Identification of immunogenic cell death-related genes involved in Alzheimer's disease.

Alzheimer's disease (AD) is the leading cause of dementia worldwide, with recent studies highlighting the potential role of immunogenic cell death (ICD) in the pathogenesis of this neurodegenerative disorder. A total of 52 healthy controls and 64 patients with AD were included. Compared to the controls, the patients with AD exhibited 2392 differentially expressed genes (DEGs), of which 1015 and 1377 were upregulated and downregulated genes, respectively. Among them, nine common genes were identified by intersecting the AD-related module genes with the DEGs and ICD-associated genes. Gene ontology (GO)analysis further revealed "positive regulation of cytokine production" as the most significant term. Moreover, the enriched molecular functions were primarily related to the inflammatory body complex, while the overlapping genes were significantly enriched in lipopolysaccharide binding. Kyoto encyclopedia of genes and genomes (KEGG) analysis also indicated that these overlapping genes were mainly enriched in immunity, inflammation, and lipid metabolism pathways. Furthermore, the following four hub genes were detected using machine learning algorithms: P2RX7, HSP90AA1, NT5E, and NLRP3. These genes demonstrated significant differences in expression between the AD and healthy control groups (P < 0.05). Additionally, the area under the curve values of these four genes were all > 0.7, indicating their potential diagnostic value for AD. We further validated the protein levels of these four genes in the hippocampus of 3xTg-AD and C57BL/6J mice, showing P2RX7 and HSP90AA1 expression levels consistent with the previously analyzed trends. Finally, the single-sample gene set enrichment analysis (ssGSEA) algorithm provided additional evidence by demonstrating the crucial role of immune cell infiltration and its link with the hub genes in AD progression. Our study results suggest that ICD-mediated elevation of HSP90AA1 and P2RX7 levels and the resulting induction of tau hyperphosphorylation and neuroinflammation are vital in the AD pathogenic mechanism.

A case of herpes simplex virus induced peripheral neuropathy and encephalitis with positive GM3 and CASPR2 antibody.

BACKGROUND: We reported on a case involving an older patient with HSV-1 encephalitis who simultaneously experienced the onset of peripheral nerve symptoms associated with the presence of anti-GM3 immunoglobulin G (IgG). CASE PRESENTATION: A 77-year-old male was admitted to hospital with high fever, weakness of both lower limbs, and an unstable gait. A CSF test revealed a strikingly increased protein level (1,002 mg/L, normative values: 150-450 mg/L) and MRI revealed hyper-signal lesions in the right temporal lobe, right hippocampus, right insula, and right cingulate gyrus. The CSF was positive for HSV PCR (HSV-1,17870). In addition, the serum samples were positive for CASPR2 antibodies (antibody titer: 1/10) and anti-GM3 immunoglobulin G (IgG) (+). The patient was diagnosed with HSV-1-induced peripheral nerve symptoms that were associated with encephalitis and the presence of anti-GM3 IgG and anti-CASPR2 antibodies. The patient had received included intravenous immunoglobulin, intravenous acyclovir, and corticosteroids therapy. At the one-year follow-up examination, he had regained the necessary skills associated with daily life. CONCLUSIONS: Herpes simplex virus infection often induces encephalitis, and reaction to the virus may trigger an autoimmune response. Early diagnosis and treatment can avoid the progression of the disease to include autoimmune encephalitis.

Blood-brain barrier damage and new onset refractory status epilepticus: An exploratory study using dynamic contrast-enhanced magnetic resonance imaging.

