CD46 accelerates macrophage-mediated host susceptibility to meningococcal sepsis in a murine model

2016 ◽  
Vol 47 (1) ◽  
pp. 119-130 ◽  
Author(s):  
Xiao Wang ◽  
Ding Zhang ◽  
Mikael Sjölinder ◽  
Yi Wan ◽  
Hong Sjölinder
Keyword(s):  
Murine Model ◽  
Host Susceptibility ◽  
Meningococcal Sepsis

Factor V Level Affects the Host Susceptibility to Group A Streptococcal Infection.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 25-25
Author(s):  
Hongmin Sun ◽  
Angela Yang ◽  
Xixi Wang ◽  
David Ginsburg
Keyword(s):  
Bacterial Infection ◽  
Murine Model ◽  
Streptococcal Infection ◽  
Host Susceptibility ◽  
Selective Agents ◽  
Transgenic Murine Model ◽  
Group A ◽  
Human Plasminogen ◽  
Fv Leiden

Abstract Group A streptococci (GAS), a common human pathogen, secrete streptokinase (SK), which activates the host’s plasminogen (PLG). SK is highly specific for human PLG, exhibiting little or no activity against other mammalian species. We demonstrated the major role of the PLG/SK interaction in GAS pathogenicity using a transgenic murine model expressing human plasminogen with increased susceptibility to human pathogenic streptococci. We hypothesize that GAS hijack the host fibrinolytic system in order to circumvent local thrombosis for systemic spread. Markedly increased mortality was also observed following GAS injection in C57BL/6J mice treated with the snake venom Ancrod, which proteolytically degrades plasma fibrinogen, supporting the critical roles of coagulation in host/pathogen interaction. However, fibrinogen also plays important roles in inflammation and immune response, it is necessary to use independent genetic models to further test the impact of coagulation in host defense against bacterial infection. The effect of variations in FV on mouse susceptibility to streptococcal infection was tested. We established a mouse model with low plasma FV level. These mice have a slightly increased bleeding time, though otherwise phenotypically normal. Subjected to streptococcal infection, these mice exhibited significantly increased mortality than wildtype controls, suggesting that the decreased thrombotic tendency in the low FV mice increases host susceptibility to infection. FV Leiden is a common prothrombotic mutation among Caucasian population with an incidence between 4% and 6%. Previous studies from Kerlin et al demonstrated the FV Leiden conferred survival advantage in patients with severe sepsis and in mice challenged with endotoxin. This may be an example of balanced gene polymorphism that maintains the FV Leiden mutant in the general gene pool by selection of bacterial infections. In order to identify the selective agents responsible for the prevalence of FV Leiden mutation, we took advantage of our plasminogen transgenic murine model for streptococcal infection to test whether streptococci is one of the selective agents. Human plasminogen transgene was introduced into FV Leiden background and the susceptibility to streptococcal infection was measured. No significant improvement of survival was observed in the FV Leiden mouse comparing with the wildtype control. Thus, streptococcal infection is not the selective agent for the prevalence of FV Leiden mutation. These observations highlight the potential role of variations in blood coagulation factors in host susceptibility to bacterial infection.

Anti-OX40ligand treatment as a novel therapeutic strategy in a murine model of colitis

2001 ◽  
Vol 120 (5) ◽  
pp. A685-A685
Author(s):  
B SINGH ◽  
V MALMSTROM ◽  
F POWRIE
Keyword(s):  
Murine Model ◽  
Therapeutic Strategy ◽  
Novel Therapeutic

404: Immune Mediated Survival Advantage and Primary Tumor Control of Cryoablation Compared to Nephrectomy in a Murine Model of Advanced Renal Cancer

2006 ◽  
Vol 175 (4S) ◽  
pp. 132-132 ◽  
Author(s):  
Sean P. Hedican ◽  
Eric R. Wilkinson ◽  
Thomas F. Warner ◽  
Fred T. Lee ◽  
Stephen Y. Nakada
Keyword(s):  
Renal Cancer ◽  
Murine Model ◽  
Primary Tumor ◽  
Survival Advantage ◽  
Tumor Control ◽  
Advanced Renal Cancer ◽  
Immune Mediated

Disseminated intravascular coagulation in meningococcal sepsis

2003 ◽  
Vol 23 (03) ◽  
pp. 125-130 ◽  
Author(s):  
S. Zeerleder ◽  
R. Zürcher Zenklusen ◽  
C. E. Hack ◽  
W. A. Wuillemin
Keyword(s):  
Organ Dysfunction ◽  
Disseminated Intravascular Coagulation ◽  
Skin Necrosis ◽  
Multiple Organ ◽  
Meningococcal Sepsis ◽  
Multiple Organ Dysfunction ◽  
Intravascular Coagulation ◽  
Therapeutic Concepts ◽  
New Therapeutic Concepts ◽  
Coagulation And Fibrinolysis

SummaryWe report on a man (age: 49 years), who died from severe meningococcal sepsis with disseminated intravascular coagulation (DIC), multiple organ dysfunction syndrome and extended skin necrosis. We discuss in detail the pathophysiology of the activation of coagulation and fibrinolysis during sepsis. The article discusses new therapeutic concepts in the treatment of disseminated intravascular coagulation in meningococcal sepsis, too.

Sign in / Sign up

Export Citation Format

Share Document