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2009 Vol.4 No.2
Published 2009-06-25

述评
Review
论著
病例分析
综述
) [HTML 1KB] [PDF 15KB] ( 1920 )
73 LU Hong-Zhou1,2,3;SUN Jian-Jun1
2009 Vol. 4 (2): 73-75 [Abstract] ( 2037 ) [HTML 1KB] [PDF 75KB] ( 1996 )
 
Review
68 LONG Jing-Xue;YUAN Shi-Shan
2009 Vol. 4 (2): 68-72 [Abstract] ( 2456 ) [HTML 1KB] [PDF 90KB] ( 3662 )
 
论著
76 QI Xian;YAO Huo-Chun;LU Cheng-Ping

Swine influenza type A H3N2 virus-induced apoptosis in porcine pulmonary alveolar macrophages in vitro

Porcine pulmonary alveolar macrophages (PAMs) were infected with A/Swine/Guangdong/1/2004, a swine influenza virus (SIV) isolate. Results showed that A/Swine/Guangdong/1/2004 was able to carry out productive replication in PAMs. DNA laddering in SIV-infected cells showed subdiploid DNA peaks at 24, 48, and 72 h post-infection by flow cytometry. Under light and electron microscopes, morphological changes in SIV-infected cells were observed, including cell shrinkage, plasma membrane blebbing, nuclear condensation, and cytoplasm vacuolization. These results indicate that SIV may induce apoptosis in PAMs in vitro, and apoptosis may play an important role in death of PAMs infected with SIV.
2009 Vol. 4 (2): 76-80 [Abstract] ( 2563 ) [HTML 1KB] [PDF 942KB] ( 2301 )
81 CHEN Hui1;WU Min2; YU Shi-Yan1,2; CHEN Jie-Liang1,2; YUAN Zheng-Hong1,2
Interferon-β induction and related signaling pathways in human hepatocyte cell lines
Interferon-β plays an important role in innate immunity against viral infection. Hepatocytes, as hepatitis viruses-harboring cells, are reported to possess the potential to inductively express interferon-β. However, a practical in vitro cell model for investigating the interplay between hepatitis B virus and host cells is rarely reported. Here, we determined the inductive expression of interferon-β by interferon-β agonists〔(Newcastle disease virus, NDV) and poly(I∶C)〕in immortalized primary hepatic cell line, PH5CH8,and hepatocarcinoma cell lines, Huh-7 and HepG2. The data demonstrated that inductive expression of interferon-β in PH5CH8 cells was significantly higher than that in Huh7 or HepG2 cells. In addition, the expression level of key molecules critical for interferon-β induction was investigated to clarify the underlying mechanism. The results showed that the background expression level was fairly low in Huh7 and HepG2 cell lines, compared to that in PH5CH8 cells. It is suggested that PH5CH8 cells possess intact potential to produce interferon-β and reconstitution of a selective interferon-deficient hepatic cell line might be achieved via introduction of related molecules critical for interferon induction.
2009 Vol. 4 (2): 81-87 [Abstract] ( 3433 ) [HTML 1KB] [PDF 440KB] ( 3955 )
88 ZHAO Shou-Song;CHEN Zi-An;ZHANG Li
Detection and significance of serum tumor necrosis factor-α and interleukin-6 in chronic hepatitis B patients superinfected with acute hepatitis E

The present study was aimed to discuss the role and clinical significance of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the deterioration of chronic hepatitis B patients superinfected with acute hepatitis E. Serum TNF-α and IL-6 in chronic hepatitis B patients superinfected with acute hepatitis E (n=30), chronic hepatitis B patients (n=20), acute hepatitis E patients(n=20), and healthy volunteers (n=20) were detected by enzyme-linked immunosorbent assay (ELISA). Main biochemical quantitative analyses of serum levels of alanine aminotransferase (ALT), aspartamine transferase (AST) and total bilirubin (TBIL), cholesterol ester (CHE), albumin (ALB),and prothrombin activity (PTA) were detected by automatic biochemical analyzer. Compared to that of chronic hepatitis B patients, acute hepatitis E patients, and healthy volunteers, the serum levels of TNF-α and IL-6 in chronic hepatitis B patients superinfected with acute hepatitis E were significantly increased (P <0.01). Compared to that of chronic hepatitis B patients and acute hepatitis E patients, the serum levels of ALT, AST and TBIL in chronic hepatitis B patients superinfected with acute hepatitis E were significantly increased (P <0.05), the serum levels of CHE, ALB and PTA reduced obviously (P <0.05). The serum levels of TNF-α and IL-6 in chronic hepatitis B patients superinfected with acute hepatitis E showed a significant positive correlation with ALT and TBIL and a significant negative correlation with PTA (P <0.05). TNF-α and IL-6 participate in the process of immune injury in chronic hepatitis B patients superinfected with acute hepatitis E. Detection of the serum levels of TNF-α and IL-6 has practical clinical value in determining the degree of liver injury and prognosis of chronic hepatitis B patients superinfected with acute hepatitis E.

