miR-202-3p negatively regulates MMP-1 to inhibit the proliferation, migration and invasion of lung adenocarcinoma cells.

Lung adenocarcinoma (LUAD) is one of the common cancers. Studies show that MMP-1 is involved in tumor progression, yet relevant regulatory mechanism in LUAD remains to be further elucidated. Here, we demonstrated from bioinformatics analysis for GEO data that MMP-1 was differentially up-regulated in LUAD. miR-202-3p, identified as the upstream regulator of MMP-1 by both bioinformatics and dual-luciferase assays, was differentially down-regulated in LUAD and presented a negative correlation with MMP-1. Following cell biological experiments proved that knocking down the expression of MMP-1 inhibited the proliferation, migration and invasion of LUAD cells, while overexpressed miR-202-3p posed a similar suppressive effect on cancer progression. Additionally, rescue assay further identified that overexpression of MMP-1 attenuated the suppressive effect of up-regulated miR-202-3p on malignant progression of LUAD cells. In all, this research suggests a mechanism by which MMP-1 under the regulation of miR-202-3p modulates the proliferation, migration and invasion of LUAD cells, which may contribute to the development of new therapeutic strategies.

Effect and mechanism of miR-146a on malignant biological behaviors of lung adenocarcinoma cell line.

The aim of the present study was to assess the expression of microRNA-146a (miR-146a) in human lung adenocarcinoma cells, its effect on cellular behaviors, and the underlying molecular mechanisms. Reverse transcription-quantitative PCR (RT-qPCR) was used to measure miR-146a expression in the human normal lung epithelial cell line, BEAS-2B, and human lung adenocarcinoma cell lines, A549, PC-9 and H1299, to determine whether miR-146a acts as an oncogene or anti-oncogene. miR-146a mimics were transfected into target cells to observe the proliferation, apoptosis, invasion and migration of human lung adenocarcinoma cells. The target genes of miR-146a were predicted using bioinformatics analysis, and binding sites were validated by dual-luciferase reporter assay. Target gene expression at the mRNA and protein levels was measured by RT-qPCR and western blot analysis, respectively. The expression levels of miR-146a in human lung adenocarcinoma cell lines were lower than its expression in BEAS-2B (P<0.01). A549 cell line is a EGFR wild-type lung adenocarcinoma cell line, which is also the most widely studied in NSCLC, and therefore this was chosen as the target cell line for further investigation. Overexpression of miR-146a in A549 cells can inhibit cell proliferation (P<0.05), promote apoptosis (P<0.05), and reduce the cells' migratory ability (P<0.01). Bioinformatics prediction indicated that interleukin-1 receptor-associated kinase 1 (IRAK1) and TNF receptor associated factor 6 (TRAF6) are the target genes of miR-146a. Dual-luciferase reporter assay showed that miR-146a could specifically bind to 3'-untranslated regions of IRAK1 and TRAF6. The protein and mRNA levels of IRAK1 and TRAF6 were significantly downregulated after miR-146a overexpression in A549 cells (P<0.01). The results of this study demonstrated that the expression of miR-146a in human lung adenocarcinoma cells was significantly lower than in normal lung epithelial cells, indicating that miR-146a acts as an anti-oncogene. miR-146a suppresses the proliferation and migration of human lung adenocarcinoma cells by downregulating the expression of IRAK1 and TRAF6.

Effect of lentiviral vector-packaged interleukin-18 gene on the malignant behavior of lung cancer.

