Allergic bronchopulmonary mycosis due to Schizophyllum commune in a patient with chronic hepatitis B.

INTRODUCTION: Schizophyllum commune (S. commune) is an opportunistic pathogenic fungus and can cause infection of the respiratory system in immunocompromised hosts. Allergic bronchopulmonary mycosis (ABPM) is the major disease caused by S. commune. However, identification of S. commune using routine mycological diagnostic methods is difficult. It is easy to make mistakes in diagnosis and treatment, resulting in deterioration of the disease. We report the first case of ABPM due to S. commune in a Chinese patient with chronic hepatitis B. CASE PRESENTATION: The patient presented cough, sputum and dyspnea for six months. The pathogen was missed during routine laboratory workup. We performed bronchoscopy examination and bronchoalveolar lavage. S. commune was identified by metagenomic next-generation sequencing (mNGS) of bronchial alveolar lavage fluid (BALF). Hence, the patient was immediately treated with 200 mg voriconazole twice daily (intravenous infusion) and 20 mg prednisone once a day (oral therapy), along with oral entecavir for hepatitis B. There was no recurrence of infection after the medication was discontinued. CONCLUSIONS: S. commune infection should be considered in the diagnosis of patients with refractory cough, sputum and dyspnea, especially in immunocompromised individuals. The mNGS technique is an effective supplementary technique for the diagnosis of S. commune infection, enabling precise clinical decision-making and appropriate treatment. Most patients have good prognosis with a combination of proper antifungal therapy and hormonal therapy.

Renal CD81 interacts with sodium potassium 2 chloride cotransporter and sodium chloride cotransporter in rats with lipopolysaccharide-induced preeclampsia.

The kidney regulates blood pressure through salt/water reabsorption affected by tubular sodium transporters. Expanding our prior research on placental cluster of differentiation 81 (CD81), this study explores the interaction of renal CD81 with sodium transporters in preeclampsia (PE). Effects of renal CD81 with sodium transporters were determined in lipopolysaccharide (LPS)-induced PE rats and immortalized mouse renal distal convoluted tubule cells. Urinary exosomal CD81, sodium potassium 2 chloride cotransporter (NKCC2), and sodium chloride cotransporter (NCC) were measured in PE patients. LPS-PE rats had hypertension from gestational days (GD) 6 to 18 and proteinuria from GD9 to GD18. Urinary CD81 in both groups tented to rise during pregnancy. Renal CD81, not sodium transporters, was higher in LPS-PE than controls on GD14. On GD18, LPS-PE rats exhibited higher CD81 in kidneys and urine exosomes, higher renal total and phosphorylated renal NKCC2 and NCC with elevated mRNAs, and lower ubiquitinated NCC than controls. CD81 was co-immunoprecipitated with NKCC2 or NCC in kidney homogenates and co-immunostained with NKCC2 or NCC in apical membranes of renal tubules. In plasma membrane fractions, LPS-PE rats had greater amounts of CD81, NKCC2, and NCC than controls with enhanced co-immunoprecipitations of CD81 with NKCC2 or NCC. In renal distal convoluted tubule cells, silencing CD81 with siRNA inhibited NCC and prevented LPS-induced NCC elevation. Further, PE patients had higher CD81 in original urines, urine exosomes and higher NKCC2 and NCC in urine exosomes than controls. Thus, the upregulation of renal CD81 on NKCC2 and NCC may contribute to the sustained hypertension observed in LPS-PE model. Urine CD81 with NKCC2 and NCC may be used as biomarkers for PE.

Hydroxy-Containing Covalent Organic Framework Combined with Nickel Ferrite as a Platform for the Recognition and Capture of Bisphenols.

