Gastric mucosal interleukin-8 and IL-8 antibody concentrations related to prevailing Helicobacter pylori infections. A Danish-Albanian study.
OBJECTIVE
Helicobacter pylori (H. pylori) appears to initiate an inflammatory cascade. Thus, phagocytes are accumulated in the gastric mucosa, in inflammatory conditions. Further, a potent chemotactic mediator, interleukin 8 (IL-8) is synthesized at such sites. The recently described IL-8 autoantibodies may, however, counteract the pro-inflammatory actions of IL-8. The aim was to study the correlation between H. pylori infection and IL-8, together with IL-8 autoantibodies in two different populations from a developed and a developing country.


METHODS
Two different endoscopically characterized populations (65 Danes and 89 Albanians) were examined. IL-8 and IL-8 autoantibodies were detected by ELISA techniques, and H. pylori was identified by histological examinations.


RESULTS
Significantly more Albanian controls and dyspeptic patients (80 out of 89 persons) were H. pylori positive as compared to 24 of 65 Danes (p < 0.001). The median IL-8 level among Albanian controls 349 pg/mg protein was significantly higher than among Danes < 61 pg/mg protein (p < 0.001), and was at the same level as found in Danish peptic ulcer patients (p > 0.05). Further, H. pylori positive patients from both countries had significantly higher levels of IL-8 as compared to H. pylori negative patients (p < 0.001). However, significantly higher levels of IL-8 autoantibodies were found in the Albanian sub-population (median 138 O.D. units versus 52 O.D. units among Danes) (p < 0.001).


CONCLUSIONS
In H. pylori related disorders, a high mucosal IL-8 production has been found. However, this investigation further demonstrates higher levels of IL-8 autoantibodies among dyspeptic patients from a developing country, which might possibly counteract the pro-inflammatory actions of IL-8 by binding the molecule. The physiological significance of an altered immune response as described here needs to be elucidated in future studies.
Nielsen
O H
OH
Department of Medicine, Glostrup Hospital, University of Copenhagen. ohn@dadlnet.dk
Horn
T
T
Prifti
S
S
Peichl
P
P
Scheibel
J H
JH
Lindley
I J
IJ
D000293:Adolescent; D000328:Adult; D000368:Aged; D001323:Autoantibodies / Q000378:metabolism*; D004381:Duodenal Ulcer / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D004382:Duodenitis / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology* / Q000378:metabolism*; D005756:Gastritis / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D016481:Helicobacter Infections / Q000276:immunology* / Q000378:metabolism*; D016480:Helicobacter pylori; D006801:Humans; D016209:Interleukin-8 / Q000276:immunology* / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D013276:Stomach Ulcer / Q000276:immunology / Q000378:metabolism / Q000382:microbiology
D001323:Autoantibodies; D016209:Interleukin-8