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Mechanism that can result in blindness
from corneal infection under study
When the immune system
rallies to fight an infection in
thetransparent outer layer of
the eye, it can do more harm
than good, according to a re
searcher who wants to iden
tify what triggerstheimmune
response and stop it.
“Everything you cannot see
is the cornea,” Dr. Fu-Shin X.
“Yu, cell biologist at the Medi
‘cal College of Georgia, said of
thelayer that collectslight for
‘the lens to focus and a person
to see. Diseases and injuries
to this front line of the eye are
the leading cause of visits to
eye doctors and some of the
" most painful eye problems.
" The durable cornea also
forms a protective physical
barrier that shields the eye
from various types of damage
ranging from trauma toinfec
tions to the deleterious ef
fects of light itself. In fact, a
healthy, intact cornea is es
sentiallyimpervious tobacte
ria that are constantly on
peopleand theirenvironment.
But when the cornea’s in
tegrity is compromised by an
injury or even the subtle, slow
loss of tissue that can result
from wearing contact lenses,
it may summon the immune
system, the traditional fighter
of infections, to the immuno
privileged site, said Dr. Yu.
That apparently noble ef
fort can result in the rapid
. loss of vision as immune sys
tem cells move in and inflam
mation sets in to help remove.
the invader and the tissue it
destroyed. “When bacteria get
in, they may trigger a domino
reaction until thereisinflam
mation and scar formation,”
Dr. Yu said. “And once that
inflammation has started,
there is almost nothing you
can doto stopit. So the conse
~ quenceis,notlikeonthehand,
for example, where a scar is
OK.” In the cornea, scars,
which are anatural part ofthe
healing process, disrupt or
derly collagen fibers so that
light can no longer penetrate
and vision is lost. Once the
damage is done, “you have
almost no solution except cor
neal transplantation,” hesaid.
“We are trying to find out
how infection or the presence
ofbacteria trigger pro-inflam
matory cytokines and things
that interfere v.ith that sig
nal,” he said. His group has
developed an organ culture
model for these studies in
whichreagentsknown toblock
signaling pathways are being
tested for efficacy in blocking
the release of these pro-in
flammatory cytokines.
Dr. Yu first compromises
the surface of the corneal
model as an injury or contact
lens might. He then infects
themodel with bacteria, treats
the corneal model with topi
cal antibiotics—as an ophthal
mologist would do for a cor
neal infection - then tries to
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block the immune system re
sponse. “We are trying to find
thingsthatinterfere with that
signal,” Dr. Yu said, hopeful
that one day his research will
giveophthalmologists another
drug that will block inflam
mation.
Today eye doctors often give
steroids to try and stop the
inflammation, once it has oc
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curred.
Dr. Yu’s work is supported
by two grants from the Na
tional Eye Institute of the
National Institutes of Health
as well as funding from the
Center for Alternatives to
Animal Testing at Johns
Hopkins University School of
Public Health.
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