A hydroxy-containing covalent organic framework (COF) was successfully obtained via a simple nitrogen-purge synthetic procedure for the first time. The COF favored a serrated AA-stacking arrangement, which enhanced the stability compared with common AA or AB arrangements. To validate the potential of the COF in environmental applications, we decorated the COF onto NiFe2O4 and used the NiFe2O4@COF nanocomposite for magnetic solid-phase extraction of trace bisphenols (BPs). The parameters affecting extraction efficiencies were systematically optimized. Under the optimum extraction conditions, calibration plots showed good linearity (5.0-1.0 × 103 ng mL-1) for six BPs, and limits of detection varied from 0.14 to 0.73 ng mL-1. Molecular polarity indexes and molecular dynamics simulations revealed why the COF could efficiently recognize and capture BPs. An adsorption mechanism related to the interaction between BP clusters and the COF was discovered. Ecotoxicological assessment of BPs further unraveled the significance of the developed method for the timely tracking of the concentration, distribution, and migration of BPs in environmental media.

Relationship between blood amyloid A and resting magnetic resonance functional brain connections in patients with obstructive sleep apnea-hypopnea syndrome.

OBJECTIVE: The aim of this study was to analyze the relationship between serum amyloid A (SAA) concentrations in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) and their magnetic resonance imaging (MRI) of resting brain function. METHODS: Male patients with OSAHS were enrolled from January to June 2019 in Suzhou Ninth People's Hospital Affiliated to Soochow University, and nineteen healthy male volunteers were selected as the normal control group. The patients with OSAHS were divided into mild, moderate, and severe groups according to their apnea-hypopnea index (AHI). Early in the morning after the polysomnography (PSG), blood samples were collected and serum levels of serum amyloid A (SAA) were measured by enzyme-linked immunosorbent assay. All subjects were scored by the Auditory Verbal Learning Test (AVLT) scale. Resting brain function images of healthy male volunteers and patients in the severe group were collected by 3.0 T magnetic resonance scanner. SPSS25.0 software was used for statistical analysis. RESULTS: The SAA of the OSAHS group (n = 43) were higher than those of control group (n = 19). The scores of AVLT-immediate and AVLT-delay in the severe OSAHS group were lower than those in the control group (P < 0.05), and it was negatively correlated with SAA. In the severe OSAHS group, the rest state Function Connection (rsFC) in temporal lobe, marginal lobe, and frontal lobe was lower than that in the control group (P < 0.05) and was significantly negatively correlated with SAA. The rsFC in bilateral parietal lobes was higher than that in the control group (P < 0.05), was significantly positively correlated with SAA, and was negatively correlated with AVLT-delay. CONCLUSIONS: The significant increase in SAA concentration in patients with OSAHS correlated with brain rsFC intensity, providing a reference role for the diagnosis, treatment, and prognosis of cognitive dysfunction in patients with OSAHS.

Preliminary study on brain resting-state networks and cognitive impairments of patients with obstructive sleep apnea-hypopnea syndrome.

BACKGROUND: To investigate functional changes in brain resting-state networks (RSNs) in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) and their correlations with sleep breathing disorders and neurocognitive performance. METHODS: In this study, 18 OSAHS patients and 18 matched healthy controls underwent neurocognitive assessment and magnetic resonance imaging (MRI). Group-level independent component analysis (ICA) and statistical analyses were used to explore between-group differences in RSNs and the relationship between functional changes in RSNs, sleep breathing disorders and neurocognitive performance. RESULTS: The OSAHS patients performed worse on neuropsychological tests than the healthy controls. Eight RSNs were identified, and between-group analyses showed that OSAHS patients displayed significantly decreased functional connectivity in the bilateral posterior cingulate gyri (PCC) within the default mode network (DMN), the right middle frontal gyrus (MFG) within the dorsal attention network (DAN), and the left superior temporal gyrus (STG) within the ventral attention network (VAN), and increased functional connectivity in the right superior frontal gyrus (SFG) within the salience network (SN). Further correlation analyses revealed that the average ICA z-scores in the bilateral PCC were correlated with sleep breathing disorders. CONCLUSIONS: Our findings demonstrate that the DMN, SN, DAN, and VAN are impaired during the resting state and are associated with decreased functionally distinct aspects of cognition in patients with OSAHS. Moreover, the intermittent hypoxia and sleep fragmentation caused by OSAHS are likely to be the main influencing factors.

Expression and diagnostic value of circulating miRNA-190 and miRNA-197 in patients with pulmonary thromboembolism.