Interleukin-18 (IL-18) is a multifunctional cytokine that exhibits antitumor, anti-infection and immunoregulatory functions. This study aimed to investigate the effects of lentiviral vector-packaged interleukin (IL)-18 gene on the malignant behavior of lung cancer and the potential underlying molecular mechanism of IL-18 anticancer activity. Human lung adenocarcinoma A549 cells transfected with human IL-18 gene-containing lentiviral expression vector were the IL-18 intervention group (group A), cells transfected with the empty lentiviral expression vector were empty vector group (group B), and cells without any intervention were the blank control group (group C). Reverse transcription-quantitative PCR and western blotting were used to determine IL-18 mRNA and protein expression levels. Cell Counting Kit-8, colony-formation, flow cytometry, invasion and wound-healing assays were used to evaluate the malignant behavior of A549 cells transfected with the IL-18 lentiviral vector. The expression levels of the T helper (Th)1 cell cytokine interferon-γ (IFN-γ) and the Th2 cell cytokine IL-4 were tested by ELISA, and western blotting was used to test the expressing of nuclear factor κB (NF-κB). The results demonstrated that IL-18 mRNA and protein expression levels in group A were significantly increased compared with groups B and C; the expression levels of IFN-γ in group A were higher and the expression levels of IL-4 in group A were lower compared with those in groups B and C; and the expression of NF-κB was increased in the cytoplasm and decreased in the nucleus in group A compared with groups B and C. The data indicated that, compared with the control groups, the IL-18 gene lentiviral expression vector increased the expression of IL-18, diminished A549 cell proliferative ability, enhanced apoptosis, decreased the invasive and metastatic capacities of the cells, promoted the secretion of IFN-γ, decreased the production of IL-4, reversed the imbalance of Th1/Th2 cell subsets and inhibited the nuclear activation of NF-κB, which collectively present an anti-lung cancer mechanism and deserve further study.

IL­21/IL­21R inhibit tumor growth and invasion in non­small cell lung cancer cells via suppressing Wnt/ß­catenin signaling and PD­L1 expression.

Lung cancer is considered to be one of the world's deadliest diseases, with non­small cell lung cancer (NSCLC) accounting for 85% of all lung cancer cases. The present study aimed to investigate the role and underlying mechanisms of interleukin­21 (IL­21), and its receptor IL­21R, in NSCLC. Lung tissues and blood samples of NSCLC were used to measure IL­21, IL­21R and programmed death 1 ligand 1 (PD­L1) expression using ELISA, western blot and immunohistochemistry analyses. Following treatment with different doses of IL­21, the proliferation, invasion and migration of human NSCLC cell line A549 was evaluated using a cell counting kit­8, colony formation, Transwell and scratch wound healing assays, respectively. Additionally, IL­21R and PD­L1 expression in A549 cells was detected using western blot analysis and immunofluorescence. IL­21R silencing was subsequently used to investigate its effects in cell proliferation, invasion and migration. PD­L1, IL­1ß and tumor necrosis factor α (TNF­α) expression were measured. Finally, Wnt/ß­catenin signaling expression was evaluated using western blot analysis following treatment with IL­21. Cells were then treated with lithium chloride (LiCl), which is an agonist of Wnt/ß­catenin signaling, and the levels of PD­L1, IL­1ß and TNF­α were detected. The results revealed that IL­21 and IL­21R expression in the lung tissues and blood samples of patients with NSCLC were decreased, while PD­L1 expression was increased, compared with normal tissues or healthy controls. Treatment of A549 cells with IL­21 upregulated IL­21R expression, downregulated PD­L1 and inhibited cell growth and metastasis in a dose­dependent manner. Following IL­21R silencing, the effects of IL­21 treatment were reversed, suggesting that IL­21 acted on A549 cells through binding to IL­21R. In addition, the results demonstrated that IL­21 treatment reduced the expression levels of proteins associated with the Wnt/ß­catenin signaling, whereas activation of Wnt/ß­catenin signaling with the LiCl agonist upregulated PD­L1, IL­1ß and TNF­α expression. In conclusion, the IL­21/IL­21R axis reduced the growth and invasion of NSCLC cells via inhibiting Wnt/ß­catenin signaling and PD­L1 expression. The present results may provide a novel molecular target for NSCLC diagnosis and therapy.

Antitumor activity of interleukin-18 on A549 human lung cancer cell line.

