Mice Deficient in Ficolin, a Lectin Complement Pathway Recognition Molecule, Are Susceptible to Streptococcus pneumoniae Infection | Zendy

Yuichi Endo | Zendy; Minoru Takahashi | Zendy; Daisuke Iwaki | Zendy; Yumi Ishida | Zendy; Naomi Nakazawa | Zendy; Toshihisa Kodama | Zendy; Tomohiro Matsuzaka | Zendy; Kazuko Kanno | Zendy; Yu Liu | Zendy; K. Tsuchiya | Zendy; Ikuo Kawamura | Zendy; Masahito Ikawa | Zendy; Satoshi Waguri | Zendy; Ikuo Wada | Zendy; Misao Matsushita | Zendy; Wilhelm Schwaeble | Zendy; Teizo Fujita | Zendy

Open Access

Mice Deficient in Ficolin, a Lectin Complement Pathway Recognition Molecule, Are Susceptible to Streptococcus pneumoniae Infection

Author(s) -

Yuichi Endo,

Minoru Takahashi,

Daisuke Iwaki,

Yumi Ishida,

Naomi Nakazawa,

Toshihisa Kodama,

Tomohiro Matsuzaka,

Kazuko Kanno,

Yu Liu,

K. Tsuchiya,

Ikuo Kawamura,

Masahito Ikawa,

Satoshi Waguri,

Ikuo Wada,

Misao Matsushita,

Wilhelm Schwaeble,

Teizo Fujita

Publication year - 2012

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.1200836

Subject(s) - ficolin , lectin pathway , mannan binding lectin , complement system , proteases , lectin , biology , innate immune system , classical complement pathway , streptococcus pneumoniae , microbiology and biotechnology , alternative complement pathway , collectin , nod2 , c type lectin , serine , immunology , immune system , enzyme , biochemistry , antibiotics

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.

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