Induction of various cytokines and development of severe mucosal inflammation by cagA gene positive Helicobacter pylori strains
Y Yamaoka
a Third Department of Internal Medicine,
Kyoto Prefectural University of Medicine, 465 Kawaramachi-Hirokoji,
Kamigyo-ku, Kyoto 602, Japan, b Department of Microbiology,
Kyoto Prefectural University of Medicine, Kyoto, Japan
Correspondence to: Dr Y
Yamaoka. Accepted for publication 10 March 1997 Background Keywords:
cytokines;
Helicobacter pylori;
cagA gene;
interleukin 8;
interleukin 1
Helicobacter pylori
strains possessing the cagA gene are thought to induce
interleukin 8 (IL-8) in gastric mucosa. However, it is still unclear
whether a relation exists between the cagA gene and the
expression patterns of cytokines other than IL-8.
Aims
To investigate the
relation between the cagA gene and the production
of various cytokine proteins using an enzyme linked immunosorbent
assay (ELISA).
Patients and methods
In 184 patients,
the cagA gene was detected by polymerase chain reaction
(PCR), and levels of production of IL-1
, IL-6, IL-7, IL-8, IL-10,
and tumour necrosis factor
(TNF-
) in antral biopsy specimens
were measured by ELISA.
Results
Mucosal levels of IL-1
, IL-6,
IL-8, and TNF-
were significantly higher in H pylori
positive than in H pylori negative patients.
Furthermore, the mucosal levels of IL-1
and IL-8 were significantly higher in specimens infected with cagA
positive strains than in those infected with cagA
negative strains. In H pylori positive
patients, the mucosal level of IL-8 was closely correlated with
that of IL-1
(p<0.0001), and the mucosal level of IL-6
was closely correlated with that of TNF-
(p<0.0001).
Conclusion
These findings suggest that the
ability to induce cytokines differs among the strains;
cagA+ strains induce various kinds of
cytokines and may cause severe inflammation, whereas
cagA
strains induce IL-8 and IL-1
only
weakly and may cause only mild inflammation. However, as most patients
infected with the cagA+ strains have
gastritis, these strains may not be equivalent to ulcerogenic strains.
(GUT 1997;41:442-451)
© 1997 by Gut
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