The classical paradigm of autoimmune pathogenesis involving specific genetic
makeup and exposure to environmental triggers has been challenged recently
by the addition of a third element, the loss of intestinal barrier function.
Regardless of HLA B27 phenotype or gastrointestinal symptoms, evidence of
ileitis, ileocolitis or colitis exists in patients with spondyloarthropathy.
The FUT2 secretory gene is a strong candidate for Crohn's susceptibility by
shaping the functional states of mucosal microbiota and may thus have
influence on the release of zonulin, the main regulator of gut permeability.
Gram negative bacteria precipitate and may be involved in the pathogenesis
of spondyloarthropathies. Susceptibility to many infectious agents is
associated with ABO blood group or secretor state. Patients who cannot
secrete ABO and Lewis blood group antigens into body fluids, an ability
controlled by a single gene on chromosome 19, are known to be at increased
risk of certain autoimmune diseases associated with human leukocyte antigen
(HLA) markers. Lewis (Le) blood group phenotype can be used to infer
secretor status. The objective of this study was to determine the
distribution of secretor state and Lewis blood group phenotype in patients
with seronegative spondyloarthropathies and healthy control subjects.
Hundred and ten (110) patients with seronegative spondyloarthropathies (58
females and 52 males) and 103 control (74 males and 29 females) subjects
participated in this study. Samples of saliva and blood were subjected to
haemagglutination inhibition tests for determination of secretor status and
Lewis phenotype. A total of 92(84%) patients and 92 (89%) control subjects
were secretors while 18 (16%) patients and 11 (11%) control subjects were
non-secretors. There was no statistically significant difference (?2 1,461
p<0,05 and degrees of freedom 1) in distribution of secretor status in
comparison to seronegative spondyloarthropathies by comparing two observed
populations. Seven patients had modified (reduced) expression of Lewis b
antigen on their erythrocytes. Reduction of Lewis b antigen expression was
not observed on erythrocytes of healthy subjects. Reduced expression of
Lewis b antigen could be a consequence of the inflammatory process within
the gut and it also suggests several pathogenic mechanisms which may be
relevant to the synthesis of Lewis antigens inside the gut or its absorption
on erythrocytes in patients with spondyloarthropathy.
Potential role of molecular mimicry between Helicobacter pylori lipopolysaccharide and host Lewis blood group antigens in autoimmunity.