2009 Vol. 4 (2): 88-91 [Abstract] ( 2458 ) [HTML 1KB] [PDF 167KB] ( 2228 )
92 LIU Jing-Ran*;Sun Zhi-Ping*;XU Tao;WU Yang; LI Dawen;QU Di
Detection of the ArlR expression in different growth phases of Staphylococcus epidermidis

Staphylococcus epidermidis (S. epidermidis) is an opportunistic pathogen that colonizes on the surface of human skin and in mucous membranes. It can form biofilms by adhering to indwelling medical devices, often causing biofilm-associated infection. Two-component signal transduction systems (TCSs) play an important role in modulating biofilm formation in bacteria. However, regulation mechanisms of TCSs in S. epidermidis are still poorly understood. In this study, the expression of response regulator ArlR of arlRS TCS in S. epidermidis growth phases was investigated. The prokaryotic expression plasmid pET28a-arlR was constructed, and ArlR protein was expressed and purified. The purified ArlR was used to immunize mice for inducing anti-ArlR antibodies. The titers of anti-ArlR in the immune sera were over 1:100000, as determined by immune dot blot technique. ArlR expression in the different growth phases in bacteria was detected by Western blot analysis. Results showed that the expression level of ArlR was lowest at 2-hour culture and highest at 4-hour culture, and declined at 6-hour and 10-hour cultures. Western blot analysis results were confirmed by the transcriptional levels of arlR determined by real-time reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. It would help to get additional insight in to arlRS TCS regulation functions in the formation of biofilms in S. epidermidis.

2009 Vol. 4 (2): 92-96 [Abstract] ( 10710 ) [HTML 1KB] [PDF 293KB] ( 2564 )
97 WANG Chuan-Qing1;HE Lei-Yan1;WANG Ai-Min1;ZHANG Wen-Hong2
Characteristics of bacterial pathogens associated with community-acquired pediatric diarrhea in Shanghai in 2007
The present study was aimed to survey the prevalence of enteric bacterial pathogens associated with acute community-acquired diarrhea in children in Shanghai. Two thousand eight hundred and seventy-one (n=2871) children with acute community-acquired diarrhea were included in this study. Bacterial pathogens were collected from stool samples and isolated by culture methods. Bacteria were identified by API system and serologic testing. The following enteric pathogens were detected: Shigella, Escherichia coli (E.coli), Salmonella, Vibrio parahaemolyticus, Vibro cholerae, Aeromonas, and Yersinia enterocolitica. The data showed that the isolation rate of Campylobacter was 11.0% (172/1556) and the prevalent peak of Campylobacter was in April (P<0.001). Children younger than 4 years were the most susceptible (P<0.05). The isolation rate of Shigella was 3.2% and the predominant serotype of Shigella was S.flexneri (63.7%). The isolation rate of E.coli causing diarrhea was 1.0%, among which, enteropathogenic E.coli (EPEC)accounted for 70.0% (21/30) and the predominant serotype of EPEC was O55/K59. Our data indicate that Campylobacter, Shigella and E.coli causing diarrhea are the predominant pathogenic bacteria associated with community-acquired pediatric diarrhea in Shanghai in 2007.It is implied that the isolation of Campylobacter and E.coli causing intestinal diseases should be surveyed routinely.
2009 Vol. 4 (2): 97-101 [Abstract] ( 2930 ) [HTML 1KB] [PDF 111KB] ( 2218 )
 