BACKGROUND: Diagnosing pulmonary thromboembolism (PTE) remains challenging due to the lack of specific clinical symptoms and biomarkers. Circulating microRNAs (miRNAs) have proved to be potential biomarkers for numerous cardiovascular diseases. The aims of this study were to quantitatively analyze the expression of plasma miRNA-190 and miRNA-197 in patients with PTE and to evaluate the diagnostic value for PTE. METHODS: Thirty patients diagnosed with PTE by computed tomographic pulmonary angiography at the emergency department were enrolled in this study, and plasma was collected immediately. For comparison, myocardial infarction (MI, n = 45) and healthy participants (NC, n = 45) were recruited as the control groups. Quantitative reverse transcription PCR (qRT-PCR) was conducted to reveal the relative expression levels of miRNA-190 and miRNA-197 in each group. The plasma concentrations of D-dimer were measured by immunoturbidimetric assay. The diagnostic value was evaluated by analyzing the area under the receiver operating characteristic curve (AUC). RESULTS: The relative expression levels of miRNA-190 and miRNA-197 in the PTE group were both significantly higher than in the MI group (t = 3.602 t = 4.791, P < .05, respectively) and the healthy control group (t = 5.814, t = 5.886, P < .05, respectively). As diagnostic indicator, the sensitivity and specificity of miRNA-190 were 75.56% and 80%, respectively, with an AUC of 0.7844 (95%CI: 0.6858-0.8831, P < .001). The sensitivity and specificity of miRNA-197 were 73.33% and 86.67%, respectively, with an AUC value of 0.7931 (95%CI: 0.6870-0.8991, P < .001). Combining miRNA-190 and miRNA-197 with D-dimer levels significantly increased the diagnostic power, improving the AUC to 0.9536 (95% CI: 0.9083-0.9989, P < .001). CONCLUSIONS: The relative expression levels of miRNA-190 and miRNA-197 in PTE patients were significantly higher than in the MI and healthy control groups, indicating that (a) both may be involved in the pathophysiological process of PTE and (b) both may serve as potential noninvasive diagnostic markers for PTE. The combination of miRNA-190, miRNA-197, and D-dimer levels showed better sensitivity and specificity, which is more conducive to the diagnosis of PTE.

Benchmarking of computational error-correction methods for next-generation sequencing data.

BACKGROUND: Recent advancements in next-generation sequencing have rapidly improved our ability to study genomic material at an unprecedented scale. Despite substantial improvements in sequencing technologies, errors present in the data still risk confounding downstream analysis and limiting the applicability of sequencing technologies in clinical tools. Computational error correction promises to eliminate sequencing errors, but the relative accuracy of error correction algorithms remains unknown. RESULTS: In this paper, we evaluate the ability of error correction algorithms to fix errors across different types of datasets that contain various levels of heterogeneity. We highlight the advantages and limitations of computational error correction techniques across different domains of biology, including immunogenomics and virology. To demonstrate the efficacy of our technique, we apply the UMI-based high-fidelity sequencing protocol to eliminate sequencing errors from both simulated data and the raw reads. We then perform a realistic evaluation of error-correction methods. CONCLUSIONS: In terms of accuracy, we find that method performance varies substantially across different types of datasets with no single method performing best on all types of examined data. Finally, we also identify the techniques that offer a good balance between precision and sensitivity.

Subthreshold depression among diabetes patients in Beijing: Cross-sectional associations among sociodemographic, clinical, and behavior factors.

