Mediators of Inflammation in Allergic Hypersensitivity Flashcards
What are the major mediators of inflammation in allergic hypersensitivity
histamine, leukotrienes and PGD(2)
initial exposure to allergen —>
production of IgE antibodies
IgE antibodies bind to
mast cell receptors
subsequent exposure to primary allergen produces
cross linking of IgE on the surface of mast cells, triggering degranulation, release of histamine
followed by activation of eicosanoid biosynthesis
LTC(4), LTD(4), and PGD (2)
how does the IgE-Ag events play out, easy description
first allergen exposure causes generation of IgE
IgE sits in mast cell receptors
subsequent exposure to allergen causes IgE to bind immunogen on antibody, causing antibodies to cross link on surface of mast cell –> release of histamine
in terms of synthesis, what temporal aspect of histamine is different from eiocosinoids?
histamine is pre-synthesized and stored, awaiting release
heparin
keeps histamine stored in an inactive complex
Decarboxylase
converts dietary histidine into histamine
histamine is converted into two forms
imidazole aldehyde (inactive form) N-methyl histamine (inactive)
Diamine oxidase
converts histamine into imidazole aldehyde (inactive form)
Histamine N-methyl transferase
N-methyl histamine
Histamine vs Prostaglandins/Thromboxane/Leukotrienes
biosynthesis
histamine is made continuously and released instantaneously
PG/TG/LT are made on demand and released instantaneously
Histamine vs PG/TG/LT
life span
histamine: short lived, enzymatic inactivation
PG/TG/LT: short lived, enzymatic or spontaneous inactivation
physiology and pathology of histamine, pg, tg, lt
local, not systemic
unwarrented systemic exposures
