IL-13） was also explored. Methods： Forty SD rats were randomly divided into a normal group（NG）, a model group（MG）, a normal moxibustion group（NMG） and a smokeless moxibustion group（SMG）. The model of UC was made by antigen immunization combined with enema with topical formalin. The rats in the normal moxibustion group accepted moxibustion at bilateral Tianshu（ST 25）, while the rats in the smokeless moxibustion group with smokeless moxibustion at bilateral Tianshu（ST 25）, each 10 min, once a day for 8 d. After treatments, the hematoxylin-eosin（HE） staining was used to observe the pathological changes of colonic tissue, the Western blotting（WB） was used to observe the expression of CD86 and CD163, two important functional phenotypes of macrophage differentiation in lung tissue of UC rats, while the enzyme-linked immunosorbent assay（ELISA） was used to assess the content of IFN-γ, TNF-α, IL-4 and IL-13, the key cytokines of macrophage differentiation in micro environment of the lung tissue. Results： Compared with the NG, the colons of rats in MG were injured more seriously, and the scores of gross observation and histological examination were significantly higher（P〈0.05）. Compared with the MG, the pathological changes of the two groups of rats with moxibustion treatment were improved, which presented with ulcer repair, inflammation dissipation, and the general score and histological score of the two groups were decreased（P〈0.05）. Compared with the NG, the expression of CD86 in the lung tissue of rats in the MG was increased（P〈0.05）, and CD163 expression was decreased（P〈0.05）. Compared with the MG and the SMG, the expression of CD86 in the lung tissue of the rats in the NMG was significantly lower than those in the MG and SMG, and CD163 was higher（P〈0.05）, while the differences were not statistically significant between the MG and the SMG（P〈0.05）. Compared with the NG, the expression of key cytokines in lung tissue of MG was abnormal, the contents of IFN-γ and TNF-α increased（P〈0.05）, while the IL-4 and IL-13 decreased（P〈0.05）. The IL-4 and IL-13 were significantly increased in lung tissue of rats in the NMG（P〈0.05）, and the IFN-γ and TNF-α were reduced（P〈0.05）, compared with those in the MG and the SMG, while the differences were not statistically significant between the MG and the SMG（P〈0.05）. Conclusion： Moxibustion can increase the expression of CD163, the important functional phenotype of macrophages in lung tissue of UC rats, and the differentiation critical cytokines IL-4 and IL-13. It can also reduce activated phenotype CD86 and its differentiation critical cytokines IFN-γ and TNF-α in the lung tissue of UC rats.

Effects of Wuwei Dilong Decoction on Inflammatory Cells and Cytokines in Asthma Model Guinea Pigs

Objective： To explore the effects and the mechanism of Wuwei Dilong Decoction （五味地龙汤 Schisandra Fruit and Earthworm Decoction） for treatment of asthma. Methods： The asthma guinea pig model was established with spray of ovalbumin （OVA）. Fifteen days later, the guinea pigs were administered by intra-gastric perfusion of Wuwei Dilong Decoction once a day for 8 consecutive days. Blood samples were taken for testing the total leucocytes, eosinophil （EOS）, lymphocytes, interferon-γ （IFN-γ） and leukotriene B4 （LTB4）. Results： In the asthma model group, the total leucocytes, EOS and lymphocytes were all increased, with significant differences as compared with the different dosage Wuwei Dilong Decoction groups （P〈0.01 or P〈0.05）. The serum LTB4 in the asthma model group was significantly increased and IFN-γ decreased. After administration of Wuwei Dilong Decoction of the large, medium and small dosages, LTB4 decreased, while IFN-7 increased （P〈0.05 or P〈0.01）. Conclusion： Wuwei Dilong Decoction can inhibit infiltration and diffusion of the inflammatory cells in the asthma model guinea pigs, and regulate LTB4 and IFN-γ, which is probably one of the important mechanisms of Wuwei Dilong Decoction for relieving asthma.

Clinical efficacy of acupuncture in treatment ofchronic urticaria and its effects on the content of IgE and the imbalance of Th1/Th2 cell function

Objective:To observe the clinical efficacy of acupuncture in treatment of chronic urticaria and the change in the content of serum immunoglobulin E(IgE),and to discuss the effect of acupuncture on the imbalance of T helper(Th)1/Th2 cell function via observing the changes in the contents of interferon-y(IFN-y)and interleukin-4(IL-4).Methods:Ninety patients meeting the inclusion criteria of chronic urticaria were randomized into an acupuncture-medication group,an acupuncture group and a Western medication group by the random number table method.The acupuncture-medication group was intervened by acupuncture,cupping,collateral-pricking bloodletting and oral administration of cetirizine hydrochloride tablets;the acupuncture group was treated with acupuncture,cupping and collateral-pricking bloodletting;the Western medication group only received oral administration of cetirizine hydrochloride tablets.Before treatment and after 6-week treatment,the changes in the symptom scores and the contents of serum IgE,IFN-γ and IL-4 in the three groups were observed.Results:There were no significant differences in the total effective rate among the three groups(all P>0.05),but the cured and markedly effective rate was significantly higher in the acupuncture-medication group than that in the Western medication group(P<0.05).After treatment,the total symptom score decreased in the three groups(P<0.05),and the improvement of total symptom score in the acupuncture-medication group was more significant than that in the Western medication group(P<0.05).The component symptom scores all decreased after treatment in the three groups(all P<0.05);the improvements of the scores of itch intensity,and skin lesion size and number were more significant in the acupuncture-medication group than in the Western medication group(all P<0.05);the improvement of the skin lesion size score was more significant in the acupuncture group than in the Western medication group(P<0.01).The contents of IgE and IL-4 dropped(all P<0.05)and the content of IFN-y increased(P<0.05)after treatment in the three groups;the post-treatment changes in the serum contents of IgE and IFN-y were more significant in the acupuncture-medication group than in the Western medication group(both P<0.05).The incidence rate of adverse reactions was significantly lower in the acupuncture-medication group and acupuncture group than in the Western medication group(both P<0.05),and the relapse rate was significantly lower in the acupuncture-medication group than in the Western medication group(P<0.05).Conclusion:Combined acupuncture and medication can enhance the cured and markedly effective rate in treating chronic urticaria.Acupuncture is equivalent to cetirizine hydrochloride tablets comparing the clinical efficacy in treatment of chronic urticaria.Acupuncture plus medication and acupuncture alone both can effectively mitigate the clinical symptoms,with low incidence of adverse reactions.The relapse rate is low when using acupuncture together with medication.Acupuncture plus medication can work better in regulating the contents of IgE and IFN-y and improving the imbalance of Th1/Th2 cell function.