OBJECTIVE: In this study, we investigated the antitumor activity of interleukin (IL)-18 on A549 human lung cancer cell line and evaluated the potential of IL-18 therapy in lung cancer. MATERIALS AND METHODS: We generated a human IL-18 lentiviral expression vector and examined three groups of A549 cells, including nontransduced cells and cells transduced with either IL-18 or an empty lentiviral expression vector. IL-18 expression, cell proliferation, and apoptosis were examined using Western blotting, methylthiazolyldiphenyl-tetrazolium bromide assay, and flow cytometry, respectively. The expression of the T helper 1 (Th1) cytokine interferon-γ (IFN-γ) and Th2 cytokine IL-4 was analyzed by enzyme-linked immunosorbent assay (ELISA). RESULTS: Compared to the other groups of cells, A549 cells transduced with the IL-18 lentiviral expression vector exhibited significant increases in IL-18 expression, apoptosis, and the fraction of cells in G0 and G1 phases of the cell cycle and significant decrease in proliferation. Furthermore, ELISA results showed that IFN-γ expression increased significantly and IL-4 decreased in A549 cells transfected with IL-18 lentivirus expression vector. CONCLUSION: Using a lentiviral expression vector, IL-18 was expressed stably and efficiently in A549 cells, which showed attenuated proliferation and tumor cell growth, and enhanced tumor cell apoptosis. IL-18 expression also induced the secretion of IFN-γ, while decreasing the production of IL-4, therefore restoring the balance between Th1/Th2 cell subsets. These findings further demonstrated the antitumor activity of IL-18 and might open new therapeutic avenues for the prevention and treatment of lung cancer.

Preliminary evaluation of the potential role of ß-elemene in reversing erlotinib-resistant human NSCLC A549/ER cells.

ß-elemene (ß-ELE) is a natural compound extracted from Curcuma zedoaria Roscoe that has shown promise as a novel anticancer drug to treat malignant tumors. Recent studies have demonstrated that ß-ELE can reverse the drug resistance of tumor cells. To the best of our knowledge, there are no reports concerning the reversal of erlotinib resistance by ß-ELE in human non-small cell lung cancer (NSCLC) cells. Therefore, the present study investigated the effects of ß-ELE on erlotinib-resistant human NSCLC A549/ER cells in vitro and its possible mechanism of action. The sensitivity of A549/ER cells to erlotinib, the cytotoxicity of ß-ELE on the growth of A549/ER cells and the effects of ß-ELE on the reversal of drug resistance in A549/ER cells were determined by MTT assay. The cell apoptosis rate, cell cycle phase distribution and intracellular rhodamine 123 (Rh123) fluorescence intensity were detected by flow cytometry. The expression level of P-glycoprotein (P-gp) was detected by western blotting. A549/ER cells had a stable drug-resistance to erlotinib. ß-ELE inhibited the proliferation of A549/ER cells in a time- and dose-dependent manner, enhanced the sensitivity of A549/ER cells to erlotinib and reversed the drug resistance in A549/ER cells. Treatment with 15 µg/ml ß-ELE combined with 10 µmol/l erlotinib caused an increased rate of cell apoptosis and G0/G1 phase arrest. Furthermore, ß-ELE reduced the efflux of Rh123 from A549/ER cells, increased the intracellular accumulation of Rh123 and decreased the expression of P-gp. The results of the present study indicated that ß-ELE could reverse drug resistance in erlotinib-resistant human NSCLC A549/ER cells in vitro through a mechanism that may involve the decreased expression of P-gp, inhibition of P-gp dependent drug efflux and the increased intracellular concentration of anticancer drugs.

Tripchlorolide induces autophagy in lung cancer cells by inhibiting the PI3K/AKT/mTOR pathway and improves cisplatin sensitivity in A549/DDP cells.

Tripchlorolide (T4) has been shown to induce A549 lung cancer cell death predominantly by activating an autophagy pathway. However, the underlying mechanism remains unclear. Herein, we demonstrated that compared with T4 treatment alone, pretreatment with wortmannin (an inhibitor of phosphatidylinositol 3-kinase), perifosine (an inhibitor of AKT) or rapamycin (an inhibitor of mTOR) combined with a subsequent T4 treatment significantly impaired the cell viability of A549 and A549/DDP lung cancer cells. We found that either treatment scheme markedly reduced the activity of P13K and AKT. Expression of LC3II increased in parallel to the increase of the T4 concentration in both A549 and A549/DDP cells and was repressed by overexpression of AKT. The expression levels of PI3-K, PI3-P, AKT, TSC2, mTOR, p70S6K and 4E-BP1 were minimally affected by the wortmannin, perifosine, or rapamycin plus T4 treatments, but their phosphorylated products were greatly affected in A549 lung cancer cells and slightly affected in A549/DDP lung cancer cells. These results indicate that T4 induces autophagy in lung cancer cells by inhibiting the PI3K/AKT/mTOR signaling pathway. We further found that T4 decreased expression of MDR1 and improved cisplatin sensitivity of A549/DDP cells. Altogether, these results have meaningful implications for tumor therapy in the future.

