Biomedical subjects

S Qin

Publications and source records attributed to S Qin.

At least 55 records · Page 3Linked to original sources

PubMed2000

[Antitumor effect of arsenic trioxide on mice experimental liver cancer].

OBJECTIVE: To investigate the antitumor activity of arsenic trioxide on mice experimental liver cancer. METHODS: Mice bearing HepA solid and ascitic liver tumor were used in vivo experiments. RESULTS: The tumor-bearing mice were treated with arsenic trioxide 2.0mg/kg/d and 3.5mg/kg/d intravenously for 7 days. After the administration of arsenic trioxide, the growth of solid tumor were obviously inhibited, the inhibitory rate were 31.63% and 42.13% respectively. Under the inspection of transmission electron microscope, some cells of the solid tumor showed the typically morphological characteristics of apoptosis. The apoptotic cells were detected by in situ TdT-mediated dUTP nick end labeling (TUNEL). The immunohistochemical staining showed that the number of bcl-2 protein positive cells decreased, but the number of bax protein positive cells increased. It also showed that arsenic trioxide could significantly prolong the mean survival time in ascitic-tumor-bearing mice, the prolonging rate of life span was 59.29% and 76.69% respectively. The sub-G1 peaks were observed by flow cytometry on the ascitic specimen and the apoptotic rate were 25.98% and 53.17% respectively. CONCLUSION: arsenic trioxide has obvious antitumor activity on HepA liver tumor-bearing mice. The mechanism of arsenic trioxide may mainly be inducing liver cancer cells to undergo apoptosis, which may be related to downregulate the expression of bcl-2 genes and upregulate the expression of bax genes.

Animals↗

PubMed2000

[An experimental study on arsenic trioxide-selectively induced human hepatocarcinoma cell lines apoptosis and its related genes].

OBJECTIVE: To study the possible apoptosis-inducing effect of arsenic trioxide on human hepatocarcinoma (HCC) cells, and its molecular mechanisms. METHODS: Arsenic trioxide action on the cell growth, apoptosis, periodicity and the expression of related genes in two human hepatocarcinoma cell lines QGY-7701 and QGY-7703, and normal humanhepatic cell line L-02 in vitro was observed by MTT assay, acridine orange (AO) /ethidiumbromide (EB) fluorescent staining, electron microscopy detection, DNA gel electrophoresis, flow cytometry, TUNEL assay and immunohistochemical staining. RESULTS: Arsenic trioxide could strongly inhibit the growth of human hepatocarcinoma cells QGY-7701 and QGY-7703 with the cell cycle arrested on S phase, and induce the apoptosis of the cells with bcl-2 gene expression down-regulated and bax and Fas gene expression up-regulated. But arsenic trioxide had no obvious effect on the normal hepatic cells. CONCLUSION: Arsenic trioxide has significant selective apoptosis-inducing effect on the human hepatocarcinoma cells, which is regulated by several genes. The results provide the credible experimental basis for clinically treating HCC with arsenic trioxide.

Antineoplastic Agents↗

PubMed2000

[Rhubarb extracts in treating complications of severe cerebral injury].

OBJECTIVE: To investigate the therapeutic effects of the Chinese medicinal herb, Rhubarb, on severe brain injury. METHODS: Rhubarb extracts in ethyl alcohol and water were used to treat 20 patients with severe cerebral injury complicated by hyperthermia, renal failure, hemorrhage in the upper digestive tract, and increased intracranial pressure. Vital signs, variations of Glasgow coma scale (GCS) and intracranial pressure (ICP) of the patients were observed. The degree of hemorrhage in the digestive tract and the change in creatinine value were also observed. Other 20 patients served as controls. RESULTS: The result of the treatment group was more marked than that of the control group. Three days after administration of the rhubarb extract, the body temperature decreased by 1.1 degrees C, ICP by 0.4 kPa (1 mm Hg = 0.1333 kPa) on average, and the incidence of hemorrhage in the digestive tract by 30%. The volume of hemorrhage of the digestive tract decreased by 700 +/- 250 ml, and the time for turning occult blood to negative by 10%. CONCLUSION: The Chinese medical herb, rhubarb, has multiple therapeutic effects on severe brain injury.

Adolescent↗

PubMed2000

Detecting residual ischemia and identifying coronary artery disease after myocardial infarction using dobutamine technetium-99m-MIBI SPECT.

