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This was
posted at alt.suppport.crohns-colitis
in August of 2000:
"The
immunodeficiency hypothesis of Crohn's disease: possible early
events in its pathogenesis." An excessive immune response
against endogenous bacteria is the current hypothesis for
the etiology of Crohn's disease, while the suppression of
this immune response, largely T-cell driven, is the goal of
standard therapy.
However,
some epidemiologic and pathophysiologic data suggest other
explanations: some deficiencies in neutrophil function detected
in some genetic disorders can be observed as a clinical and
pathologic syndrome indistinguishable from Crohn's disease;
Crohn's disease itself has a well-known abnormal neutrophil
function; neutrophil function can be impaired by some bacteria
that are also involved in other chronic inflammatory disorders;
and neutrophil function is known to be suppressed directly
by some 20th century environmental risk factors for Crohn's
disease. These factors have also played a role in a shift
in the dominant gut flora with similar effects.
"This
paper supports the idea that the interaction of environmental
and genetic factors can give rise to some cases of Crohn's
disease, with an impaired mucosal neutrophil function; therefore,
the intramucosal microbes are not effectively cleared. A proximate
defect in the mucosal immune response is proposed by this
hypothesis, which at the same time encompasses existing data.
In this case, new strategies to alter intestinal flora and
stimulate neutrophil function could be taken into account
for future therapeutic approaches. "
(Korzenik, J.R. Dig Dis Sci 2000; 45(6): 1121-1129.)
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Research on immunodeficiency in Crohn's disease