Primary lymphoepithelioma-like carcinoma of the lung: An unusual cancer and clinical outcomes of 14 patients.

Advanced lung cancer is considered to exhibit a poor prognosis; however, the pulmonary lymphoepithelioma-like carcinoma (LELC), a rare subtype of non-small cell lung cancer (NSCLC), exhibits an improved prognosis, compared with non-LELC. The present study aimed at investigating the clinical manifestation, imaging characteristics, pathology, tumor markers, treatment and prognosis of primary LELC of the lung. A total of 14 patients with pulmonary LELC were confirmed by surgery and pathology. Clinical data of those patients were retrospectively reviewed including age, sex, smoking history, symptoms, computed tomography (CT) results, Epstein-Barr virus-encoded RNA (EBER) status, treatment and outcomes. In the present study, there were 7 males and 7 females who ranged in age between 22 and 64 years (mean, 51.21±11.37 years) and who all were from eastern China. The tumor-node-metastasis stage ranged between stages I and IV, with 71.43% of the patients at advanced stage (stages III and IV). The results of the present study identified 100% positive expression of EBER. Tumors located centrally were of significantly increased size, compared with peripheral tumors (P<0.05), and lymphadenopathy was more common in patients with advanced stage (P<0.05). The majority of patients were treated with surgery, platinum-based chemotherapy or radiotherapy. At time of writing, 12 patients were alive and the longest survival time was 60 months. Pulmonary LELC typically affected young patients and was not associated with smoking history; however, pulmonary LELC was associated with Epstein-Barr virus infection in the Asian population. The majority of patients were in early or locally advanced stages and exhibit an improved prognosis compared with other types of NSCLC. Pulmonary LELC was sensitive to chemotherapy and surgery, with postoperative chemotherapy-based multimodality treatment recommended.

Clinicopathological significance of oestrogen receptor expression in non-small cell lung cancer.

Objective To investigate the expression and clinicopathological significance of the oestrogen receptor (ER) in non-small cell lung cancer (NSCLC). Methods ER expression was examined by immunohistochemical staining of tumour tissue and adjacent normal lung tissue from 67 NSCLC patients. The relationships between ER expression and clinicopathological features were analysed. Results A higher percentage of NSCLC tissues (28/67, 41.79%) than adjacent normal lung tissues (10/55, 18.18%) were ER positive. ER expression correlated with tumour differentiation but not with gender, age, tumour histological type, tumour size, lymph node metastasis, or clinical TNM staging. The median survival times of patients with ER-positive ( n = 28) and -negative ( n = 39) tumours were 36 and 27 months, respectively. The 1-, 3-, and 5-year survival rates were higher for patients with ER-positive tumours than for patients with ER-negative tumours. Conclusion ER expression could be a useful prognostic biomarker and therapeutic target for patients with NSCLC.

[The efficacy and safety of moxifloxacin in the treatment of patients with acute exacerbation of chronic obstructive pulmonary disease].