OBJECTIVE: To evaluate dobutamine technetium-99m methoxy isobutyl nitrile (sestamibi) single-photon emission computed tomography (Dobu-ECT) in detecting residual ischemia and identifying coronary vessel disease after myocardial infarction. METHODS: Sixty-two patients with confirmed myocardial infarction were studied with Dobu-ECT at the time of coronary artery angiography. Dobutamine was administered intravenously in incremental rates from 5 to 40 micrograms.kg-1.min-1 at 3-minute intervals. At the highest infusion rate, 7.4 x 10(8) Bq 99mTc-MIBI was injected intravenously, and tomographic imaging was performed after one hour. Resting images were taken after 24 hours, with a second dose of 99mTc-MIBI. RESULTS: The sensitivity of Dobu-ECT in detecting residual ischemia of myocardial infarction was 76%, which was higher than dobutamine electrocardiography (Dobu-ECG). Regardless of the single-, double- or triple-vessel diseases, Dobu-ECT was superior to Dobu-ECG in identifying residual ischemia (56% vs 4%, 86% vs 27%, 100% vs 47%, P < 0.01, respectively). The incidence of residual ischemia in patients receiving thrombolytic therapy was 67%, lower than patients without thrombolysis (72%) or those with an old myocardial infarction (94%). But the differences were not statistically significant. Dobu-ECT detected only 56% of ischemias in non-infarct related myocardium. Eighty-two percent of all significantly stenosed vessels were detected with Dobu-ECT, and 84% of patients with multivessel disease could be accurately identified. The sensitivity of Dobu-ECT was significantly greater for detecting severe stenosis over moderate stenosis. The sensitivity for detecting stenosis in the right coronary artery was greater than left anterior descending or left circumflex, but its specificity was lower. CONCLUSION: Dobu-ECT can identify residual ischemia, as well as its location and extent after myocardial infarction. Dobu-ECT can also accurately detect significantly stenosed vessels.

Adult↗

PubMed2000

[Dural arterovenous fistula involving cavernous sinus].

OBJECTIVE: To study the pathogenesis and treatment of dural arteriovenous fistulas (DAVFS) involving the cavernous sinus. METHODS: 32 cases were embolized with particle by microcatheterization via endovascular approach and ervation by digital substraction angiography. Of the 32 cases, 14 were embolized by microsoils through superior petrosal sinus approach into the cavernous sinus. RESULTS: In 28 of the 32 cases the fistulas were completely embolized angiographically. The fistulas were partly embolized in 4 of the 32 cases. The carotid artery was compressed for 6 months. One week later, the fistula disappeared angiographically. No fistulas were found during the follow-up for 6 months to 8 years. CONCLUSION: Endovascular treatment of DAVFS involving the cavernous sinus is effective.

Adolescent↗

PubMed2000

[The diagnosis and treatment of Lyme disease: a report of six cases].

We retrospectively analyzed the clinical features, diagnosis, treatment, and prognosis of 6 cases of Lyme disease from November, 1994 to December, 1998. According to our report, doxycycline, penicillin, and ceftriaxone are effective drugs for Lyme disease. The shorter the disease course is, the better the treatment effect will be. Patients in phase III usually need repeated treatment.

Adolescent↗

PubMed1999

Chemokine and chemokine receptor interactions provide a mechanism for selective T cell recruitment to specific liver compartments within hepatitis C-infected liver.

The role played by chemokines in regulating the selective recruitment of lymphocytes to different tissue compartments in disease is poorly characterized. In hepatitis C infection, inflammation confined to portal areas is associated with a less aggressive course, whereas T cell infiltration of the liver parenchyma is associated with progressive liver injury and cirrhosis. We propose a mechanism to explain how lymphocytes are recruited to hepatic lobules during bursts of necroinflammatory activity in chronic hepatitis C infection. We report here that lymphocytes infiltrating hepatitis C-infected liver express high levels of the chemokine receptors CCR5 and CXCR3. However, whereas the CCR5 ligands macrophage inflammatory protein-1alpha and -1beta were largely confined to vessels within portal tracts, the CXCR3 ligands IFN-inducible protein-10 and monokine-induced by IFN-gamma were selectively up-regulated on sinusoidal endothelium. In vitro, human hepatic sinusoidal endothelial cells secreted IFN-inducible protein-10 and monokine-induced by IFN-gamma in response to stimulation with IFN-gamma in combination with either IL-1 or TNF-alpha. This suggests that intrahepatic Th1 cytokines drive the increased expression of IFN-inducible protein-10 and monokine-induced by IFN-gamma and thereby promote the continuing recruitment of CXCR3-expressing T cells into the hepatic lobule in chronic hepatitis C infection.

