Rare causes of anemia in children: Two cases of idiopathic pulmonary hemosiderosis.

Idiopathic pulmonary hemosiderosis (IPH) is a rare cause of diffuse alveolar hemorrhage (DAH) with unknown etiology. Hemoptysis, dyspnea, anemia, diffuse infiltration in chest radiography and presence of hemosiderin-loaded macrophages (HLMs) in the sputum, gastric content or bronchoalveolar lavage fluid (BALF) are the major characteristics for diagnosis of IPH. Here we present two pediatric patients with IPH. Patient 1 was repeatly misdiagnosed with bronchopneumonia because of diffuse infiltration in her chest X ray, but her anemia was repeatedly ignored. Patient 2 was misdiagnosed with nutritional anaemia because she did not have dyspnea or hemoptysis, and her chest computed tomography (CT) only revealed mild alveolar infiltrates. IPH must be included in the differential diagnosis in patients with long-term anemia who respond poorly to the hematopoietic supplements. CT is superior to X-ray in detecting alveolar hemorrhage.

Pseudobronchial crista-like change in children: A case report.

Pseudobronchial crista-like change is an unusual type of inflammatory granulation tissue hyperplasia in the endobronchial membrane caused by chronic retention of bronchial foreign bodies. Here, we report a case of pseudobronchial crista-like change in a 4-year-old boy who required admission for intermittent cough for >10 days and wheezing for 2 days. The main manifestation was persistent and non-healing lobar pneumonia. Initial electronic bronchoscopy showed cristae at the distal left main bronchus, which was misdiagnosed as bronchial opening stenosis. Repeat electronic bronchoscopy was performed after standard antibiotic treatment proved ineffective. Foreign bodies were observed at the opening of the basal branch of the left lower lobe. The left main bronchial cristae were clamped. The cristae appeared to be a pseudobronchial crista-like change caused by long-term retention of bronchial foreign bodies. After CT-confirmation of no abnormal blood supply at the cristae, the bronchial foreign bodies were removed, and the distal cristae of the left main bronchus were cut-off by laser, followed by balloon dilatation. To our knowledge, no similar cases have been reported so far in our review of domestic and foreign literature. Insufficient clinical understanding of Pseudobronchial Crista-like Change increase the risk of misdiagnosis and missed diagnosis. Detailed exploration and careful identification under bronchoscopy are helpful for the timely diagnosis and treatment of Pseudobronchial Crista-like Change.

DUSP1 regulates hippocampal damage in epilepsy rats via ERK1/2 pathway.

OBJECTIVE: To investigate the effects of DUSP1 on the hippocampal injury of young rats with epilepsy (EP) through mediating ERK1/2 signaling pathway. METHODS: Young SD rats were selected and divided into Control, EP, EP + LV-GFP, EP + LV-DUSP1, EP + LV-siDUSP1, and EP + LV-siDUSP1 + U0126 groups. Morris Water Maze Test was used to detect the spatial learning and memory. Nissl staining and TUNEL staining were conducted and the inflammatory factors and oxidative stress-related indicators were also measured. Western blotting was utilized to detect the expression of DUSP1 and ERK1/2 pathway. EP cell model was constructed in vitro to verify the in vivo results. RESULTS: Compared with Control group, young rats in EP group had decreased spatial learning and memory abilities and increased apoptotic rate and decreased number of Nissl positive cells. Besides, the up-regulated levels in inflammatory factors (IL-1ß, IL-6), MDA content, and p-ERK1/2/ERK1/2 protein expression, as well as the down-regulated levels in DUSP1 protein expression and SOD content were also observed in EP rats. The EP rats treated with LV-DUSP1 showed obvious improvements regarding the above indicators, while those treated with LV-siDUSP1 had aggravated injury. But the effect of LV-siDUSP1 can be reversed by the treatment with ERK1/2 pathway inhibitor U0126. Further in vitro investigation verified the in vivo results. CONCLUSION: DUSP1 may ameliorate the oxidative stress and inflammatory injury, as well as improve spatial learning and memory abilities via inhibiting ERK1/2 pathway, eventually playing protective roles in hippocampal injury of young rats with EP.

Effect of renin-angiotensin-aldosterone system inhibitors on all-cause mortality and major cardiovascular events in patients with diabetes: A meta-analysis focusing on the number needed to treat and minimal clinical effect.