OBJECTIVE: To compare the effectiveness and safety of moxifloxacin and cefoperazone-sulbactam therapy in acute exacerbation of chronic obstructive pulmonary disease (COPD). METHODS: This was a prospective, randomized, multicentre study conducted between December 2011 and December 2012 involving 21 hospitals in Fujian. A total of 202 patients with AECOPD requiring antibiotic therapy were enrolled. Of these patients randomized to either treatments, 102 patients [male 60, female 42, (69.8 ± 6.5) y] received moxifloxacin (400 mg qd) and 100 [male 56, female 44, (69.6 ± 6.7) y] received cefoperazone-sulbactam (3.0 q 8 h). Clinical effectiveness, bacterial eradication and drug safety were evaluated. RESULTS: The clinical effectiveness rate was 90.2% (92/102) in the moxifloxacin group and 88.0% (88/100) in the cefoperazone-sulbactam group. The bacterial eradication rate was 51.9% (14/27) and 48.3% (14/29) in the 2 groups respectively. The differences between groups were not statistically significant in terms of clinical and microbiological effectiveness (χ² = 0.251, χ² = 0.072, both P > 0.05). The length of hospital stay and antibiotic-days were shorter in the moxifloxacin group [(8.7 ± 2.4) vs (11.7 ± 3.0) d; (6.7 ± 2.2) vs (8.7 ± 2.3) d], the differences being significant between the 2 arms. (t = 6.360, t = 7.732, P < 0.05). Both drugs were well tolerated with no significant differences in numbers of drug-related adverse events (P > 0.05). CONCLUSIONS: Moxifloxacin was equivalent to cefoperazone-sulbactam therapy for clinical success, bacteriologic eradication and showed superiority over the control group in shortening the length of hospital stay and antibiotic-days. Additionally, the drug safety of moxifloxacin was good.

Therapeutic effects of sorafenib on the A549/DDP human lung adenocarcinoma cell line in vitro.

The aim of the present study was to observe the effects of sorafenib on the proliferation, apoptosis and invasion of A549/DDP cisplatin-resistant lung adenocarcinoma cells cultured in vitro. The A549/DDP cisplatin-resistant lung adenocarcinoma cell strain was cultured in vitro, the cell culture group incubated in culture medium only was set as the control group (Group S0) and the four concentration gradients of sorafenib were added to the culture groups as the experimental groups: S1, 2 µmol/l; S2, 4 µmol/l; S3, 8 µmol/l; and S4, 16 µmol/l. The MTT assay was used to determine the growth inhibition rate of the cells, which were respectively subjected to sorafenib treatment for 24, 48 and 72 h. Flow cytometry was used to determine the rate of apoptosis of cells in each group following sorafenib treatment for 72 h. Furthermore, the Transwell invasion experiment was used to determine the effect on A549/DDP cell invasion following sorafenib treatment for 24 h. Based on the MTT assay, it was found that the inhibition rates of A549/DDP cisplatin-resistant lung adenocarcinoma cells in groups S1-4 following sorafenib treatment for 24 h were 4.58±2.82, 14.93±2.62, 37.58±7.13 and 58.39±8.15%, respectively. For 48 h, inhibition rates in S1-4 were 14.98±2.93, 26.28±7.31, 63.00±3.05 and 78.84±3.96%, respectively, and for 72 h, inhibition rates were 18.80±2.82, 32.71±2.55, 75.51±4.73 and 87.50±3.36%, respectively. The difference in the inhibition rates of cells among the experimental groups for the same incubation time showed statistical significance (P<0.05). Flow cytometric analysis indicated that the rate of apoptosis in the control group was 8.88±0.81% following sorafenib treatment for 72 h, and the rates of apoptosis in groups S1-4 were, 12.84±0.24, 17.27±0.78, 21.98±0.75 and 49.67±1.38%, respectively. The rate of apoptosis in each experimental group was higher compared with that in the control group (P<0.05). The difference in the rate of apoptosis among the experimental groups was statistically significant (P<0.05). The Transwell assay showed that the number of cells permeating the septum in the control group was 82.7±2.3/high power lens (HP), while the average number of cells permeating septum in groups S1-4 following treatment with sorafenib for 24 h was 58.2±2.5, 41.3±1.3, 22.6±2.1 and 14.7±1.1/HP, which was significantly lower compared with the control group. The number of cells permeating the septum in each experimental group decreased with the enhancement of the concentration gradient. The differences were statistically significant (P<0.05). In conclusion, sorafenib inhibits the proliferation of A549/DDP cisplatin­resistant lung adenocarcinoma cells in a time­ and concentration­dependent manner. In addition, sorafenib induces apoptosis in A549/DDP cisplatin­resistant lung adenocarcinoma cells, thus reducing their invasiveness.

Survivin expression in human lung cancer and the influence of its downregulation on the biological behavior of human lung cancer cells.