BACKGROUND: This study explores the prevalence of subthreshold depression (SubD) and its association with factors in type 2 diabetes mellitus (T2DM) patients. METHODS: This cross-sectional study involved 808 outpatients with T2DM from ten hospitals in Beijing between September 2015 and January 2016. All participants completed the Patient Health Questionnaire 9-item (PHQ-9) to evaluate depressive status, with scores between 5 and 14 considered SubD. Conditional logistic regression was conducted to investigate the variables associated with SubD in T2DM patients. RESULTS: T2DM patients with SubD comprised 11.6% (n = 94) of the sample. The odd ratios for the variables having significant positive associations with SubD were: being a women (OR = 1.90; 95%CI: 1.09-3.32), divorced/widowed (OR = 3.27; 95%CI: 1.46-7.30), comorbidity of cerebrovascular disease (OR = 2.00; 95%CI: 1.06-3.76), more diabetic complications (OR = 8.04; 95%CI: 2.77-23.31), and higher HbA1c in men (OR = 2.41; 95%CI: 1.25-4.64). Being older (OR = 0.78; 95%CI: 0.62-0.98), exercising more (OR = 0.44; 95%CI: 0.22-0.91) and poverty (OR = 0.36; 95%CI: 0.19-0.69) were negatively related to SubD. LIMITATIONS: The sample was mainly recruited from hospital settings, which limits generalization. The study's cross-sectional design precludes making causal inferences. CONCLUSIONS: The proportion of SubD was estimated to be 11.6% among T2DM patients in Beijing. Having more diabetic complications and being divorced/widowed made the odds of having SubD 8-fold and 3-fold higher than not having it, respectively. The relationship between SubD and diabetes necessitates early screening for milder forms of depression, which can alleviate the social burden and individual impairment from major depression or other chronic diseases.

Minimization of hepatitis B infection among children in Jiangsu, China, 12years after integration of hepatitis B vaccine into the expanded program on immunization.

BACKGROUND: China has integrated hepatitis B vaccine into the Expanded Program on Immunization since 2002. We aimed to survey the seroprevalence of and immunity to hepatitis B virus (HBV) in children born from 2002 to 2014 in Jiangsu, China. METHODS: Totally 3442 children (M:F=2072:1370) at the age of 7months to 12years (5.5±3.6), from five cities and rural areas across Jiangsu province, were enrolled. Blood samples were measured for HBV markers by ELISA and quantitative microparticle enzyme immunoassay. HBV DNA was tested by real-time PCR and S region was amplified by nested PCR. RESULTS: Twelve (0.35%) children were positive for hepatitis B surface antigen (HBsAg) and 34 (0.99%) were HBsAg negative and positive for antibody against hepatitis B core antigen (anti-HBc). Totally 2542 (73.85%) children had anti-HBs levels ⩾10mIU/ml and 535 (15.54%) with 2-9.9mIU/ml. All 12 HBsAg-positive children had detectable HBV DNA with a mean level of 6.1±1.7logIU/ml (3.3-8.1logIU/ml); 8 were genotype C and 4 were genotype B. No mutation was detected in the a determinant of HBsAg. HBV DNA was not detected in all the 34 children with positive anti-HBc and negative HBsAg. CONCLUSION: HBsAg prevalence among children in Jiangsu born after the introduction of universal vaccination against hepatitis B has significantly decreased. No mutation of S gene is associated with vaccine failure in the cohort of children.

Regulation of Th1/Th2 balance through OX40/OX40L signalling by glycyrrhizic acid in a murine model of asthma.

BACKGROUND AND OBJECTIVE: Glycyrrhizic acid (GA) has been reported to have attenuating airway inflammation effects in asthma mouse model. However, the potential molecular mechanisms by which GA exerts anti-inflammatory effects on ovalbumin (OVA)-induced allergic asthma have not been well elaborated. METHODS: The effect of GA on OVA-sensitized and challenged mice was investigated. The effect of GA on anti-OX40 mAb stimulated splenocytes from asthma mice model was also examined. RESULTS: In OVA-induced asthmatic mice, GA treatment prevented the decrease of T helper1 cytokine (interferon (IFN)-γ) and the increase of T helper2 cytokines (interleukin (IL)-4, IL-5, IL-13) in bronchoalveolar lavage fluid (BALF), reduced serum immunoglobulin (Ig)E and OVA-specific IgE levels, prohibited the protein and mRNA expression of OX40 and OX40 Ligand (OX40L) in lung tissues, and the expression of OX40 in CD4(+) T cells and OX40L in CD11b(+) monocytes and CD19(+) B cells in spleens in a dose-dependent manner compared with the vehicle treatment (all P < 0.05). Moreover, OVA significantly increased the activation of p38 mitogen-activated protein kinase (MAPK) in lung tissues, whereas GA and anti-OX40L mAb markedly reduced phosphorylation of p38 MAPK. In addition, GA could inhibit the T cell proliferation and modulate the balance of Th1/Th2 in anti-OX40 mAb stimulated CD4(+) T cells from asthmatic spleens (all P < 0.05). CONCLUSIONS: GA may exert a therapeutic effect on OVA-induced experimental asthma partly by regulating the Th1/Th2 balance through suppressing OX40-OX40L signalling and p38 MAPK activity. GA may be a promising treatment for asthma.