AIMS: To assess the effectiveness of renin-angiotensin-aldosterone system (RAAS) inhibitors, angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) separately to prevent all-cause mortality, myocardial infarction (MI), stroke and heart failure (HF) in patients with diabetes considering the number needed to treat (NNT) and minimal clinical effect (MCE). METHODS: Data from 17 morbidity-mortality trials in patients with diabetes were used to calculate NNTs and evaluate MCE to prevent all-cause mortality, myocardial infarction, stroke, and heart failure. RESULTS: A total of 17 trials involving 42,037 patients were included in this meta-analysis. Mean follow-up was 3.7 years. ACEIs significantly reduced the risk of all-cause mortality, MI and HF; the corresponding mean NNTBs were 48, 62 and 78, respectively, but ARBs were only associated with a reduction in heart failure. The clinical significance assessment of the included trials indicated that most of the statistically significant trial results had no definitive clinical significance, and only some of them had possible clinical significance. CONCLUSIONS: Among patients with diabetes, ACEIs reduced all-cause mortality, MI and HF, whereas ARBs could only prevent HF. However, none of the results of these trials had clear clinical significance, and most had only possible clinical significance.

Biological effects of chlamydiaphage phiCPG1 capsid protein Vp1 on chlamydia trachomatis in vitro and in vivo.

The researches on chlamydia in recent years show that chlamydia bacteriophage may be a potential and effective means to solve the clinical infection of chlamydia trachomatis (Ct). We investigated the biological effect of chlamydiaphage phiCPG1 capsid protein Vp1 on Ct both in McCoy cells and genital tract of mice. Different concentrations of Vp1 were co-incubated with Ct E serotype strain in McCoy cells. Female BALB/c mice were used to establish Ct E strain-induced urogenital infection model. They were randomly divided into five groups and given different treatments on the fifth day after Ct inoculation. Animals in groups 1 and 2 were given 30 µL different concentrations of Vp1 in the genital tract respectively, those in group 3 were intramuscularly injected with 30 µL Vp1, those in the infected group did not receive any intervention, and those in the control group received 30 µL PBS in the genital tract. The vaginal discharge was collected to identify the live chlamydia by cell culture and gene fragment by real time PCR different days after infection. Inhibition rate of 100 µg/mL and 50 µg/mL Vp1 proteins against Ct E strain in the McCoy cell cultures was 91% and 79% respectively. The number of intracellular Ct inclusion in the McCoy cells co-cultured with vaginal discharge of group 1 and group 2 was less than in the infected group, and that in group 1 was less than in group 2, on the 7th day after Ct inoculation. Real-time PCR showed that chlamydia concentration of the vaginal discharge in group 2 was lower than in the infected group, and that in group 1 was lower than in group 2 on the 10th day. It was suggested that Vp1 capsid proteins had inhibitory effect on the proliferation of Ct serovar E strain in cell culture and mouse genital tract.

Whole Genome Analysis Reveals New Insights into Macrolide Resistance in Mycoplasma pneumoniae / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>Mutations in 23S rRNA gene are known to be associated with macrolide resistance in Mycoplasma pneumoniae (M. pneumoniae). However, these mutations alone do not fully explain the high resistance rates in Asia. The aim of this study was to investigate other possible mutations involved in macrolide resistance in M. pneumoniae.</p><p><b>METHODS</b>The whole genomes of 10 clinical isolates of M. pneumoniae with macrolide resistance were sequenced by Illumina HiSeq2000 platform. The role of the macrolide-specific efflux transporter was assessed by efflux-pump inhibition assays with reserpine and carbonyl cyanide m-chlorophenyl-hydrazone (CCCP).</p><p><b>RESULTS</b>A total of 56 single nucleotide polymorphisms (SNPs) were identified in 10 clinical isolates in comparison to the reference strains M129 and FH. Strikingly, 4 of 30 SNPs causing non-synonymous mutations were clustered in macrolide-specific efflux system gene macB encoding macrolide-specific efflux pump protein of the ATP-binding cassette transporter family. In assays of the minimal inhibitory concentrations (MIC) of macrolide antibiotics in the presence of the efflux pump inhibitors caused a significant decrease of MICs, even under detectable levels in some strains.</p><p><b>CONCLUSION</b>Our study suggests that macrolide efflux pump may contribute to macrolide resistance in M. pneumoniae in addition to the common point mutations in 23S rRNA gene.</p>