The aim of the present study was to detect the expression of survivin in human lung cancer and to investigate the influence of its downregulation on the biological behavior of A549 lung cancer cells. The high expression of survivin in human lung cancer was verified by immunohistochemistry. Survivin small interfering RNA (siRNA) and unrelated sequence were synthesized and the siRNA lentiviral vector was constructed. The vector was transfected into A549 lung cancer cells, in which the clone with stable expression was screened out. We blocked the expression of survivin mRNA and protein by RNA interference (RNAi) technique. The downregulation of survivin mRNA and protein expression was confirmed by real-time quantitative PCR and western blotting. The proliferative activity and growth rate of A549 cells were determined by colony formation assay and mononuclear cell direct cytotoxicity assay (MTT assay). The reconstituted basement membrane (RBM) penetrating capacity was determined by cell invasion assay. The cell movement and migratory capacity were detected by wound-healing repair assay. The results showed that the sequence-specific siRNA significantly downregulated the expression of survivin at both the mRNA and protein levels. Downregulation of survivin expression dramatically decreased the invasive and metastatic capacities of the cells, suppressed the proliferation, decelerated the rate of growth, reduced the number of clones on soft agar and decreased the capacity of RBM penetration and migration. In conclusion, survivin, which plays an important role in carcinogenesis and development of lung cancer, can be effectively downregulated using the RNAi technique.

Effects and mechanism of downregulation of survivin expression by RNA interference on proliferation and apoptosis of lung cancer cells.

The survivin protein, a member of the inhibitors of apoptosis (IAP) family, has gained popularity as a therapeutic target for cancer due to its selective expression in tumor cells and its significant involvement in tumor cell viability. The aim of this study was to investigate the effect of the survivin-small interfering RNA (siRNA) plasmid on survivin expression in the human lung cancer cell line, A549, and to observe its effects on apoptosis and proliferation of A549 cells. A549 human lung cancer cells were transfected with survivin-targeting siRNA. The downregulation of survivin expression was determined by real-time polymerase chain reaction and western blotting. The proliferation of A549 cells was determined by MTT assay. The apoptotic rate and cell cycle distribution were analyzed by flow cytometry (FCM). Caspase-9 activity was also detected to study the apoptosis of lung cancer cells induced by siRNA against survivin. The sequence-specific siRNA efficiently and specifically downregulated the expression of survivin at both the mRNA and protein levels. Downregulation of survivin expression dramatically suppressed the proliferation of A549 cells and arrested the cells at the G (1)/G (0) phase. Caspase-9 activity was significantly increased in A549 cells transfected with siRNA against survivin. In this study, we found that survivin-specific siRNA can efficiently suppress the expression of survivin, increase apoptosis and inhibit A549 cell proliferation. Our findings further indicate the possibility that the antitumor effects of survivin-siRNA are mediated through the activation of caspase-9.

Tripchlorolide induces cell death in lung cancer cells by autophagy.

It has been demonstrated that triptolide inhibits the growth of several types of cancer cells in vitro and prevents tumor growth in vivo by inducing apoptosis and autophagy. Here we showed that Tripchlorolide (T4) significantly suppressed the proliferation of A549 cells in a dose- and time-dependent manner. This suppressive effect was diminished when cells were pretreated with 3-Methylamphetamine (3-MA). After the cells were treated with T4, the LC3 II protein expression was significantly increased, and autophagosomes were observed by TEM. However, almost no apoptosis was observed in A549 treated with T4. These results suggest that T4 induces A549 cell death predominantly through the activation of the autophagy pathway instead of the apoptosis pathway.

[Clinical features of 127 cases of novel influenza A (H1N1) infection in Fujian Province].