OBJECTIVE: This study was undertaken to characterize the blood-brain barrier (BBB) dysfunction in patients with new onset refractory status epilepticus (NORSE) using dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI). METHODS: This study included three groups of adult participants: patients with NORSE, encephalitis patients without status epilepticus (SE), and healthy subjects. These participants were retrospectively included from a prospective DCE-MRI database of neurocritically ill patients and healthy subjects. The BBB permeability (Ktrans) in the hippocampus, basal ganglia, thalamus, claustrum, periventricular white matter, and cerebellum were measured and compared between these three groups. RESULTS: A total of seven patients with NORSE, 14 encephalitis patients without SE, and nine healthy subjects were included in this study. Among seven patients with NORSE, only one had a definite etiology (autoimmune encephalitis), and the rest were cryptogenic. Etiology of encephalitis patients without SE included viral (n = 2), bacterial (n = 8), tuberculous (n = 1), cryptococcal (n = 1), and cryptic (n = 2) encephalitis. Of these 14 encephalitis patients without SE, three patients had seizures. Compared to healthy controls, NORSE patients had significantly increased Ktrans values in the hippocampus (.73 vs. .02 × 10-3 /min, p = .001) and basal ganglia (.61 vs. .003 × 10-3 /min, p = .007) and a trend in the thalamus (.24 vs. .08 × 10-3 /min, p = .017). Compared to encephalitis patients without SE, NORSE patients had significantly increased Ktrans values in the thalamus (.24 vs. .01 × 10-3 /min, p = .002) and basal ganglia (.61 vs. .004 × 10-3 /min, p = .013). SIGNIFICANCE: This exploratory study demonstrates that BBBs of NORSE patients were impaired diffusely, and BBB dysfunction in the basal ganglia and thalamus plays an important role in the pathophysiology of NORSE.

Netrin-1 Monoclonal Antibody-Functionalized Nanoparticle Loaded with Metformin Prevents the Progression of Abdominal Aortic Aneurysms.

Background: Abdominal aortic aneurysms (AAAs) are a global health and economic burden. Therapeutic strategies to inhibit the progression of AAAs are currently lacking. Recently, the therapeutic effect of metformin on aneurysms has attracted considerable interest. However, the unfavorable pharmacokinetic properties of metformin limit its feasibility for AAA treatment. Methods and Results: We constructed a metformin-loaded netrin-1-responsive AAA-targeted nanoparticle (Tgt-NP-Met) for AAA management. Evaluation of the therapeutic effect of Tgt-NP-Met was performed by in vitro and in vivo experiments. Our results showed that the binding of netrin-1 monoclonal antibodies enhanced the AAA-targeting capability of nanoparticles (NPs). Moreover, Tgt-NP-Met administration prevented AAA development and reduced the aneurysm diameter in apolipoprotein E (ApoE)-deficient (ApoE-/-) mice that received continuous infusion of angiotensin II. Furthermore, metformin prevented AAA progression by inhibiting the transformation of vascular smooth muscle cells (VSMCs) from a contractile phenotype to a synthetic phenotype, which is mediated by macrophage infiltration and activation. Conclusion: Our findings identify metformin as a functional suppressor for macrophage-mediated phenotypic transformation of VSMCs and Tgt-NP-Met as an efficient therapeutic strategy for AAA management.

Gardnerella vaginalis purulent meningitis in an adolescent male: a case report.

BACKGROUND: We report a rare case of Gardnerella vaginalis found in the cerebrospinal fluid of a young boy. CASE PRESENTATION: A 14-year-old boy was admitted to hospital with headache, vomiting, fever, drowsiness and positive meningeal irritation signs on examination. Cerebrospinal fluid (CSF) shows white blood cell and protein were elevated, and glucose was low. Traditional aerobic and anaerobic culture of CSF did not grow any organisms. However, metagenomic next-generation sequencing (mNGS) reveals G. vaginalis in his CSF. The patient was diagnosed with purulent meningitis, and treated with intravenous meropenem and linezolid for a week, followed by oral administration of amoxicillin for two weeks. He recovered without sequelae. CONCLUSIONS: Purulent meningitis caused by Gardnerella vaginalis is extremely rare. Metagenomic next-generation sequencing of CSF should be highlighted for early diagnosis. With effective antibiotic treatment, the prognosis was excellent.

Umbilical cord blood stem cells transplantation in a patient with severe progressive supranuclear palsy: a case report.

BACKGROUND: Progressive supranuclear palsy is a neurodegenerative condition that worsens over time. Given the lack of targeted treatments, patients with severe progressive supranuclear palsy have very low life expectancy. CASE PRESENTATION: We present a case of a 61-year-old Chinese man with severe progressive supranuclear palsy and treated with umbilical cord blood stem cells transplantation. After the umbilical cord blood stem cells therapy, his neurologic symptoms stopped deteriorating, his muscle rigidity was mildly improved, and he remains alive for more than 8 years. CONCLUSIONS: Umbilical cord blood stem cells transplantation may be an alternative therapy for patients with severe progressive supranuclear palsy.