[Therapeutic effects of glycyrrhizic acid on asthma airway inflammation in mice and its mechanism].

OBJECTIVE: To explore the therapeutic effects and mechanism of glycyrrhizic acid (GA) on airway inflammation in a murine model of asthma. METHODS: A total of 70 female BALB/c mice were randomly divided into 5 groups (n = 14 each) of control, asthmatic and three treatments with low, medium and high doses of GA. Mice in the asthmatic and the treatment groups were sensitized and challenged by ovalbumin (OVA). Mice of the treatment groups were injected intraperitoneally with GA (25, 50, 100 mg/kg) 30 min before each OVA challenge. The control mice received an aerosol inhalation of normal saline instead of OVA. Within 24 hours after the last OVA challenge, bronchoalveolar lavage fluid (BALF) was collected for counting total cells and eosinophils (Eos) in other 8 mice in each group. Interleukin (IL)-12p70, IL-10, IL-4 and interferon gamma (IFN-γ ) were measured in BALF by enzyme-linked immunosorbent assay (ELISA). Histological studies of lung were conducted with hematoxylin and eosin staining (HE) and the expressions of CD86, major histocompatibility complex (MHC)-II, CD40, OX40 ligand (OX40L) on CD11c(+) dendritic cells (DCs) in spleens were evaluated with flow cytometry (FCM). RESULTS: Compared with the control group, the number of total cells and eosinophils was higher in BALF in asthmatic group ((124.3 ± 39.7)×10(7)/L, (26.3 ± 17.2)×10(7)/L vs (55.3 ± 22.8)×10(7)/L, (0.6 ± 0.4) ×10(7)/L), the expressions of IL-10 and IL-4 increased ((49 ± 12, 169 ± 29) ng/L vs (34 ± 4, 89 ± 37) ng/L) and the levels of IFN-γ and IFN-γ/IL-4 ratio decreased in BALF ((122 ± 56 ) ng/L, (0.7 ± 0.4) vs (89 ± 37) ng/L, 2.9 ± 0.8)), the expressions of CD86, MHC-II, CD40, OX40L on CD11c(+) DCs increased in spleens ((38.4 ± 15.7)%, (90.4 ± 3.4)%, (25.4 ± 10.2)%, (29.6 ± 9.9)% vs (18.8 ± 4.4)%, (73.1 ± 11.3)%, (3.8 ± 2.2)%, (5.0 ± 1.6)%) (all P < 0.05). Compared with the asthmatic group, total cell counts and the eosinophil numbers significantly decreased by the treatment of GA at a dose of 100 mg/kg ( (62.1 ± 21.7)×10(7)/L, (2.2 ± 1.7)×10(7)/L), the levels of IL-12p70, IL-10, IFN-γ and the ratio of IFN-γ/IL-4 increased ((44 ± 14, 132 ± 13, 208 ± 66) ng/L, (1.8 ± 0.6)) and the level IL-4 decreased (122 ± 38) ng/L. The expressions of MHC-II, CD40, OX40L on CD11c(+) DCs decreased ((75.8 ± 15.9)%, (11.1 ± 5.9)%, (11.8 ± 3.4)%)) (all P < 0.05). The asthmatic mice induced an infiltration of inflammatory cells around airways and blood vessels. Administration of GA significantly reduced the infiltration of inflammatory cells in peribronchial areas compared with asthmatic mice especially at a dose of 50 mg/kg 100 mg/kg. CONCLUSION: GA effectively ameliorates the airway inflammation of asthma via inhibiting the Th2 responses though modulating the expressions of CD86, MHC-II, CD40, OX40L on CD11c(+) DCs.

Low titers of measles antibody in mothers whose infants suffered from measles before eligible age for measles vaccination.