Biological Effects of Chlamydiaphage phiCPG1 Capsid Protein Vp1 on Chlamydia Trachomatis In Vitro and In Vivo / 华中科技大学学报（医学）（英德文版）

The researches on chlamydia in recent years show that chlamydia bacteriophage may be a potential and effective means to solve the clinical infection of chlamydia trachomatis (Ct).We investigated the biological effect of chlamydiaphage phiCPG1 capsid protein Vp1 on Ct both in McCoy cells and genital tract of mice.Different concentrations of Vp1 were co-incubated with Ct E serotype strain in McCoy cells.Female BALB/c mice were used to establish Ct E strain-induced urogenital infection model.They were randomly divided into five groups and given different treatments on the fifth day after Ct inoculation.Animals in groups 1 and 2 were given 30 μL different concentrations of Vp1 in the genital tract respectively,those in group 3 were intramuscularly injected with 30 μL Vp1,those in the infected group did not receive any intervention,and those in the control group received 30 μL PBS in the genital tract.The vaginal discharge was collected to identify the live chlamydia by cell culture and gene fragment by real time PCR different days after infection.Inhibition rate of 100 μg/mL and 50 μg/mL Vpl proteins against Ct E strain in the McCoy cell cultures was 91％ and 79％ respectively,The number of intracellular Ct inclusion in the McCoy cells co-cultured with vaginal discharge of group 1 and group 2 was less than in the infected group,and that in group 1 was less than in group 2,on the 7th day after Ct inoculation.Real-time PCR showed that chlamydia concentration of the vaginal discharge in group 2 was lower than in the infected group,and that in group 1 was lower than in group 2 on the 10th day.It was suggested that Vp1 capsid proteins had inhibitory effect on the proliferation of Ct serovar E strain in cell culture and mouse genital tract.

Could lengthening minocycline therapy better treat early syphilis?

Syphilis is a sexually transmitted disease caused by Treponema pallidum. Minocycline, a representative tetracycline derivative, has the greatest antimicrobial activity among all tetracyclines. There are few reports about treating syphilis with minocycline because there is a lack of efficacy data from controlled trials. We compared the rates of serological cure in patients with early syphilis who were treated with minocycline or benzathine penicillin G (BPG).During the study period, a total of 40 syphilis patients received the BPG treatment, which was a single intramuscular dose of 2.4 million units of BPG, and 156 patients were treated with minocycline; 77 patients were placed in the 2-week, standard minocycline therapy group and received 100 mg of minocycline orally, twice daily for 14 days, and 79 patients were placed in the 4-week, lengthened minocycline therapy group and received 100 mg of minocycline orally, twice daily for 28 days. The outcome of interest was the rate of serological cure in these patients.At the end of the 2-year follow-up, the serological cure rate of the 4-week, lengthened minocycline therapy group (87.34%) was higher than that of both the 2-week, standard minocycline therapy group (72.73%) and the BPG treatment group (77.50%). In addition, the curative effect of the 4-week, lengthened minocycline therapy was significantly greater than that of the 2-week, standard minocycline therapy in patients who were aged >40 years; exhibited an initial rapid plasma reagin titer ≥1: 32; or exhibited secondary syphilis (P = 0.000, 0.008, 0.000; <0.05).Minocycline appears to be an effective agent for treating early syphilis, especially when applied as a 4-week, lengthened therapy.

Semaphoring mAb: a new guide in RIT in inhibiting the proliferation of human skin carcinoma.

Semaphoring is a transmembrane receptor which participates in many cytokine-mediated signal pathways that are closely related to the angiogenesis, occurrence and development of carcinoma. The present study was designed to access the effect of mono-antibody (mAb) guided radioimmunotherapy (RIT) on skin carcinoma and investigate the potential mechanisms. Semaphoring mAb was acquired from mice (Balb/c), purified with rProtein A column; purity, concentration and activity were tested with SDS-PAGE and indirect ELISA; specificity and expression on the cutanuem carcinoma line and tissue were tested by Western blotting; morphology change was assessed by microscopy. MTT assay and colony inhibition tests were carried out to test the influence on the proliferation of tumor cells; Western blotting was also carried out for expression of apoptosis-associated (caspase-3, Bax, Bcl-2) and proliferation-related (PI3K, p-Akt, Akt, p-ERK1/2, ERK1/2) proteins and analyse the change in signal pathways (PI3K/Akt and MEK/ERK). The purity of purified semaphorin mAb was 96.5% and the titer is about 1?106. Western blotting showed semaphoring mAb to have specifically binding stripes with semaphoring b1b2 protein, B16F10, and A431 cells at 39KDa, 100KDa and 130KDa, respectively. Positive expression was detected both in cutanuem carcinoma line and tissue and it mostly located in cell membranes. MMT assay revealed dose-relate and time-relate inhibitory effect of semaphorin mAb on A431 and B16F10. Colony inhibition tests also showed dose-relate inhibitory effects. Western blotting demonstrated the expression of apoptosis and proliferation-related protein and changes in signal pathway. In conclusion, we demonstrated that semaphorin is highly expressed on the tumor cell-surfaces and RIT with semaphorin mAb has effect in inhibiting proliferation and accelerating apoptosis of tumor cells.