Long non-coding RNA MALAT1 suppresses the proliferation and migration of endothelial progenitor cells in deep vein thrombosis by regulating the Wnt/ß-catenin pathway.

Deep vein thrombosis (DVT) is one of the most common circulating vascular diseases with an incidence of ~0.1% worldwide. Although anticoagulant medication remains to be the main therapeutic approach for patients with DVT, existing thrombus and pulmonary embolisms still pose as a threat to patient life. Therefore, effective targeted therapies need to be developed and studies are required to improve understanding of this condition. Endothelial progenitor cells (EPCs) originate from the bone marrow, are located in the peripheral blood and are involved in thrombus resolution. Long non-coding RNAs (lncRNAs) are non-coding RNAs that are >200 nucleotides in length. LncRNAs are associated with the development of numerous vascular diseases. Among these lncRNAs, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) is downregulated in human atherosclerotic plaques. Furthermore, MALAT1 polymorphism resulted in vascular disease in Chinese populations. In the present study, the expression profile and potential functions of MALAT1 in DVT were investigated. The results revealed that MALAT1 was upregulated in DVT tissues. Furthermore, MALAT1 was able to regulate the biological behaviors of EPCs, including proliferation, migration, cell cycle arrest and apoptosis. In addition, the Wnt/ß-catenin signaling pathway is a promising downstream target of MALAT1 in DVT. The changes in biological behaviors in EPCs caused by silenced MALAT1 were reversed by inhibition of the Wnt/ß-catenin signaling pathway. In summary, the data indicated the roles of MALAT1 in the pathogenesis of DVT, and the MALAT1/Wnt/ß-catenin axis could be a novel therapeutic target for the treatment of DVT.

Exosomal miR-638 Inhibits Hepatocellular Carcinoma Progression by Targeting SP1.

PURPOSE: Exosomal microRNAs (miRNAs) play essential roles in the development of hepatocellular carcinoma (HCC). Nevertheless, the role and mechanism of exosomal miR-638 in HCC development remain largely unknown. METHODS: Exosomes were isolated and confirmed via transmission electron microscopy and western blot. The abundances of miR-638 and specificity protein 1 (SP1) were measured via quantitative reverse transcription polymerase chain reaction or western blot. Cell proliferation was investigated by Cell Counting Kit-8, colony formation assay, apoptosis, cell cycle distribution and related protein expression. Cell migration and invasion were detected via transwell assay and western blot. Co-culture experiment was performed to assess exosome transfer from HCC cells to endothelial cells. The target correlation between miR-638 and SP1 was analyzed via dual-luciferase reporter and RNA immunoprecipitation assays. The subcutaneous xenograft experiment was conducted to test the function of miR-638 in vivo. RESULTS: The miR-638 level declined in exosomes from serum or HCC cell medium. miR-638 overexpression repressed HCC cell proliferation by decreasing viability and colony formation and inducing apoptosis and cell cycle arrest at G1 phase, and decreased abilities of migration and invasion. Exosomal miR-638 from HCC cells could transfer to human umbilical vein endothelial cells (HUVECs) and suppress HUVEC proliferation, migration and invasion. SP1 was a target of miR-638 and overexpression of SP1 reversed the effect of miR-638 on HCC cells. Overexpression of miR-638 reduced xenograft tumor growth via decreasing SP1. CONCLUSION: Exosomal miR-638 inhibited HCC tumorigenesis by targeting SP1. This study indicated the potential clinical implications of miR-638 in HCC.

WITHDRAWN: Analysis of Risk Factors for Postoperative Infection and Neurological Complications in Patients with Acute Stanford A AD According to CT angiography Information.

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Association of SLCO1B1 Polymorphisms and Atorvastatin Safety and Efficacy: A Meta-analysis.

