3.4 Complement system
When the host recognizes the danger signal, the complement system will
be activated. Complement can regulate the early innate immune response,
which is essential to protect the host from the uncontrolled
transmission of invasive pathogens. In the early stage of sepsis,
complement-related activated products will increase, such as
anaphylactoid toxins C3a, C4A, and c5a[35].
Complement activation products C3a, C5a, and c5b induce anti-microbial
response and pro-inflammatory effect through crosstalk with a variety of
signal transduction pathways. With the progress of complement
activation, continuous production of C5a may lead to congenital immune
paralysis, resulting in weakened inflammation and bacterial killing[36]. C5a and C5aR can induce an inflammatory
response and participate in multiple organ failures during sepsis.
Sommerfeld[37] et al. Found that in the mild to
moderate sepsis model, c5ar1 deficient mice had a higher survival rate
than the wild group, and the c5ar1 deficient group could also improve
liver injury in sepsis. In addition, complement-mediated neutrophil
dysfunction, apoptosis, and systemic inflammatory response also affect
the progression of sepsis.