BACKGROUND: Resurgence or outbreak of measles recently occurred in both developed and developing countries despite long-standing widespread use of measles vaccine. Measles incidence in China has increased since 2002, particularly in infants and in persons >or= 15 years of age. It is speculated that infants may acquire fewer measles IgG from their mothers, resulting in the reduced duration of protection during their early months of life. This study aimed to clarify the reason of increased susceptibility to measles in young infants in China. Measles IgG in 24 measles infants

Influence of maternal antibody against hepatitis B surface antigen on active immune response to hepatitis B vaccine in infants.

Transplacentally acquired maternal antibodies in infants may inhibit active immune responses to vaccines. In this study, we compared the immunogenicity of the recombinant hepatitis B vaccine, which was intramuscularly injected at 0, 1, and 6 months of age, in 71 infants born to mothers with positive or negative antibody against hepatitis B surface antigen (anti-HBs). Forty-one infants born to anti-HBs positive mothers were all positive at birth. At 2 months after the second injection, anti-HBs in 30 infants with negative maternal antibody was significantly higher than that in 41 infants with positive maternal anti-HBs (191.1mIU/ml vs. 96.2mIU/ml, P=0.018). At one month after the full immunization, the anti-HBs levels had no statistical difference between maternal anti-HBs negative and positive groups, but the antibody response in infants with high maternal anti-HBs (>1000mIU/ml) was significantly inhibited. Nevertheless, all infants had anti-HBs higher than the protective level. In conclusion, passively acquired maternal anti-HBs in infants may to some extent impair the antibody response to hepatitis B vaccine. The long-term efficacy of hepatitis B vaccine in infants with high titers of maternal anti-HBs remains to be further evaluated.

[The effects of imiquimod on an animal model of asthma].

