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anaphylactoid reaction 40 anaphylaxis
Antibody Concentration in Serum
PRIMARY SECONDARY
Logarithmic
increase
IgM
Steady state
Total Ab
IgG
(immediate hypersensitivity) reaction following an antigen
that has been systemically administered. This allergic reaction
is a consequence of the binding of antigen to immunoglobulin
E (IgE) antibodies on mast cells in the connective
tissue throughout the body, resulting in a disseminated
release of inflammatory mediators.
anaphylactoid reaction
A response resembling anaphylaxis, except that it is not attributable
to an allergic reaction mediated by immunoglobulin E
(IgE) antibody. It is due to the nonimmunologic degranulation
of mast cells such as that caused by drugs or chemical
compounds such as aspirin, radiocontrast media, chymopapain,
bee or snake venom, or gum acacia that cause release of
the pharmacological mediators of immediate hypersensitivity
including histamine and other vasoactive molecules.
anaphylatoxin inactivator
A 300-kDa globulin carboxyl peptidase in serum that
destroys the anaphylatoxin activity of C5a, C3a, and C4a by
cleaving their carboxyl-terminal arginine residues.
anaphylatoxin inhibitor (anaINH)
A 300-kDa globulin carboxyl peptidase that cleaves the carboxyl
terminal arginine of anaphylatoxin. The enzyme acts
on all three forms, including C3a, C4a, and C5a, inactivating
rather than inhibiting them.
anaphylatoxins
Substances generated by the activation of complement that
leads to increased vascular permeability as a consequence of
the degranulation of mast cells with the release of pharmacologically
active mediators of immediate hypersensitivity.
These biologically active peptides of low molecular weight are
derived from C3, C4, and C5. They are generated in serum
during fixation of complement by antigen–antibody complexes,
immunoglobulin aggregates, etc. Small blood vessels,
mast cells, smooth muscles, and leukocytes in peripheral blood
are targets of their action. Much is known about their primary
structures. These complement fragments are designated C3a,
C4a, and C5a. They cause smooth muscle contraction, mast
cell degranulation with histamine release, increased vascular
permeability, and the triple response in skin. They induce
anaphylactic-like symptoms upon parenteral inoculation.
anaphylaxis
A shock reaction that occurs within seconds following the
injection of an antigen or drug or after a bee sting to which
a susceptible subject has immunoglobulin E (IgE)-specific
antibodies. There is embarrassed respiration due to laryngeal
Decline
Negative
phase
Hydrophobic site
IgM
Total Ab
Schematic representation of humoral and cellular events in the primary and secondary (anamnestic) antibody responses.
C3a/C3a57-77 –
Receptor interactions
Model C3a Peptide –
Receptor interactions
IgG
Effector site
Anaphylatoxin-receptor interactions.
and bronchial constriction and shock associated with decreased
blood pressure. Signs and symptoms differ among species
based on the primary target organs or tissues. Whereas IgE
is the anaphylactic antibody in humans, IgG1 may mediate
anaphylaxis in selected other species. Type I hypersensitivity
occurs following the crosslinking of IgE antibodies by a
specific antigen or allergen on the surfaces of basophils in the
blood or mast cells in tissues. This causes the release of the
pharmacological mediators of immediate hypersensitivity,
with a reaction occurring within seconds of contact with the
antigen or allergen. Eosinophils, chemotactic factor, heparin,
histamine, and serotonin, together with selected other substances,
are released during the primary response. Acute phase
reactants are formed and released in the secondary response.
Secondary mediators include slow-reacting substance of