14th ICID - Poster Abstracts - International Society for Infectious ...

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When citing these abstracts please use the following reference: Author(s) of abstract. Title of abstract [abstract]. Int J Infect Dis 2010;14S1: Abstract number. Please note that the official publication of the International Journal of Infectious Diseases 2010, Volume 14, Supplement 1 is available electronically on http://www.sciencedirect.com Final Abstract Number: 73.010 Session: Animal Models, Pathogenesis & Host Defenses Date: Friday, March 12, 2010 Time: 12:30-13:30 Room: Poster & Exhibition Area/Ground Level Type: Poster Presentation An animal model to study antimicrobial effects on community-acquired methicillin-resistant Staphylococcus aureus infection M. Ip, E. T. Y. Leung, C. Wong, K. To Chinese University of Hong Kong, , Shatin, Hong Kong, China Background: Outbreaks of Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) infections have been reported worldwide, and a main concern is the severity of infection with fatal necrotizing pneumonia and toxic shock. Studies showed that the expression of virulence proteins by Staphylococcus aureus depends on the strain types and could be modulated by different agents including antibiotics. The objective of the study was to establish a murine infection model to study the in-vivo effects of commonly used antimicrobials on the severity of CA-MRSA pneumonia. Methods: 6-to-8-week-old BALB/c mice were divided into groups of six in individually ventilated cages and injected with intranasal injection of a representative strain of CA-MRSA. The bacterial inoculum was titrated with varying concentration ranging 1 x 107 – 5 x 108 cfu, with controls receiving same volume of broth medium. Mice were sacrificed on Day 2, 3 and 4 of infection and the lungs were dissected, placed in formalin, embedded in paraffin blocks and sectioned for histological examination. The severity of pneumonia was scored according to size of leukocyte infiltration and level of alveolar integrity and epidermis damage. Sub-inhibitory concentrations of antimicrobial agents (half of MIC per body weight) of vancomycin, ciprofloxacin, gentamicin were administered at different timepoints after bacterial inoculation. Results: The severity of pneumonia varies with the bacterial inocula titrated. All infected mice developed pneumonia after 24 hours of infection after inoculation of at least 1 x 108 cfu bacteria. The endpoint for outcome of pneumonia was interpreted at 24 hours. Incubation of 48 and 72 hours led to increasing mortality of mice and masked the histological effects of pneumonia. The most significant effects was in the ciprofloxacin group, with 33% (2/6) mice in ciprofloxacintreated group died and the the remainder (4/6) developed severe pneumonia of Grade 5 histologically (in terms of size and extent of necrotizing lesions) than the infected-control group. The non-infected-control group remained healthy. Conclusion: A murine model for CA-MRSA pneumonia to study effects of different drugs was established. The choice of antimicrobials that minimizes release of toxins and reduces the severity of pneumonia is an invaluable approach in improving treatment outcome in CA-MRSA infections.
When citing these abstracts please use the following reference: Author(s) of abstract. Title of abstract [abstract]. Int J Infect Dis 2010;14S1: Abstract number. Please note that the official publication of the International Journal of Infectious Diseases 2010, Volume 14, Supplement 1 is available electronically on http://www.sciencedirect.com Final Abstract Number: 73.011 Session: Animal Models, Pathogenesis & Host Defenses Date: Friday, March 12, 2010 Time: 12:30-13:30 Room: Poster & Exhibition Area/Ground Level Type: Poster Presentation Increased killing of liver NK cells by Fas/FasL and NKG2D/NKG2DL contributes to hepatocyte necrosis in virus-induced liver failure T. Chen 1 , Y. Zou 1 , M. Han 1 , H. Wang 1 , W. Yan 1 , G. Song 1 , Z. Wu 1 , X. Wang 1 , C. Zhu 1 , X. Luo 2 , Q. Ning 1 1 Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, Hubei, China, 2 Tonji Hospital, Wuhan, China Background: The role of liver NK cells in virus-induced severe viral hepatitis and subsequently hepatic failure is not well defined. Methods: In this study, we investigated the role of liver NK cells in the development of hepatocyte necrosis in fulminant hepatic failure (FHF) and acute-on-chronic liver failure (ACLF) due to viral infection. A mouse model of FHF induced by murine hepatitis virus strain 3 (MHV-3) was used to study the role of liver NK cells. Samples from patients with hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) were examined. Results: Following MHV-3 infection, the number of NK cells in livers of Balb/cJ mice increased markedly, peaked at 48 h post-infection, and remained at a high level until sacrifice. In peripheral blood, spleen, and bone marrow, this number decreased significantly. Expression of CD69, cytotoxic activity, and intracellular IFN- and TNF- production by liver NK cells at 48 h postinfection were all significantly upregulated. Highly activated liver NK cells were cytotoxic to MHV- 3-infected hepatocytes and this effect was markedly inhibited by anti-FasL plus anti-NKG2D monoclonal antibodies. Furthermore, the accumulation of hepatic NK cells and increase in the expression of natural cytotoxicity receptors (NKP30 and NKP46) on the peripheral NK cells from patients with HBV-ACLF were correlated with disease progression. Conclusion: These results indicate the pivotal involvement of NK cells in the pathogenesis of FHF and HBV-ACLF, and the synergetic effect of Fas-FasL and NKG2D-NKG2DL pathway in liver NK cell mediation of hepatocyte toxicity.
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