OBJECTIVE: To study the mechanism of imiquimod on asthma animals. METHODS: (1) 40 mice and 48 rats were divided into 4 groups: control, asthma, dexamethasone and imiquimod groups. The asthma model was established. The mice and rats in the imiquimod group were exposed to an aerosol of 0.15% imiquimod. Lung inflammation and airway responsiveness were measured 24 h after the last ovalbumin (OVA) challenge. The expression of Interleukin-4 (IL-4), interferon gamma (IFN-gamma), eotaxin, macrophage-derived chemokine (MDC), thymus and activation-regulated chemokine (TARC), T-bet, GATA-3, STAT6 mRNA in the lung were determined by reverse transcription polymerase chain reaction (RT-PCR). The levels of eotaxin, MDC, and TARC in sera were tested by enzyme linked immunosorbent assay (ELISA). The expression of T-bet, GATA-3 and STAT6 proteins in the lung were measured by Western blot. (2) Parabronchial lymphnodes (PBLN) were isolated and cultured. The PBLN cells were divided into blank control, positive control, dexamethasone and drug groups (1 - 3 subgroups), cultured for different hours, and the expressions of IL-4 and IFN-gamma in supernatants were determined by ELISA, The mRNA expressions of the cytokines in cells weredetected by RT-PCR. (3) Flow cytometry was used to detect intracellular IL-4 and IFN-gamma production in spleen T lymphocytes. (4) CD(4)(+) T cell of spleen pellets were subject to assessment of T-bet and GATA-3 protein and mRNA expression respectively. RESULTS: The expiration resistance was determined before and after injection of acetylcholine chloride (20 - 160 microg/ml), and expiration resistances of the asthmatic group (6.26 +/- 0.85), (11.55 +/- 3.09), (28.74 +/- 5.94), (3710.83 +/- 197.49) cm H(2)Oxml(-1)xs(-1), were significantly elevated compared with those of the control group (1.34 +/- 0.16), (3.47 +/- 0.49), (9.29 +/- 1.27), (25.22 +/- 5.44) cm H(2)Oxml(-1)xs(-1), D = 88.98, 56.00, 45.00, 108.00, all P < 0.01). The numbers of eosinophils and lymphocytes, the thicknesses of WA/Pi and ASM/Pi in the asthmatic group [(26.0 +/- 1.6)/mm(2), (45.2 +/- 3.2)/mm(2), 12.0 +/- 1.4, 6.7 +/- 0.6] were all significantly higher than those of the imiquimod group [(12.4 +/- 2.9)/mm(2), (24.2 +/- 3.7)/mm(2), 9.2 +/- 0.6, 4.0 +/- 0.5, D or q = 193.00, 16.92, 185.50, 7.66, all P < 0.01]. In the imiquimod group, the mRNA and protein expressions of T-bet (0.48 +/- 0.08, 0.48 +/- 0.17) were significantly increased compared with those of the asthmatic group (0.08 +/- 0.12, 0.18 +/- 0.06, D = 120.96, 177.98, all P < 0.01), the mRNA and protein expressions of GATA-3 in the imiquimod group were both significantly decreased compared with those of the asthmatic group (D = 166.96, 310.97, all P < 0.01). In the control group, only low concentrations of IFN-gamma [(22 +/- 5, 31 +/- 5) pg/ml] were detected in PBLN cell cultures. After 24 or 48 h stimulation, the concentrations of IFN-gamma in drug 2 subgroup [(149 +/- 31), (154 +/- 28) pg/ml] and drug 3 subgroup [(166 +/- 30), (158 +/- 31) pg/ml] were increased significantly; Levels of IL-4 [druug 2 subgroup: (23 +/- 5), (39 +/- 11) pg/ml, drug 3 subgroup: (43 +/- 13), (56 +/- 12) pg/ml] were increased slowly compared with those in the OVA group (drug 2 subgroup 24 h IL-4, D = 9.90; drug 3 subgroup 24 h IL-4, D = 8.79, drug 2 subgroup 48 h IL-4, D = 8.80, drug 3 subgroup 48 h IL-4, D = 8.10, drug 2 subgroup 24 h IFN-gamma, q = 4.80, drug 3 subgroup 24 h IFN-gamma, q = 6.40, drug 2 subgroup 48 h IFN-gamma, q = 3.95, drug 3 subgroup 48 h IFN-gamma, q = 4.31, all P < 0.05). After imiquimod treatment, the mRNA and protein levels of T-bet in imiquimod group CD(4)(+) T cells were increased significantly compared with those in OVA group, and the mRNA and protein levels of GATA-3 were decreased significantly in CD(4)(+) T cells of imiquimod group compared with those in OVA group. The eotaxin, MDC and TARC levels of serum in asthma group [(593 +/- 41) pg/ml, (170 +/- 20) pg/ml, (221 +/- 25) pg/ml] were significant different from those in control group [(288 +/- 66) pg/ml, (100 +/- 33) pg/ml, (84 +/- 49) pg/ml], (eotaxin: q = 12.20, MDC: q = 8.00, TARC: q = 10.50, all P < 0.01). MDC and TARC levels of serum in imiquimod group [(84 +/- 13) pg/ml, (163 +/- 35) pg/ml] decreased as compared with those in asthma group (MDC: q = 9.80, TARC: q = 4.50, all P < 0.01) and MDC levels in imiquimod group were no different with normal group (q = 1.80, P > 0.05). eotaxin levels of serum in imiquimod group [(501 +/- 76) pg/ml] increased as compared with those from normal group (q = 8.50, P < 0.01), and decreased as compared with those from asthma group (q = 3.70, P < 0.05). (4) The expression of eoaxin, MDC, TARC and STAT(6) on the bronchial epithelium in imiquimod group was decreased as compared with asthma group, but increased as compared with normal group. The eotaxin, MDC and TARC mRNA expression of the lung in asthma group (0.85 +/- 0.11, 0.96 +/- 0.10, 0.94 +/- 0.28) had significant differences from those in the control group (0.45 +/- 0.08, 0.39 +/- 0.09, 0.24 +/- 0.08, eotaxin: q = 3.00, MDC: q = 15.40, TARC: q = 5.90, all P < 0.01) and those in imiquimod group (0.65 +/- 0.17, 0.66 +/- 0.12, 0.66 +/- 0.34, eotaxin: q = 1.50, MDC: q = 8.10, TARC: q = 2.40, all P < 0.05). CONCLUSION: These findings suggested that imiquimod can inhibit the airway inflammation of asthma animals by reducing GATA-3 mRNA and protein expression and increasing T-bet, STAT(6) mRNA and protein expression.