Cell Movement↗

PubMed1999

Human G protein-coupled receptor GPR-9-6/CC chemokine receptor 9 is selectively expressed on intestinal homing T lymphocytes, mucosal lymphocytes, and thymocytes and is required for thymus-expressed chemokine-mediated chemotaxis.

TECK (thymus-expressed chemokine), a recently described CC chemokine expressed in thymus and small intestine, was found to mediate chemotaxis of human G protein-coupled receptor GPR-9-6/L1.2 transfectants. This activity was blocked by anti-GPR-9-6 monoclonal antibody (mAb) 3C3. GPR-9-6 is expressed on a subset of memory alpha4beta7(high) intestinal trafficking CD4 and CD8 lymphocytes. In addition, all intestinal lamina propria and intraepithelial lymphocytes express GPR-9-6. In contrast, GPR-9-6 is not displayed on cutaneous lymphocyte antigen-positive (CLA(+)) memory CD4 and CD8 lymphocytes, which traffic to skin inflammatory sites, or on other systemic alpha4beta7(-)CLA(-) memory CD4/CD8 lymphocytes. The majority of thymocytes also express GPR-9-6, but natural killer cells, monocytes, eosinophils, basophils, and neutrophils are GPR-9-6 negative. Transcripts of GPR-9-6 and TECK are present in both small intestine and thymus. Importantly, the expression profile of GPR-9-6 correlates with migration to TECK of blood T lymphocytes and thymocytes. As migration of these cells is blocked by anti-GPR-9-6 mAb 3C3, we conclude that GPR-9-6 is the principal chemokine receptor for TECK. In agreement with the nomenclature rules for chemokine receptors, we propose the designation CCR-9 for GPR-9-6. The selective expression of TECK and GPR-9-6 in thymus and small intestine implies a dual role for GPR-9-6/CCR-9, both in T cell development and the mucosal immune response.

Antibodies, Monoclonal↗

PubMed1999

Involvement of receptor aggregation and reactive oxygen species in osmotic stress-induced Syk activation in B cells.

Syk has been shown to be activated by osmotic stress, however, the mechanisms involved are largely unknown. In this study, we demonstrated that cell shrinkage, rather than osmolarity, was responsible for osmotic stress-induced Syk activation. Osmotic stress-induced Syk activation depended partly upon aggregation of surface receptors. Moreover, intracellular reactive oxygen species were involved in mediating osmotic stress-induced Syk activation, with osmotic stress-induced Syk activation being inhibited by the pretreatment of cells with N-acetyl-cysteine and reduced glutathione. When cells were treated with the combination of sodium chloride and hydrogen peroxide, there was a synergistic activation of Syk. In conclusion, osmotic stress-induced Syk activation required suramin-inhibitable surface receptor aggregation and accumulation of intracellular reactive oxygen species.

Acetylcysteine↗

PubMed1999

The chemokine receptor CCR4 in vascular recognition by cutaneous but not intestinal memory T cells.

Lymphocytes that are responsible for regional (tissue-specific) immunity home from the blood to the intestines, inflamed skin or other sites through a multistep process involving recognition of vascular endothelial cells and extravasation. Chemoattractant cytokine molecules known as chemokines regulate this lymphocyte traffic, in part by triggering arrest (stopping) of lymphocytes rolling on endothelium. Here we show that many systemic memory T cells in blood carry the chemokine receptor CCR4 and therefore respond to its ligands, the chemokines TARC and MDC. These cells include essentially all skin-homing cells expressing the cutaneous lymphocyte antigen and a subset of other systemic memory lymphocytes; however, intestinal (alpha4beta7+) memory and naive T cells respond poorly. Immunohistochemistry reveals anti-TARC reactivity of venules and infiltration of many CCR4+ lymphocytes in chronically inflamed skin, but not in the gastrointestinal lamina propria. Moreover, TARC induces integrin-dependent adhesion of skin (but not intestinal) memory T cells to the cell-adhesion molecule ICAM-1, and causes their rapid arrest under physiological flow. Our results suggest that CCR4 and TARC are important in the recognition of skin vasculature by circulating T cells and in directing lymphocytes that are involved in systemic as opposed to intestinal immunity to their target tissues.

Chemokine CCL17↗

PubMed1999

Multiple activation steps of the N-formyl peptide receptor.

