Vibrio cholerae bengal serogroup-O139 capsular polysaccharide and protein conjugates thereof

• 1. 一种霍乱弧菌O139荚膜多糖结合疫苗及其制备方法 [P] . 中国专利： CN102085363B . 2013.06.26
• 2. 一种霍乱弧菌O139荚膜多糖结合疫苗及其制备方法 [P] . 中国专利： CN102085363A . 2011-06-08
• 3. VIBRIO CHOLERAE BENGAL SEROGROUP-0139 CAPSULAR POLYSACCHARIDE, PROTEIN CONJUGATES THEREOF AND ANTIBODIES INDUCED THEREBY [P] . 世界知识产权组织专利： WO9515178A1 . 1995-06-08

  机译： 霍乱弧菌孟加拉血清型0139胶囊状多糖，蛋白质与其结合，并因此而产生抗体

• 4. (vibrio cholerae) bengal serogroup-0139 capsular polysaccharide, protein conjugates thereof and antibodies induced thereby [P] . AU1179695A . 1995-06-19

  机译： （霍乱弧菌）孟加拉血清群-0139荚膜多糖，其蛋白缀合物和由此诱导的抗体

• 5. PEPTIDES MIMICKING VIBRIO CHOLERAE O139 CAPSULAR POLYSACCHARIDE AND THEIR USE TO ELICIT PROTECTIVE IMMUNE RESPONSE [P] . AU2003253301A1 . 2004-07-14

  机译： 模仿霍乱弧菌O139多糖的多肽及其在引起保护性免疫反应中的用途

• 1. Survival and proliferation of the lysogenic bacteriophage CTXΦ in Vibrio cholerae [J] . Fenxia, Fan, Biao, 中国病毒学：英文版 . 2015,第001期
• 2. SYNTHESIS OF THE REPEATING UNIT OF THE O-ANTIGENIC POLYSACCHARIDE OF Vibrio cholerae O-10 [C] . Sarkar S., Chatterjee N., Gupta S. J International Carbohydrate Symposium . 2013
• 3. The capsular polysaccharide of Vibrio cholerae O139 Bengal: Induction and modulation of host-cell mediated immune responses. [D] . Trigiani-Fernandez, Ellen Ruth. 2001
• 4. Vibrio cholerae O139 Conjugate Vaccines: Synthesis and Immunogenicity of V. cholerae O139 Capsular Polysaccharide Conjugates with Recombinant Diphtheria Toxin Mutant in Mice [O] . Zuzana Kossaczka, Joseph Shiloach, Virginia Johnson, 2000
• 5. Vibrio cholerae O139 Conjugate Vaccines: Synthesis and Immunogenicity of V. cholerae O139 Capsular Polysaccharide Conjugates with Recombinant Diphtheria Toxin Mutant in Mice [O] . Kossaczka, Zuzana, Shiloach, Joseph, Johnson, Virginia, 2000
• 6. Isolation and Characterization of a Vibrio cholerae Strain Unable to Secrete Cholera Toxin, and Cloning and Characterization of Genes from Vibrio cholerae that Confer a Congo Red Dye Binding Phenotype on Escherichia coli. [R] . Coker, C. 1996

• 1. BACKGROUND： Vibrio vulnifi cus inside the body could activate the NF-!B signaling pathwayand initiate the inflammatory cascade. The lung is one of the earliest organs affected by sepsisassociated with acute lung injury. High mobility group protein B1 （HMGB1） is an important late-actingpro-infl ammatory cytokine involving in the pathophysiology of sepsis. It is also involved in the injuryprocess in the lung, liver and intestine. There has been no report on the involvement of HMGB1 inVibrio vulnifi cus sepsis-induced lung injury.METHODS： Sixty rats were randomly divided into a normal control group （group A, n=10） anda Vibrio vulnificus sepsis group （group B, n=50）. Sepsis was induced in the rats by subcutaneousinjection of Vibrio vulnificus （concentration 6×108 cfu/mL, volume 0.1 mL/100g）） into the left lowerlimbs. The rats in group B were sacrifi ced separately 1, 6, 12, 24, and 48 hours after the infection.Their lungs were stored as specimens, lung water content was measured, and lung pathology wasobserved under a light microscope. The expressions of the HMGB1 gene and protein in the lungswere detected by RT-PCR and Western blot. Data were analyzed with one-way analysis of variance（ANOVA） and the LSD method for pair-wise comparison between the two groups. P〈0.05 wasconsidered statistically signifi cant.RESULTS： Compared to group A （0.652±0.177）, HMGB1 mRNA expression in the lungs ofgroup B was signifi cantly higher at 0 hour （1.161±0.358, P=0.013）, 24 hours （1.679±0.235, P=0.000）,and 48 hours （1.258±0.274, P=0.004） （P〈0.05）, and peaked at 24 hours. Compared to group A（0.594±0.190）, HMGB1 protein expression at 6 hours （1.408±0.567, P=0.026） after infection wassignificantly increased （P〈0. 05）, and peaked at 24 hours （2.415±1.064, P=0.000） after infection.Compared to group A （0.699±0.054）, lung water content was significantly increased at 6 hours（0.759±0.030, P=0.001）,12 hours （0.767±0.023, P=0.000）, 24 hours （0.771±0.043, P=0.000） and 48hours （0.789±0.137, P=0.000） after infection （P〈0.05）. Compared to group A, pathological changesat 12 hours in group B indicate marked pulmonary vascular congestion, interstitial edema andinfl ammatory infi ltration. Alveolar cavity collapse and boundaries of the alveolar septum could not beclearly identifi ed.CONCLUSION： Vibrio vulnifi cus sepsis can lead to injury in rat lungs, and increased HMGB1expression in lung tissue may be one of the mechanisms for injury from Vibrio vulnifi cus sepsis. [J] . Qiao-meng Qiu ,Zhong-wang Li ,Lu-ming Tang . 世界急诊医学杂志(英文) . 2011,第4期
• 2. Isolation, Identification and Antimicrobial Susceptibility Profile Analysis of iVibrio cholerae/iO1 from Stool Samples of Bangladesh [J] . Muhammad Ekhlas Uddin ,Tanzina Akter ,Papia Sultana . 微生物学（英文） . 2018,第3期
• 3. Survival and proliferation of the lysogenic bacteriophage CTXφ in Vibrio cholerae [J] . Fenxia Fan ,Biao Kan . 中国病毒学 . 2015,第001期
• 4. Acquisition and dissemination mechanisms of CTXΦ in Vibrio cholerae： New paradigm for dif residents [J] . Bhabatosh Das1 ,G Balakrish Nair1 ,Rupak K Bhadra2 . 世界医学遗传学杂志 . 2014,第002期
• 5. 北京港口水产中非O1/O139群霍乱弧菌MLST分型研究 [C] . Fu Pubo ,付溥博 ,Zhang Lin . 2018分析检测技术与仪器发展创新论坛 . 2018
• 6. 霍乱弧菌O139血清群mshA基因的克隆、表达及其融合蛋白免疫性的初步研究 [A] . 尹铁球 . 2006