anaphylatoxin


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anaphylatoxin

 [an″ah-fil´ah-tok″sin]
a substance produced by complement activation that causes the release of histamine and other mediators of immediate hypersensitivity from basophils and mast cells, thereby producing signs and symptoms of immediate hypersensitivity (anaphylaxis) without involvement of IgE.

an·a·phyl·a·tox·in

(an'ă-fil-ă-tok'sin),
Low molecular weight cleavage products (C3a, C4a, and C5a); generated by the activation of the complement cascade. They are proinflammatory; can cause permeability, smooth muscle contraction, and mask cell degranulation.
Synonym(s): anaphylotoxin
[anaphylaxis + toxin]

anaphylatoxin

/ana·phyl·a·tox·in/ (-fil´ah-tok″sin) a substance produced in blood serum during complement fixation which serves as a mediator of inflammation by inducing mast cell degranulation and histamine release; on injection into animals, it causes anaphylactic shock.

anaphylatoxin

[an′əfī′lətok′sin]
a fragment (C3a, C4a, or C5a) that is produced during the pathways of the complement system. Along with other mechanisms, it mediates changes in mast cells leading to the release of histamine and other immunoreactive or inflammatory reactive substances. If the degranulation of mast cells is too strong, it can cause allergic reactions.

anaphylatoxin

(1) Any antigen that reacts with an IgE and precipitates an anaphylactic reaction by stimulating histamine release.
(2) Activated complement fragments (C3a, C4a and C5a) that bind to mast cells and basophils and trigger the release of inflammatory mediators.

an·a·phyl·a·tox·in

, anaphylotoxin (an'ă-fil'ă-tok'sin, an'ă-fil'ō-tok'sin)
1. A substance postulated to be the immediate cause of anaphylactic shock and that is assumed to result from the in vivo combination of specific antibody and the specific sensitizing material.
2. The small fragment (C3a) split from the third component (C3) of complement, which produces a local wheal following intracutaneous injection.

anaphylatoxin

Any substance that can directly cause degranulation of MAST CELLS thereby bringing about an acute allergic reaction.

anaphylatoxin

a substance produced in blood serum when complement is activated; serves as a mediator of inflammation by inducing mast cell degranulation, histamine release and increased vascular permeability, and on injection into animals, it causes anaphylactic shock.

anaphylatoxin inhibitor
a specific serum carboxypeptidase, one of the complement proteins.
References in periodicals archive ?
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 [17].
The two lowest bands (Figure 2, bands 1 and 2) likely correspond to the SELDI-TOF peaks with m/z 9,100 and 10,100 and were identified by database searches as anaphylatoxin C3a and calgranulin A.
In addition, serum anaphylatoxin activity was searched for in this patient and her children, all of whom had well-documented hereditary angioedema.
Anaphylatoxin and immune complexes work additively: that's why C5-deficient animals are highly resistant to the induction of immune complex-induced arthritis.
C3a, together with C4a and C5a, the small fragments of C3, C4, and C5, respectively, are called the complement anaphylatoxins.
3; also known as lysine carboxypeptidase, kininase I, anaphylatoxin inactivator, or plasma carboxypeptidase B) and the more recently identified carboxypeptidase U (CPU; EC 3.
9]), anaphylatoxins (C3a, C4a, and C5a), and fibrinopeptides A and B (19).
These protein fragments (C3a and C5a) are potent inflammatory mediators and also act as anaphylatoxins, directly triggering mast cells.
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).
Histamine-releasing factors from macrophages (4) or T lymphocytes (5) and anaphylatoxins from complement system activation also lead to activation and subsequent degranulation of mast cells (6).