demonstrated that the anaphylatoxins
C3a are essential for liver regeneration.
and infectious and non-infectious inflammatory diseases.
When the complement system is activated, the generation of anaphylatoxins
C3a and C5a can degranulate mast cells.
Subsequent steps of the complement cascade lead to formation of several effector molecules, including opsonization of pathogens, formation of the membrane attack complex inducing osmotic lysis of cells, and recruitment and activation of inflammatory cells by the anaphylatoxins
complement C3a and C5a (25).
In addition, HD is considered an important source of oxidative stress in ESRD, due to the production of interleukins and anaphylatoxins
(powerful activators of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase) during HD sessions.
Through interactions with C3a and C5a receptors, these anaphylatoxins
trigger the production of pro-inflammatory innate immune proteins, such as cytokines, in leukocytes and thus contribute to inflammation (Cohen et al.
Anaphylactic or anaphylactoid reactions may also be secondary to complement activation with liberation of anaphylatoxins
Excessive activity of this pathway-leads to the presence of high circulating levels of C3a and C5a, potent anaphylatoxins
involved in local inflammatory responses .
These protein fragments (C3a and C5a) are potent inflammatory mediators and also act as anaphylatoxins
, directly triggering mast cells.
In the mammalian cell, Anaphylatoxins
are able to trigger j) degranulation (release of substances) of endothelial cells, mast cells or phagocytes, which produce a local inflammatory response .
C3a, C4a and C5a, known as anaphylatoxins
, can release vasoactive amines and lysosomal enzymes, enhance vascular permeability, and cause smooth muscle to contract (Guo and Ward 2005).
Although inhibition of the complement system is an absolute necessity for normal pregnancy, there is an increase in the concentrations of the anaphylatoxins
C3a, C4a and C5a in the maternal circulation (1).