Bacterial Pathogenesis, Molecular Basis of
567
elicit an inflammatory response resulting
in damage to kidney tissue and eventually
impairment of normal kidney function.
Thesameorganismisalsoresponsiblefor
rheumatic heart disease in which antibod-
ies directed against a number of
S. pyogenes
products include those against M protein,
a cell surface protein of
S. pyogenes
that
shares epitopes with proteins on the sur-
face of cardiac tissue. Hence the formation
of antibodies against M protein results in
the production of a set of antibodies that
may also recognize the host tissue, leading
to an immune response against the host.
Alternatively,
the
interaction
of
pathogens with antibodies may make
them more susceptible to phagocytosis.
The
process
of
coating
cells
with
antibodies termed
opsonization
leads to
their
recognition
by
phagocytic
cells
and other cells of the immune system.
This
interaction
may
also
lead
to
hypersensitivity
reactions
since
many
of
these
cells
will
release
molecules
that result in the development of an
inflammatory response. Some pathogens
directly attack the immune response (e.g.
P. aeruginosa
)b
yp
r
o
d
u
c
i
n
gp
r
o
t
e
o
l
y
t
i
c
enzymes that can degrade certain classes of
antibodies and complement components.
Others evade the immune response by
cloaking themselves in exopolysaccharide
capsules (e.g.
Klebsiella pneumoniae
,
H.
influenzae
), which are believed to impair
the ability of antibodies to bind and to
prevent phagocytosis, or by periodically
changing
their
surface
antigens
to
render
existing
antibodies
ineffective
(antigenic variation).
Neisseria gonorrhoeae
,
the causative organism of gonorrhea,
provides a good example for antigenic
variation. This organism is capable of
using a variety of methods in order to vary
the amount and composition of the pili on
itssurface.Inthisway,itpresentsanever-
changing surface to the host response,
resulting in a decreased ability of the
host to clear the organism. Still other
organisms utilize a process of molecular
mimicry in which they present a surface
marker that the host recognizes as ‘‘self’’
and thus does not respond with a normal
immune response. Good examples of this
mimicry are the hyaluronic acid capsule of
S. pyogenes
or the sialic acid capsule of
N.
meningitidis
. The importance of evading
the immune response is illustrated by
opportunistic pathogens that are limited
to immunocompromised hosts but cannot
survive in a host whose immune system
is intact.
5.5
Invasion and Intracellular Survival
In order to persist and perpetuate the
infection, some pathogens need to gain
access to deeper regions of the host
through a process generally known as
invasion. The ability of pathogens to
invade normally phagocytic cells such
as the macrophages, which function to
engulf pathogens, is not very surprising.
However, pathogens have had to evolve
more elaborate mechanisms in order
to invade nonphagocytic cells. The fact
that some invasive pathogens can invade
an extremely diverse population of cells
while others are restricted to speciFc cell
types implies that host cell receptors are
important in invasion. Integrins that play
a role in host cell interactions including
attachment, phagocytosis, and the binding
of proteins present in the extracellular
matrix have been identiFed as receptors.
Yersinia pseudotuberculosis
,
Mycobacterium
tuberculosis
,a
n
d
Legionella pneumophila
have all been shown to utilize members of
the integrin family of proteins as receptors.
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