[Expression of TFPI-2 gene and its promoter methylation in acute myeloid leukemia].

The aim of this study was to detect the mRNA expression of tissue factor pathway inhibitor-2 ( TFPI-2) and its methylation in bone marrow mononuclear cells from acute myeloid leukemia (AML) patients and to explore its significance in AML. Bone marrow mononuclear cells were isolated from newly diagnosed AML patients (n = 33), complete remission AML patients (n = 19), relapsed/refractory AML patients (n = 12) and iron deficiency anemia patients (control group, n = 15). Expression of TFPI-2 mRNA was detected with real-time quantitative PCR (RT-PCR) and the methylation of CpG island in its promoter was detected with methylation-specific PCR (MSP). The results showed that the expression of TFPI-2 mRNA in newly diagnosed AML, complete remission AML and relapsed/refractory AML patients was much lower than that in the controls (P < 0.05). Furthermore, its expression in relapsed/refractory AML patients was lower than that in newly diagnosed AML patients (P = 0.006). Compared with complete remission AML patients, the expression of TFPI-2 mRNA in newly diagnosed AML patients was significantly reduced (P = 0.030). The percentage of TFPI-2 promoter methylation in AML patients was 64.63% (42/64). In newly diagnosed AML group, complete remission AML group and relapsed/refractory AML group,the percentages of TFPI-2 promoter methylation were 66.67% (22/33), 52.63% (10/19) and 83.33% (10/12) (P > 0.05), respectively. The optical density ratio of TFPI-2 mRNA expression was 0.165 (0.005-2.099) in methylated AML patients, and 0.597 (0.011-2.787) in unmethylated AML patients (P < 0.05). Methylation of TFPI-2 gene promoter was not detected in control patients. After 2 courses of chemotherapy, the level of TFPI-2 mRNA was much higher in the CR group than that in the non-CR group (P < 0.05). It is concluded that the down-regulation or silence of TFPI-2 gene potentially results from its promoter methylation, and the expression level of TFPI-2 and the methylation status of its promoter may be used as indicators of risk stratification and evaluation of disease progress.

The complete mitochondrial genome of the Hybris subjacens (Neuroptera:Ascalaphidae).

The mitochondrial genome of Hybris subjacens (Neuroptera: Ascalaphidae) is a circular molecule of 15,873 bp in length, containing 37 typical animal mitochondrial genes: 13 protein-coding genes (PCGs), 2 ribosomal RNAs, 22 transfer RNAs and a non-coding AT-rich region. Its gene order and arrangement are identical to the common type found in most insect mitogenomes. All PCGs start with a typical ATN codon except for COI and ND1 which use CTT and TTG as their start codon, respectively; all PCGs terminate in the common stop codon TAA or TAG, except for the COI and ND5 which use single T as their stop codons. The non-coding AT-rich region is 1051 bp long, located between rrnS and tRNA(lle) genes. It contains some structures of repeated motifs and microsatellite-like elements characteristic of the neuropterids.

Ischemic postconditioning mediates cardioprotection via PI3K/GSK-3ß/ß-catenin signaling pathway in ischemic rat myocardium.