The human N-formyl peptide receptor (FPR) is representative of a growing family of G protein-coupled receptors (GPCR) that respond to chemokines and chemoattractants. Despite the importance of this receptor class to immune function, relatively little is known about the molecular mechanisms involved in their activation. To reveal steps required for the activation of GPCR receptors, we utilized mutants of the FPR which have previously been shown to be incapable of binding and activating G proteins. For this study, the FPR mutants were expressed in human myeloid U937 cells and characterized for functions in addition to G protein coupling, such as receptor phosphorylation and ligand-induced receptor internalization. The results demonstrated that one of the mutants, R123G, though being unable to activate G protein, was capable of undergoing ligand-induced phosphorylation as well as internalization. Receptor internalization was monitored by following the fate of the ligand as well as by directly monitoring the fate of the receptor. The results with the R123G mutant were in contrast to those obtained for mutants D71A and R309G/E310A/R311G which, though being expressed at the cell surface and binding ligand, were incapable of being phosphorylated or internalized upon agonist stimulation. These results suggest that following ligand binding at least two "steps" are required for full activation of the wild-type FPR. That these observations may be of more general importance in GPCR-mediated signaling is suggested by the highly conserved nature of the mutants studied: D71, R123, and the site represented by amino acids 309-311 are very highly conserved throughout the entire superfamily of G protein-coupled receptors. Models of receptor activation based on the observed results are discussed.

Animals↗

PubMed1999

Switch in chemokine receptor expression upon TCR stimulation reveals novel homing potential for recently activated T cells.

When naive T lymphocytes are activated and differentiate into memory/effector cells, they down-regulate receptors for constitutive chemokines such as CXCR4 and CCR7 and acquire receptors for inflammatory chemokines such as CCR3, CCR5 and CXCR3, depending on the Th1/Th2 polarization. This switch in chemokine receptor usage leads to the acquisition of the capacity to migrate into inflamed tissues. Using RNase protection assays, staining with specific antibodies, and response to recombinant chemokines, we now show that following TCR stimulation, memory/effector T cells undergo a further and transient switch in receptor expression. CCR1, CCR2, CCR3, CCR5, CCR6 and CXCR3 are down-regulated within 6 h, while CCR7, CCR4, CCR8 and CXCR5 are up-regulated for 2 to 3 days. Up-regulation of CCR7 following TCR stimulation was observed also among resting peripheral blood T cells and required neither co-stimulation nor exogenous IL-2. On the other hand IL-2 down-regulated CXCR5, up-regulated CCR8 and facilitated the recovery of CCR3 and CCR5. Upon TCR stimulation, Th1 and Th2 cells produced comparable sets of chemokines, including RANTES, macrophage inflammatory protein-1beta, I-309, IL-8 and macrophage-derived chemokine, which may modulate surface chemokine receptors and contribute to cell recruitment at sites of antigenic recognition. Altogether these results show that following TCR stimulation effector/memory T cells transiently acquire responsiveness to constitutive chemokines. As a result, T cells that are activated in tissues may either recirculate to draining lymph nodes or migrate to nearby sites of organized ectopic lymphoid tissues.

Base Sequence↗

PubMed1999

Expression and function of CXC and CC chemokines in human malignant liver tumors: a role for human monokine induced by gamma-interferon in lymphocyte recruitment to hepatocellular carcinoma.