BACKGROUND: Atorvastatin is the best-selling statin in the market. However, some patients have to reduce drug doses or discontinue atorvastatin therapy mainly due to adverse drug reactions (ADRs). Genetic factors play an important role in the occurrence of ADRs. AIM: This study aimed to investigate the association between SLCO1B1 polymorphisms (c.521T>C or c.388A>G) and atorvastatin safety and efficacy. METHODS: We systematically searched PubMed, Web of Science and Embase to screen relevant studies published before Sep 2018. This meta-analysis was performed to identify the relationship between SLCO1B1 c.521T>C or c.388A>G polymorphisms and atorvastatin-related ADRs by the odds ratios (ORs) and 95% confidence intervals (CIs). The relationship of SLCO1B1 polymorphisms and lipid-lowering effects [low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC)] was assessed in pooled data by calculating the mean difference (MD) with 95% CIs. All statistical tests were performed by the Review Manager 5.3 software. RESULTS: A total of 13 studies involving 1,550 atorvastatin users were included in this analysis. There was a significant association between the SLCO1B1 c.521T>C polymorphism and atorvastatin-related ADRs associated with risk allele C (dominant model: OR=1.57, P=0.01). Allele C is associated with increased lipid-lowering efficacy in people with Hyperlipidemias as compared to allele T (LDL-C/dominant model: MD=6.19, P<0.00001 and (TC)/dominant model: MD=2.07, P=0.008). No association between the SLCO1B1 c.388A>G polymorphism and ADRs or efficacy was observed (P>0.05). CONCLUSION: SLCO1B1 c.521T>C polymorphism is a valuable biomarker for the evaluation of atorvastatin safety and efficacy.

TRIM32 overexpression improves chemoresistance through regulation of mitochondrial function in non-small-cell lung cancers.

BACKGROUND: TRIM32 is overexpressed in several human cancers. However, its expression pattern, biological characteristics and mechanisms in human non-small cell lung cancer (NSCLC) have not been reported. METHODS: We examined TRIM32 protein in 115 cases of NSCLC specimens. TRIM32 plasmid transfection and siRNA knockdown was carried out in NSCLC cell lines. AnnexinV/PI and JC-1 staining were performed to examine the change of apoptosis and mitochondrial membrane potential. Western blot was used to detect change of downstream proteins. RESULTS: We found that TRIM32 protein was upregulated in 69 cases and positively correlated with advanced TNM stage. TRIM32 overexpression also correlated with poor survival of NSCLC patients. Biological assays demonstrated that TRIM32 overexpression promoted while it depletion inhibited cell growth, colony formation and invasion. In addition, TRIM32 maintained NSCLC cell viability and reduced apoptosis when treated with cisplatin. JC-1 and CellRox staining demonstrated that TRIM32 could maintain mitochondrial membrane potential and reduce Reactive Oxygen Species (ROS) production after cisplatin treatment. Western blot analysis showed that TRIM32 overexpression downregulated caspase 3 cleavage and cytochrome c release. TRIM32 also positively regulated Bcl-2 protein expression and NF-κB signaling. Inhibition of NF-κB abolished the effects of TRIM32 on Bcl-2. CONCLUSION: Taken together, our results indicated that TRIM32 is overexpressed in NSCLC and regulates cisplatin resistance, possibly through NF-κB and Bcl-2.

Simultaneous determination of plasma methotrexate and 7-hydroxy methotrexate by UHPLC-MS/MS in patients receiving high-dose methotrexate therapy.

The plasma concentrations of methotrexate (MTX) and its major metabolite 7-hydroxy methotrexate (7-OH-MTX) are highly correlated with the toxicities in patients with high-dose MTX therapy. Routine monitoring of MTX and 7-OH-MTX plasma levels is useful for dose adjustment of rescue drugs and toxicity prevention. A UHPLC-MS/MS method for simultaneous determination of plasma MTX and 7-OH-MTX was developed, validated, and applied in 181 plasma samples. The ion transition was m/z 455.2 → 308.2 for MTX and m/z 471.2 → 324.1 for 7-OH-MTX. The flow rate was 0.4 mL/min with a run time of 2.6 min. The calibration range was 0.002-2 µM for MTX, and 0.01-10 µM for 7-OH-MTX. The intra-day and inter-day inaccuracy and imprecision were -5.50% to 10.93% and less than 9.20% for both analytes. The internal standard (MTX-D3) normalized recovery and matrix factor were consistent at four quality control levels. 14 h, 38 h, and 62 h after dosing, MTX and 7-OH-MTX plasma levels were significantly higher in patients with impaired renal function compared to those with normal renal function. 7-OH-MTX plasma levels were significantly higher in patients with impaired liver function compared to those with normal liver function.