Previous studies have shown that PI3K/GSK-3ß/ß-catenin signaling pathway plays a vital role in ischemic preconditioning. The present study attempts to evaluate whether PI3K/GSK-3ß/ß-catenin signaling pathway might be responsible for the cardioprotection in ischemic postconditioning. Male Sprague-Dawley rats underwent 30 min of left anterior descending coronary artery occlusion and 2 h of reperfusion. One hundred twenty rats were randomized into six groups: sham, ischemia/reperfusion (I/R), ischemic postconditioning (Post), 15 µg · kg wortmannin (PI3K inhibitor) plus ischemic postconditioning (Wort + Post), wortmannin plus I/R (Wort + I/R), and 0.6 mg · kg SB216763 (GSK-3ß inhibitor) plus I/R (SB + I/R). Wortmannin and SB216763 were administered, respectively, 10 and 5 min before reperfusion. Myocardial infarct size; number of apoptotic cardiomyocytes; total Akt, GSK-3ß; phosphorylated Akt, GSK-3ß; ß-catenin in cytosol and nucleus; and Bcl-2 protein were assessed. It was found that Post and SB + I/R reduced infarct size (32.3% [SD, 2.8%], 32.7% [SD, 2.1%], vs. 53.4% [SD, 3.2%], respectively, P < 0.05) and apoptotic index of cardiomyocytes (23.2% [SD, 1.8%], 23.8% [SD, 1.8%], vs. 47.3% [SD, 5.8%], respectively, P < 0.05); compared with I/R, wortmannin abolished the cardioprotection of ischemic postconditioning. Post and SB + I/R increased phosphorylated Akt, phosphorylated GSK3ß, ß-catenin in cytosol and nucleus, and Bcl-2 expression versus I/R. These results indicate that ischemic postconditioning could induce myocardial protection via PI3K/GSK-3ß/ß-catenin signaling pathway, activation of which results in accumulation of ß-catenin and upregulation of its target genes Bcl-2.

A single tube modified allele-specific-PCR for rapid detection of erythromycin-resistant Mycoplasma pneumoniae in Beijing / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Mycoplasma pneumoniae (M. pneumoniae) is one of the common pathogens causing atypical pneumonia. In recent years, resistance to macrolides has become more common, especially in China. Previous studies have confirmed that the mutation at position 2063 in domain V of the 23S rRNA is the most prevalent, followed by the mutation at position 2064. Reported molecular detection methods for the identification of these mutations include direct sequencing, restriction fragment length polymorphism analysis, real-time polymerase chain reaction (PCR) with high-resolution melt analysis, and nested PCR-linked with capillary electrophoresis, etc. The most commonly used method for monitoring resistance-conferring mutations in M. pneumoniae is direct DNA sequencing of PCR or nested PCR products. However, these methods are time-consuming, labor-intensive or need expensive equipments. Therefore the development of rapid and sensitive methods is very important for monitoring the resistance globally.</p><p><b>METHODS</b>In this study, we reported a fast and cost-effective method for detecting 2063 and/or 2064 macrolide resistant mutations from specimens using a modified allele-specific PCR analysis, and all results were compared with the sequencing data. We also analyzed the clinical courses of these samples to confirm the modified allele-specific PCR results.</p><p><b>RESULTS</b>Among 97 M. pneumoniae specimens, 88 were found to possess mutations by this method, and all modified allele-specific PCR analysis results were consistent with the sequencing data. The data of the clinical courses of these 97 cases showed that they suffered from severe pneumonia. Erythromycin showed better efficacy on cases from which no macrolide resistance mutation was found on their specimens. However, in some cases from which mutations were detected, erythromycin monotherapy had poor efficacy, and on these patients severe symptoms improved only when azithromycin was added to the treatment.</p><p><b>CONCLUSIONS</b>The drug-resistant M. pneumoniae is very common in Beijing, China. Our modified allele-specific PCR analysis can identify erythromycin resistant mutations more rapidly from specimens than any other method currently available. Erythromycin is still effective for treating patients infected with the mutation negative M. pneumoniae, but this treatment fails to work on mutant organisms. This method can facilitate clinicians in selecting appropriate therapy within short timescales.</p>

Synthesis, structure, and bioevaluation of 2,5-bis(arylmethenyl)cyclopentanones.

Curcumin is an excellent lead compound with a variety of bioactivity. Recent articles reported that curcumin's instability and low bioavailability in vivo are mainly due to its easily decomposable beta-diketone moiety. With the aim of bioactive curcumin analogs with better pharmacokinetic property, we present here 11 bis(arylmethenyl)cyclopentanones similar to curcumin and without beta-diketone moiety by reacting relevant arylaldehydes and cyclopentanones. The analogs were structurally determined by 1HNMR and MS spectra, and the crystal structure of 6 was analyzed by X-ray diffraction. Their antibacterial activities in vitro against seven Gram-positive and Gram-negative bacteria were tested, and their inhibition of TNF-alpha and IL-6 secretion in LPS-induced mouse macrophages was investigated using enzyme-linked immunosorbent assay. It was observed that several derivatives displayed higher activity when compared with curcumin, and most of the analogs exhibited activities against the ampicillin-resistant Gram-negative Enterobacter cloacae.