Chemotactic cytokines (chemokines) play an important role in the recruitment of lymphocytes to tissue by regulating cellular adhesion and transendothelial migration. This study examined the expression and function of CXC (human monokine induced by gamma-interferon [HuMig], interleukin-8 [IL-8], and interferon-inducible protein-10 [IP-10]) and CC (macrophage inflammatory protein-1alpha [MIP-1alpha], MIP-1beta, regulated upon activation normal T lymphocyte expressed and secreted (RANTES), and macrophage chemoattractant protein-1 [MCP-1]) chemokines and their respective receptors on lymphocytes infiltrating human liver tumors. Chemokine and chemokine receptor expression was assessed by immunohistochemistry, flow cytometry, in situ hybridization and ribonuclease (RNAse) protection assays and function by in vitro chemotaxis of tumor-derived lymphocytes to purified chemokines and to HepG2 tumor cell culture supernatants. Tumor-derived lymphocytes showed strong chemotactic responses to both CC and CXC chemokines in vitro and expressed high levels of CXCR3 (HuMig and IP-10 receptor) and CCR5 (RANTES, MIP-1alpha, and MIP-1beta receptor). Expansion of tumor-derived lymphocytes in recombinant IL-2 increased expression of CXCR3. The corresponding chemokines were detected on vascular endothelium (HuMig, IL-8, MIP-1alpha, and MIP-1beta) and sinusoidal endothelium (HuMig, MIP-1alpha, MIP-1beta) in hepatocellular carcinoma. In vitro, HepG2 cells secreted functional chemotactic factors for tumor-derived lymphocytes that could be inhibited using anti-CCR5 or anti-CXCR3 monoclonal antibodies (MoAbs). Thus, lymphocytes infiltrating human liver tumors express receptors for and respond to both CXC and CC chemokines. The relevant chemokine ligands are expressed in hepatocellular carcinoma (HCC), particularly HuMig, which was strongly expressed by tumor endothelium, suggesting that they play a role in lymphocyte recruitment to these tumors in vivo. The ability of HepG2 cells to secrete lymphocyte chemotactic factors in vitro suggests that the tumor contributes to lymphocyte recruitment in vivo.

Aged↗

PubMed1999

Competitive repopulation of retrovirally transduced haemopoietic stem cells.

Gene transfer into haemopoietic stem cells (HSC) may be useful in gene therapy for a variety of inherited and acquired human diseases. Cell division is required for retroviral transduction, and cytokine stimulation is often used to increase mitosis of quiescent HSC. Exposure to cytokines has been shown to have an unfavourable effect on the engraftment of these cells when competed with unmanipulated HSC. We now show that a similar engraftment defect is present when HSC are manipulated and transduced with the human multiple drug resistance (MDR) gene. The extent of the unfavourable competition depended on the relative numbers of cytokine-treated and fresh cells when the two populations of cells were administered simultaneously into marrow-ablated isogenic mice. When the manipulated transduced cells were given 2 or 4 d before the unmanipulated cells there was a much greater engraftment of the manipulated cells. The data suggested that the manipulated cells were at a relative disadvantage for marrow engraftment as compared to fresh cells, presumably due to the more efficient homing and engraftment properties of these latter unmanipulated cells. However, the manipulated cells had no intrinsic inability to engraft when they were the predominant donor cell population. In all cases the percent of MDR transduced cells in the engrafting manipulated cells remained relatively constant at about 25-30%. These results have implications for the use of manipulated transduced stem cells in gene therapy, suggesting that administering them before adding fresh cells can overcome their engraftment defect.

Animals↗

PubMed1999

Interleukin-8 receptor modulates IgE production and B-cell expansion and trafficking in allergen-induced pulmonary inflammation.

We examined the role of the interleukin-8 (IL-8) receptor in a murine model of allergen-induced pulmonary inflammation using mice with a targeted deletion of the murine IL-8 receptor homologue (IL-8r-/-). Wild-type (Wt) and IL-8r-/- mice were systemically immunized to ovalbumin (OVA) and were exposed with either single or multiple challenge of aerosolized phosphate-buffered saline (OVA/PBS) or OVA (OVA/OVA). Analysis of cells recovered from bronchoalveolar lavage (BAL) revealed a diminished recruitment of neutrophils to the airway lumen after single challenge in IL-8r-/- mice compared with Wt mice, whereas multiply challenged IL-8r-/- mice had increased B cells and fewer neutrophils compared with Wt mice. Both Wt and IL-8r-/- OVA/OVA mice recruited similar numbers of eosinophils to the BAL fluid and exhibited comparable degrees of pulmonary inflammation histologically. Both total and OVA-specific IgE levels were greater in multiply challenged IL-8r-/- OVA/OVA mice than in Wt mice. Both the IL-8r-/- OVA/OVA and OVA/PBS mice were significantly less responsive to methacholine than their respective Wt groups, but both Wt and IL-8r mice showed similar degrees of enhancement after multiple allergen challenge. The data demonstrate that the IL-8r modulates IgE production, airway responsiveness, and the composition of the cells (B cells and neutrophils) recruited to the airway lumen in response to antigen.

Allergens↗

PubMed1999

Expression of specific chemokines and chemokine receptors in the central nervous system of multiple sclerosis patients.