Rab11a promotes proliferation and invasion through regulation of YAP in non-small cell lung cancer.

Rab11a, an evolutionarily conserved Rab GTPases, plays important roles in intracellular transport and has been implicated in cancer progression. However, its role in human non-small cell lung cancer (NSCLC) has not been explored yet. In this study, we discovered that Rab11a protein was upregulated in 57/122 NSCLC tissues. Rab11a overexpression associated with advanced TNM stage, positive nodal status and poor patient prognosis. Rab11a overexpression promoted proliferation, colony formation, invasion and migration with upregulation of cyclin D1, cyclin E, and downregulation of p27 in NSCLC cell lines. Nude mice xenograft demonstrated that Rab11a promoted in vivo cancer growth. Importantly, we found that Rab11a induced YAP protein and inhibited Hippo signaling. Depletion of YAP abolished the effects of Rab11a on cell cycle proteins and cell proliferation. Furthermore, immunoprecipitation showed that Rab11a interacted with YAP in lung cancer cells. In conclusion, the present study suggestes that Rab11a serves as an important oncoprotein and a regulator of YAP in NSCLC.

HCRP1 is downregulated in non-small cell lung cancer and regulates proliferation, invasion, and drug resistance.

HCRP1 has been reported to have tumor suppressive function. However, its expression pattern and function in human non-small cell lung cancer (NSCLC) remain obscure. This study aims to explore clinical significance of HCRP1 in NSCLC. Immunohistochemical results showed high HCRP1 protein in normal bronchial epithelial tissue and downregulated HCRP1 expression in 47/98 lung cancer specimens. HCRP1 downregulation correlated with clinical stage (p = 0.0203), nodal status (p = 0.0168), and poor patient prognosis (log-rank, p = 0.0076). Univariate analysis showed that TNM stage (p < 0.0001) and HCRP1 (p = 0.0098) were significant prognostic factors; Cox regression model showed that TNM stage serves as an independent prognostic factor (p = 0.0011). We also found that HCRP1 was downregulated in lung cancer cells compared with normal HBE cells. HCRP1 plasmid transfection in H1299 cells inhibited proliferation, cell cycle progression, and invasion. HCRP1 depletion in A549 cells showed the opposite biological effects. In addition, we found that HCRP1 could inhibit MAPK and AKT signaling with downregulation of ERK and AKT phosphorylation, cyclin proteins, Bcl2 and MMP9, while HCRP1 depletion activated ERK and AKT signaling. The level of EGFR phosphorylation was also inhibited by HCRP1. In addition, we found that HCRP1 depletion confers multidrug resistance in H1299 cells. We employed paclitaxel and cisplatin in A549 cells with HCRP1 depletion. HCRP1 depletion decreased the effect of paclitaxel and cisplatin in A549 cells. Treatment with EGFR inhibitor AG1478 and AKT inhibitor LY249004 abolished the effect of HCRP1 depletion on drug resistance. In conclusion, the present study demonstrate that HCRP1 is downregulated in NSCLC and regulates proliferation, invasion, and drug resistance through modulation of EGFR signaling.

Discoidin domain receptors: a promoter of the aggressive behavior of ameloblastomas.