OBJECTIVE: to investigate the clinical features of 127 cases of the novel influenza A/H1N1 infection in Fujian Province. METHODS: this study included 127 human cases with the novel influenza A/H1N1 infection in Fujian Province from May 2009 to July 2009. Data were collected and reviewed from hospital medical records. The statistical analyses were performed with SPSS 11.5. RESULTS: the median age of the 127 patients (55 were females) was 21 years (range 0.4 - 58). The median incubation period was 2 d (range 1 - 12 d). The typical clinical symptoms included fever, cough, sputum, and sore throat. The duration of symptoms in patients less than 5 years old and in patients more than 5 years old were (8.2 +/- 4.1) and (5.4 +/- 3.0) d respectively, the difference between these 2 groups being significant (z = 3.182, P < 0.01). There was also a statistically significant difference in the duration of symptoms between the high-temperature group and the low-temperature group [(6.8 +/- 3.2) vs (4.8 +/- 2.1) d, Hc = 9.729, P < 0.05]. The duration of symptoms in the high, the normal and the low white blood cell groups were (6.3 +/- 4.7) d, (5.4 +/- 2.8) d, and (8.5 +/- 4.2) d respectively, but the differences were not statistically significant (Hc = 4.729, P = 0.094). However, the duration of symptoms in the higher lymphocyte count group was significantly longer than that in the lower and normal lymphocyte count groups [(6.8 +/- 3.3) vs (5.4 +/- 3.4), (5.2 +/- 3.2) d, Hc = 10.105, P < 0.01]. Chest radiography showed patchy infiltrates in 6 patients, and their duration of symptoms was longer than patients with normal chest radiography [(8.1 +/- 5.7) vs (5.6 +/- 3.1) d], but the difference was not statistically significant (z = 1.286, P > 0.05). 125 patients received antiviral treatment with oseltamivir and they all had a good prognosis. There was a statistical difference in the duration of symptoms between the patients who used oseltamivir within 48 h after disease onset and patients who used the drug beyond 48 h [(4.7 +/- 2.2) vs (7.4 +/- 4.1) days, z = 4.907, P < 0.01]. All of the patients survived. CONCLUSIONS: the clinical symptoms of this series of patients with the novel influenza A (H1N1) infection appeared to be mild. There were several factors associated with longer duration of symptoms, including aged 5 years or younger, higher fever (body temperature > 38 degrees C), higher white blood cell count and lymphocyte count. The early use of anti-retroviral treatment with oseltamivir was useful in shortening the duration. The novel influenza A (H1N1) infection was a self-limited disease, and patients with no complications had a good prognosis.

[Effects of interleukin-18 on asthmatic airway inflammation: experimental study of guinea pig asthmatic model].

OBJECTIVE: To investigate the effects of Interleukin-18 (IL-18) on asthmatic airway inflammation. METHODS: Thirty healthy adult male guinea pigs were randomly divided into 3 equal groups: asthmatic model group (Group A, undergoing intraperitoneally injection of ovalbumin (OVA) once and spraying of OVA aerosol once a day for 5 days; control group (Group B), undergoing intraperitoneally injection of OVA once and spraying of normal saline aerosol once a day for 5 days; and interleukin (IL)-18 intervention group (Group C, undergoing intraperitoneally injection of OVA once and intraperitoneal injection of IL-18 on the days 1, 3, 8. 10. 15, 17, and 19. Twenty-four hours after the final spraying or IL-18 injection the bronchalveolar lavage fluid (BALF) of the left lungs were obtained. HE staining was conducted to the sediment to examine the numbers of eosinophils, neutrophils, and monocytes. ELISA was used to detect the Th1/Th2 cytokines in the BALF. The left lungs underwent pathological examination. RESULTS: The number of EOS in BALF of Groups A was (98 +/- 58) x 10(6)/L, significantly higher than those of Group B, (12 +/- 10) x 10(6)/L, and Group C, (29 +/- 10) x 10(6)/L (P < 0.01 and P < 0.05). The numbers of neutrophils in the BALF of Group A was (24 +/- 16) x 10(6)/L, significantly higher than those of Group B and C [(9 +/- 7) x 10(6)/L and (10 +/- 5) x 10(6)/L respectively, both P < 0.05]. The concentration of IFN-gamma and IL-2 in group A were both significantly lower than those of Group B and Group C (P < 0.05 and P < 0.01). The concentration of IL-4 in Group A was significantly higher than those of Groups B and C (both P < 0.05). The concentration of IL-5 of Group A was significantly higher than those of Group Bs and C (both P < 0.01). CONCLUSION: IL-18 effectively inhibits asthmatic airway inflammation by regulating the Th1/Th2 balance.