期刊
CRITICAL REVIEWS IN IMMUNOLOGY
卷 35, 期 3, 页码 173-184出版社
BEGELL HOUSE INC
DOI: 10.1615/CritRevImmunol.2015012177
关键词
pneumococci; complement; C1q; colonization; adherence and invasion; host-pathogen interaction
类别
资金
- Swedish Research Council [K2012-66X-14928-09-5]
- Foundation of Torsten Soderberg
- Foundation of Osterlund
- Foundation of Greta and Johan Kock
- Foundation of King Gustav V's 80th Anniversary
- Foundation of Knut and Alice Wallenberg
- Foundation of Inga-Britt and Arne Lundberg
- Foundation of Ake Wiberg
- Foundation of Royal Physiographic Society in Lund
- Skane University Hospital
- Swedish Society for Medical Research
The fight between a human host and a bacterial pathogen is highly complicated; each party tries to outshine the other in the race for survival. In humans, the innate immune system-in particular the complement system-functions as the first line of defence against invading pathogens. During the course of evolution, however, pathogens, in order to survive and perpetuate within a host, developed multiple strategies to counteract the host complement system and to colonize. One such pathogen is Streptococcus pneumoniae (pneumococcus), a gram-positive bacterial pathogen often commensal in the human respiratory tract. Depending on the host's susceptibility, pneumococci can transform into an infectious agent, disseminating within the human host and causing mild to life-threatening diseases. This transition from commensal to infectious agent is a highly complex process, and understanding of this mechanism is essential in controlling the pathogenicity of pneumococci. Using its intricate arsenal of weapons, such as surface-presenting adhesins as well as recruitment of host factor, pneumococci successfully colonize the host, a prerequisite for establishing infection. This review describes C1q, the first subunit of the classical complement pathway, and its role in pneumococcus-host interactions, whereby pneumococci exploit C1q as a molecular bridge facilitating host cellular adherence and invasion, a function not akin to the role of C1q in the defence mechanism.
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