Untitled - D Ank Unlimited

kininases 433 Klebsiella immunity
Raynaud’s phenomenon, and primary biliary cirrhosis
patients with features of systemic sclerosis.
kininases
An enzyme in the blood that degrades kinins to inactive
peptides. Inactivation occurs when any of the eight bonds
in the kinin are cleaved. Plasma contains two kininases.
Kininase I, or carboxy peptidase N, cleaves the C terminal
arginines of kinins and of anaphylatoxins. It differs from
pancreatic carboxy peptidase B with respect to molecular
weight, subunit structure, carbohydrate content, antigenic
properties, substrate specificity, and inhibition pattern. The
purified enzyme has a molecular weight of 280 kDa. The
site of synthesis of carboxy peptidase N is believed to be the
liver. Kininase II, a peptidyl dipeptidase, cleaves the C terminal
Phe–Args of kinins and also liberates angiotensin II
from angiotensin I. (Angiotensin is another vasoactive substance.)
The vascular endothelia of both lung and peripheral
vascular beds are rich in this enzyme. Peptidyl dipeptidase
is also present outside the circulatory system and has different
functions at these sites. Other enzymes with kininase
activity are present in the spleen and kidney (cathepsin) and
the endothelial cells of the gastrointestinal tract.
kininogens
The precursors of kinins, kininogens are glycoproteins
synthesized in the liver. Plasma kininogens comprise two,
possibly three, classes of compounds with species variation:
(1) Low molecular weight kininogens (LMKs) are
acidic proteins with molecular weights of about 57 kDa
and are susceptible to conversion into kinins by kininogenconverting
enzymes (kallikreins) of tissue origin. Forms
I and II represent the main plasma kininogens. (2) High
molecular weight kininogens (HMKs) are α glycoproteins
with molecular weights of 97 kDa that may be converted
into kinins both by plasma and tissue kallikreins. HMKs
exist in forms a and b that differ both in enzyme sensitivity
and generated kinin.
kinins
A family of straight chain polypeptides generated by
enzymatic hydrolysis of plasma α 2 globulin precursors,
collectively called kininogens. They exert potent vasomotor
effects, causing vasodilatation of most vessels in the body
but vasoconstriction of the pulmonary bed. They also cause
smooth muscle contraction and pain and increase vascular
permeability and promote the diapedesis of leukocytes.
Peptide kinins are released during inflammatory responses.
Kissmeyer-Nielsen, F.
Danish immunologist who sponsored the Sixth
Histocompatibility or Transplantation Workshop in 1975.
Six HLA-D alleles were described and the HLA-C locus
was demonstrated at the workshop.
Kitasato, Shibasaburo (1892–1931)
Co-discoverer, with Emil von Behring, of antitoxin antibodies.
Klebsiella immunity
Most healthy adults have high levels of natural resistance
against Klebsiella pneumoniae. The organism classically
induces lung infection, leading to a massive confluent lobar
consolidation with polymorphonuclear leukocytes, edema,
and abscess formation with extensive cavity formation.
Type-specific antibodies to the carbohydrate capsule are
critical to recovery. These antibodies that appear within 2
weeks following infection serve as opsonins to facilitate
the killing of this microorganism by phagocytes. Immunity
F. Kissmeyer-Nielsen.
Shibasaburo Kitasato.
to K. pneumoniae is long lasting. This microorganism is
believed to play a part in the development of ankylosing
spondylitis (AS) because AS patients develop high levels
of serum immunoglobulin A (IgA) against the microbe.
AS is associated with HLA-B27 antigen. The mechanism
has been claimed to be (1) molecular mimicry, in which
antibody against this antigen will bind to self-antigenic
determinants, leading to destructive immunity, or (2) that
Klebsiella plasmids may encode the formation of a bacterial
modifying factor that reacts with HLA-B27, rendering it
susceptible to immune attack. The main virulence factor of
the microbe is the capsule that helps it resist phagocytosis.
Despite reports of several enterotoxins, the main pathologic
effect is associated with the production of an endotoxin.
The extracellular toxic complex (ETC) contains endotoxin,
capsule, and protein and is lethal when injected into mice;
it leads to pathologic changes that resemble those produced
in K. pneumoniae lobar pneumonia in humans. Vaccines
are aimed at developing antibodies against capsule
K