病例分析
101 YIN Ke-Shan;OU Qiang, SHEN Yong;LU Hong-Zhou
First import case report of the novel influenza type A H1N1 virus in Shanghai
A novel influenza type A H1N1 virus causes acute respiratory infectious disease. Its clinical symptoms include fever, nasal discharge, sore throat, cough, headache, and diarrhea. Antiviral drugs, such as oseltamivir and zanamivir, are effective treatments. In this article, we report on the first import case of this novel influenza type A H1N1 virus infection in Shanghai, in order to improve the ability of the medical community to recognize this novel influenza.
2009 Vol. 4 (2): 101-102 [Abstract] ( 2382 ) [HTML 1KB] [PDF 46KB] ( 2149 )
 
综述
103 TANG Guo-Fang;LI Zhong-Yu;WU Yi-Mou
Mechanism of interferon-γ-mediated anti-Chlamydia infection
Chlamydia is an intracellular bacterium that infects many vertebrates, including humans. Previous studies have shown that interferon-γ(IFN-γ) plays an important role in defense against Chlamydia infection. IFN-γ-mediated anti-Chlamydia effector mechanisms may include the exhaustion of tryptophan, the induction of iron loss, and/or the activation of inducible nitric oxide synthase (iNOS). However, Chlamydia has evolved to develop mechanisms to escape IFN-γ functions. In this review, we will discuss IFN-γ-mediated effector mechanisms in the control of Chlamydia infection.
2009 Vol. 4 (2): 103-107 [Abstract] ( 2456 ) [HTML 1KB] [PDF 116KB] ( 2491 )
108 LI Qiong;WU Shu-Yan;HUANG Rui
Role of autophagy in bacterial infections and immune responses
Autophagy is an important form of programmed cell death that regulates the growth and development of cells. It acts as a ‘two-edge sword’. On one side, autophagy eliminates microbes; on the other, many bacteria have developed distinct mechanisms to regulate and interfere with autophagy for their own replication and survival. Autophagy is an important event in the innate immune response. It can initiate a response to bacteria and bacterial toxins through Toll-like receptor mechanisms or mucosal immune system. Effector cells of the cellular immune system can regulate autophagy by secreting different cytokines, allowing the organism to re-tune its adaptive immune response. Autophagy may play a pivotal role in regulating the immune polarization of Th1/Th2 in fighting intracellular bacteria.
2009 Vol. 4 (2): 108-111 [Abstract] ( 3087 ) [HTML 1KB] [PDF 77KB] ( 5364 )
112 Wang Xue-Qin1;Zhou Dao-Guo2
Salmonella invasion
Salmonella enterica serovar Typhimurium encodes two type Ⅲ protein secretion/translocation systems within the pathogenicity island 1 (SPI-1) and island 2 (SPI-2). These translocation systems inject a panel of bacterial effector proteins into host cells to promote bacterial entry into the host cells via the“trigger”mechanism. The translocated effectors exploit the host actin cytoskeleton leading to macropinocytosis and bacteria entry. In this review, we present a workingn model based on recent advances in understanding contributions from individual Salmonella effectors. First, activation of the type Ⅲ secretion system and the delivery of bacterial effector proteins(Ⅰ). Injection of the exchange factor SopE and the inositol polyphosphatase SopB results in the activation of CDC42 and Rac1(Ⅱ), leading to the recruitment of ruffling-associated molecules. SipA and SipC function to lower the critical concentration of actin, stimulating the bundling activity of plastin and stabilizing fibrous actin (F-actin), and nucleating the actin assembly (Ⅲ). SopB promotes membrane fission process by decreasing the local concentration of PIP2 at the base of the membrane ruffles and by recruiting VAMP8 (Ⅳ). The combined activities of these effectors result in a localized and pronounced outward extension of the membrane ruffles, resulting in the engulfment of Salmonella in an enclosed membrane compartment. Salmonella delivers another effector protein, SptP, which reverses the activation of these small G proteins by stimulating their intrinsic GTPase activity and therefore facilitating cell recovery (Ⅴ).
2009 Vol. 4 (2): 112-128 [Abstract] ( 2564 ) [HTML 1KB] [PDF 3967KB] ( 2242 )
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