Discoidin domain receptors 1 and 2 (DDR1 and DDR2) are members of the receptor tyrosine kinases, which regulate fundamental cellular processes concerning proliferation, differentiation, adhesion, motility, and apoptosis. The dysregulation of these receptors is linked to a number of human diseases, including fibrotic disorders, atherosclerosis, and cancer. However, there have been no studies that analyzed the expression of these DDRs in ameloblastomas (ABs). In this study, we investigated the expression level and distribution of both DDRs in ABs and determined whether these receptors could predict the prognosis of the disease. Real-time reverse transcription polymerase chain reaction, western blot, and immunohistochemical analyses were performed to detect the DDR mRNA and protein expression levels in normal oral mucosa (NOM) and ABs. The relationship of the DDRs with the clinicopathology and prognosis of ABs was analyzed statistically. The mRNA expression levels of DDR1 and DDR2 were found to be increased by 3.42- and 3.66-fold in ABs versus NOM, respectively. Recurrent ABs displayed higher DDR mRNA expression than did primary ABs (P < 0.05). Using western blot analysis, the DDR proteins were found to be lower in NOM than in ABs (P < 0.05), and primary ABs showed lower expression levels than did recurrent ones (P < 0.05). Immunohistochemically, the DDR protein expressions were markedly higher in ABs than in NOM (P < 0.05), and AB patients with higher DDR protein expression showed higher recurrence (P < 0.05). Multivariate analysis with the Cox proportional hazards model indicated the expression of both DDRs to be an independent prognostic factor of ABs. It was suggested that the up-regulation of DDR expression might play an important role in the tumorigenesis and aggressiveness of ABs. Thus, DDR protein expression may be considered as a good biomarker for indicating the prognosis of ABs.

Nanog, a novel prognostic marker for lung cancer.

OBJECTIVE: To investigate the expression of the stem cell marker Nanog in lung cancer tissues and the correlations between Nanog expression and clinic-pathologic characteristics as well as prognosis of lung cancer. METHODS: 163 patients with lung cancers enrolled in the study. The expression of Nanog in the cell lines and lung cancers were evaluated by RT-PCR, immunofluorescence and immunohistochemisty. Then, the correlations between Nanog expression status and clinic-pathologic characteristics and prognosis of lung cancer patients were analyzed. RESULTS: It showed that Nanog are higher expressed in lung cancer tissues compared to their normal counterparts in both mRNA and protein levels, and Nanog expression was observed to be positively correlated with tumor differentiation and clinical stages of lung cancer patients (P = 0.001 and 0.001). Nanog were mainly localized at the cytoplasm in the brown color in the lung cancers. In addition, nuclear staining of Nanog was more observed in poorly differentiated lung cancers compared to others (P = 0.01). Furthermore, survival analyses showed that over-expression of Nanog protein predicted a worse prognosis for lung cancer patients (P = 0.001). CONCLUSION: Nanog can be an important prognostic marker for lung cancer, which may present a new therapeutic target for lung cancer patients in the future.

Nanog siRNA plus Cisplatin may enhance the sensitivity of chemotherapy in esophageal cancer.

BACKGROUND: Cancer stem cells are regarded as the origin of tumors that can proliferate, relapse, and metastasize. Nanog, with its capacity to maintain the pluripotency and regulate proliferation and prevent differentiation, is one of the most important core markers of cancer stem cells. Studying the role of Nanog in esophageal squamous cell carcinoma (ESCC), therefore, has important implications. METHODS: In the present study, we first detected the expression of Nanog in the ESCC and cell lines by RT-PCR, immunofluorescence, and immunohistochemisty. Then, we used small interfering RNA (siRNA) to block Nanog expression while evaluating the effect of Nanog siRNA on cell apoptosis and the combined effects with Cisplatin in ESCC cell lines. RESULTS: The results showed that both mRNA and protein-level Nanog are overexpressed in ESCC tissues compared with their normal counterparts, and the increased occurrence of Nanog expression was positively correlated with TNM stages and histopathological differentiation of ESCC patients (p < 0.01). At the same time, Nanog siRNA efficiently decreased Nanog expression and induced cell apoptosis. Treatment with Nanog siRNA in combination with Cisplatin, therefore, enhanced chemosensitivity. CONCLUSION: The present study's results suggest that detecting Nanog might be helpful for diagnosing ESCC, and Nanog siRNA combined with Cisplatin may be a feasible strategy to enhance the sensitivity of chemotherapy in patients with ESCC.

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 (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-gamma (IFN-gamma) 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-gamma decreased. After administration of Wuwei Dilong Decoction of the large, medium and small dosages, LTB4 decreased, while IFN-gamma 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-gamma, which is probably one of the important mechanisms of Wuwei Dilong Decoction for relieving asthma.