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Inducing Meningococcal Meningitis Serogroup C in Mice via Intracisternal Delivery
Published on: November 5, 2019
Mice deficient in ficolin, a lectin complement pathway recognition molecule, are susceptible to Streptococcus
Yuichi Endo1, Minoru Takahashi, Daisuke Iwaki
1Department of Immunology, Fukushima Medical University School of Medicine, Fukushima 960-1295, Japan. yendo@fmu.ac.jp
Abstract:
Mannose-binding lectin (MBL) and ficolin are complexed with MBL-associated serine proteases, key enzymes of complement activation via the lectin pathway, and act as soluble pattern recognition molecules in the innate immune system. Although numerous reports have revealed the importance of MBL in infectious diseases and autoimmune disorders, the role of ficolin is still unclear. To define the specific role of ficolin in vivo, we generated model mice deficient in ficolins. The ficolin A (FcnA)-deficient (Fcna(-/-)) and FcnA/ficolin B double-deficient (Fcna(-/-)b(-/-)) mice lacked FcnA-mediated complement activation in the sera, because of the absence of complexes comprising FcnA and MBL-associated serine proteases. When the host defense was evaluated by transnasal infection with a Streptococcus pneumoniae strain, which was recognized by ficolins, but not by MBLs, the survival rate was significantly reduced in all three ficolin-deficient (Fcna(-/-), Fcnb(-/-), and Fcna(-/-)b(-/-)) mice compared with wild-type mice. Reconstitution of the FcnA-mediated lectin pathway in vivo improved survival rate in Fcna(-/-) but not in Fcna(-/-)b(-/-) mice, suggesting that both FcnA and ficolin B are essential in defense against S. pneumoniae. These results suggest that ficolins play a crucial role in innate immunity against pneumococcal infection through the lectin complement pathway.
Insights
Ficolins, key innate immune molecules, are crucial for defense against Streptococcus pneumoniae infection. Mice lacking ficolins showed reduced survival, highlighting their essential role in the lectin complement pathway.
Area of Science:
- Immunology
- Infectious Disease
Background:
- Mannose-binding lectin (MBL) and ficolins are pattern recognition molecules in the innate immune system, activating complement via the lectin pathway.
- While MBL's role in disease is known, ficolin's function remains unclear.
Purpose of the Study:
- To define the in vivo role of ficolins in host defense.
- To investigate ficolin's involvement in Streptococcus pneumoniae infection.
Main Methods:
- Generated ficolin A (FcnA)-deficient (Fcna(-/-)) and FcnA/ficolin B double-deficient (Fcna(-/-)b(-/-)) mice.
- Evaluated host defense via transnasal infection with Streptococcus pneumoniae.
- Assessed complement activation and survival rates in deficient mice.
Main Results:
- Ficolin-deficient mice showed reduced complement activation and significantly lower survival rates after S. pneumoniae infection.
- Reconstitution of the FcnA-mediated lectin pathway improved survival in Fcna(-/-) mice, but not in Fcna(-/-)b(-/-) mice.
- Both FcnA and ficolin B are essential for defense against S. pneumoniae.
Conclusions:
- Ficolins play a critical role in innate immunity against pneumococcal infection.
- Ficolins function through the lectin complement pathway to protect against S. pneumoniae.
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