[The antitumor effect and immuno-mechanism of IL-23 in mouse mammary cancer].

AIM: To study the antitumor effect of IL-23 in mouse mammary cancer and the change of its immune function. METHODS: IL-23/MA-891, LXSN/MA-891 and the parental MA-891 cells were inoculated in the subcutaneous tissues of mice, respectively. The mouse models were used to observe the tumorigenic activity of IL-23/MA-891 cells. On the thirtieth day, the spleens and tumors of the mice in three groups were extracted and then IFN-gamma, TNF-alpha, IL-12 and IL-4 were detected by ELISA. The expression of MHC-I, MHC-II, CD80 and CD86 in tumor cells, the ratio of positive cells of CD11c, and the selection of CD4 and CD8 in the spleens were detected by flow cytometry, respectively. CD4 and CD8 in three groups were immuno-stained and then they were examined by microscope. RESULTS: The tumor in the mouse inoculated with IL-23/MA891 cells developed much more slowly than that in the other two groups. Meanwhile, the spleen cells of this group secreted higher IFN-gamma, TNF-alpha and IL-12 than the other two groups (P<0.01), but the secretion of IL-4 in the three groups had no difference (P>0.05). In IL-23/MA891 group, CD4+, CD8+ lymphocytes, CD11c+ cells in spleens and infiltration of CD4+, CD8+ lymphocytes in tumor tissues were also markedly higher than those in LXSN/MA-891 and MA-891 groups (P<0.01). The expression of MHC-I, MHC-II, CD80 and CD86 in IL-23/MA-891 groups was also higher than that in the other two groups (P<0.01). CONCLUSION: In the mice the antitumor effect of the mammary cancer cells transferred by IL-23 gene is obvious, which can enhance the cellular immune function and play an important role in inhibiting the growth of tumor.

[Inhibitory effect of IL-27 gene on tumor formation activity of Eca109 cells in nude mice and its mechanisms].

BACKGROUND & OBJECTIVE: Cytokine-based biotherapy is a hot spot in tumor research. This study was to explore the inhibitory effect of interleukin-27 (IL-27) on tumor formation activity of human esophageal carcinoma cell line Eca109 in nude mice, and investigate its antitumor mechanisms. METHODS: IL-27 gene was transfected into Eca109 cells with retrovirus vector and stable clones were selected by G418. The expression of IL-27 gene was detected by reverse transcription-polymerase chain reaction (RT-PCR). The secretion of IL-27 from Eca109/IL-27 cells and interferon-gamma (IFN-gamma) in peripheral blood mononuclear cells (PBMCs) were detected by ELISA. Cell proliferation in vitro was assessed by MTT assay. Eca109/IL-27, Eca109/LXSN and Eca109 cells were subcutaneously injected into nude mice to observe the growth of transplanted tumors. The expression of CD16 and FasL in tumor-infiltrating lymphocytes (TIL) and the expression of Fas in tumor cells were detected by flow cytometry. RESULTS: IL-27p28 and IL-27EBI3 were expressed in Eca109/IL-27 cells, but not in Eca109/LXSN and Eca109 cells (P<0.01). IL-27 secretion was significantly higher in Eca109/IL-27 cells than in Eca109/LXSN and Eca109 cells (P<0.01). The proliferation rates of the 3 cell lines were similar (P> 0.05). IFN-gamma secretion was significantly higher in Eca109/IL-27 cell-stimulated PBMCs than in Eca109/LXSN cell-and Eca109 cell-stimulated PBMCs [(56.28+/-1.61) pg/mL vs. (12.70+/-0.82) pg/mL and (11.06+/-0.64) pg/mL, P<0.01]. As compared with those in Eca109 and Eca109/LXSN groups, the tumor growth in nude mice was significantly slower in Eca109/IL-27 group (P<0.05), the expression of CD16 and FasL in TIL and the expression of Fas in tumor cells were up-regulated in Eca109/IL-27 group (P<0.05). CONCLUSION: IL-27 gene may inhibit the tumor formation activity of Eca109 cells in nude mouse by activating natural killer (NK) cells through Fas/FasL pathway.