Chemokines direct tissue invasion by specific leukocyte populations. Thus, chemokines may play a role in multiple sclerosis (MS), an idiopathic disorder in which the central nervous system (CNS) inflammatory reaction is largely restricted to mononuclear phagocytes and T cells. We asked whether specific chemokines were expressed in the CNS during acute demyelinating events by analyzing cerebrospinal fluid (CSF), whose composition reflects the CNS extracellular space. During MS attacks, we found elevated CSF levels of three chemokines that act toward T cells and mononuclear phagocytes: interferon-gamma-inducible protein of 10 kDa (IP-10); monokine induced by interferon-gamma (Mig); and regulated on activation, normal T-cell expressed and secreted (RANTES). We then investigated whether specific chemokine receptors were expressed by infiltrating cells in demyelinating MS brain lesions and in CSF. CXCR3, an IP-10/Mig receptor, was expressed on lymphocytic cells in virtually every perivascular inflammatory infiltrate in active MS lesions. CCR5, a RANTES receptor, was detected on lymphocytic cells, macrophages, and microglia in actively demyelinating MS brain lesions. Compared with circulating T cells, CSF T cells were significantly enriched for cells expressing CXCR3 or CCR5. Our results imply pathogenic roles for specific chemokine-chemokine receptor interactions in MS and suggest new molecular targets for therapeutic intervention.

Acute Disease↗

PubMed1999

[Detection of NV-HB/s DNA and c-myc mRNA in mice inoculated with hepatitis B nucleic acid vaccine--NV-HB/s].

OBJECTIVE: To explore the persistence period of plasmid in mice muscles injected with NV-HB/s and the possible influence on oncogene C-myc. METHODS: Anti-HBs was detected by ELISA; NV-HB/s was detected by In-situ and Southern-blot hybridization separately; C-myc mRNA was detected by In-situ hybridization. RESULTS: All mice injected with NV-HB/s were positive of anti-HBs after 1 month of immunization; NV-HB/s was negative when detected by In-situ hybridization; By Southern-blot hybridization, the positive rates of NV-HB/s were decreasing from 100% in 2 months to 25% after 6 months of inoculation. CONCLUSIONS: NV-HB/s would be disintegrated little by little after injected into mouse muscles; no C-myc activation was observed in 6 months after NV-HB/s inoculation.

Animals↗

PubMed1999

[A study on the roles of CD86 in antigen-induced eosinophil infiltration into airways and airway hyperresponsiveness].

OBJECTIVE: To explore the effect of CD86 on antigen-induced eosinophil infiltration into the airways and airway hyperresponsiveness in sensitized mice, and further elucidate the role of CD86 in the pathogenesis of bronchial asthma. METHODS: Female BALB/c mice (n = 8 for each group) were sensitized and challenged with ovalbumin to induce airway eosinophilia and airway hyperresponsiveness. Airway responsiveness was espressed by the provocative concentration of acetylcholine causing 50% increase in respiratory resistance (PC50). Effect of anti-CD86 monoclonal antibody (mAb) on antigen-induced changes of eosinophil numbers in brochoalveolar lavage fluid (BALF) and airway reactivity was observed. CD86 expression on BALF cells was detected by flow cytometry and concentrations of interleukin-4 and interleukin-5 in homogenized supernatant of lung tissue were determined by ELISA. RESULTS: In sensitized mice challenged with ovalbumin 20 minutes once a day for 6 days, the number of BALF eosinophils was (9.2 +/- 1.5) x 10(8)/L. However, no eosinophil could be found in the BALF from mice without ovalbumin sensitization and challenge. Also, ovalbumin treatment led to PC50 value decrease from (0.66 +/- 0.13) g/L to (0.17 +/- 0.07) g/L (P < 0.01). CD86 expression on BALF cells from ovalbumin sensitized- and challenged-mice (36.4 +/- 6.2) was much higher than that from control mice (12.3 +/- 3.6, P < 0.01). In mice treated with intravenous injection of anti-CD86 mAb before each challenge, BALF eosinophils decreased by 67% (P < 0.01), and PC50 value increased by 69% (P < 0.01). Our results showed that anti-CD86 mAb prevented antigen-induced airway eosinophilia and airway hyperresponsiveness accompanied by a decrement of levels of both interleukin-4 and interleukin-5 in lung tissue. CONCLUSIONS: Anti-CD86 mAb is able to inhibit antigen-induced airway eosinophilia and to ameliorate airway hyperresponsiveness, possibly by inhibiting production of interleukin-4 and interleukin-5. These data suggested that the blockade of airway antigen-presenting cells' functions couid be of value in treatment of human asthma.

Acetylcholine↗