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Journal of Clinical Microbiology, January 2000, p. 68-70, Vol. 38, No. 1
Department of Pediatrics, Tohoku University
School of Medicine, Sendai,1 and Third
Department of Internal Medicine, Hokkaido University School of
Medicine, Sapporo,2 Japan, and
Departments of Medicine and Microbiology and Immunology,
Vanderbilt University School of Medicine, Nashville,
Tennessee3
Received 26 July 1999/Returned for modification 31 August
1999/Accepted 9 October 1999
cagA+ Helicobacter pylori
strains have been linked to more severe gastric inflammation, peptic
ulcer disease, and gastric cancer in adults, but there have been few
studies of cagA in children. We examined the relationship
between H. pylori cagA status and clinical status in
Japanese children. Forty H. pylori-positive children were
studied: 15 with nodular gastritis, 5 with gastric ulcers, and 20 with
duodenal ulcers. H. pylori status was
confirmed by biopsy-based tests and serum anti-H.
pylori immunoglobulin G (IgG) antibody. As controls, 77 asymptomatic children with sera positive for anti-H.
pylori IgG were enrolled. Levels of IgG antibodies to CagA in
serum were measured by an antigen-specific enzyme-linked immunosorbent
assay. In 16 patients with successful H. pylori eradication, posttreatment levels of CagA and H. pylori IgG
antibodies also were studied. The CagA antibody seropositivities of
asymptomatic controls (81.8%) and patients with nodular gastritis,
gastric ulcers, and duodenal ulcers (80.0 to 95.0%) were not
significantly different. Compared with pretreatment levels of CagA
antibodies, posttreatment levels decreased progressively and
significantly. We conclude that, as in Japanese adults, a high
prevalence of cagA+ H. pylori
strains was found in Japanese children, and that there was no
association with nodular gastritis or peptic ulcer disease. In
the assessment of eradicative therapies, monitoring of serum anti-CagA antibodies does not appear to offer any direct benefit over
monitoring of anti-H. pylori antibodies.
It is widely recognized that
colonization with Helicobacter pylori induces a persistent
gastric tissue response and is an important risk factor for peptic
ulcer disease and gastric cancer (4). However, the majority
of H. pylori-positive persons are asymptomatic throughout
their lifetime, and it is not known why only a subset of positive
patients develop ulcer disease and cancer. Variation in clinical
outcomes has been attributed to differences in bacterial strains,
hosts, and environmental factors.
H. pylori strains are genetically diverse (13,
33). Although of unknown function, the cytotoxin-associated gene
A (cagA) has been identified as a possible marker of
virulence of H. pylori (5). Since the
cytotoxin-associated gene product (CagA, 120 to 140 kDa) encoded
by cagA is immunodominant (10, 34), a specific
immune response to the CagA protein is induced as long as H. pylori colonization persists (6). Therefore, serum
immunoglobulin G (IgG) antibodies to the CagA antigen may be a
reliable marker of carriage of a cagA+ H. pylori strain (10, 12) which includes the
cag pathogenicity island (9, 35). In Western
populations, cagA+ H. pylori strains
induce more severe gastric mucosal inflammation than cagA
gene-negative strains (10, 15, 20) and are associated with
higher risks of peptic ulcer disease (11, 12, 15) and gastric cancer (6, 16). However, there is wide geographical variation in the prevalence of cagA+ strains
(1, 29, 37) and in their genotype (28), and it is
unknown whether cagA+ strains represent a
universal marker for these H. pylori-associated diseases.
Among adults in Japan, there is no clear relationship between
cagA+ H. pylori strains and enhanced
risk of disease (21).
Childhood is the critical period for acquisition of H. pylori (2, 27). As in adults, H. pylori
appears to be associated with both a tissue response (gastritis) and
duodenal ulcer in children (32). However, there have
been few studies of CagA seroprevalence in children (7,
20), and its role in peptic ulcer disease has not been
studied. In this study, we examined whether H. pylori CagA
status was associated in Japanese children with nodular gastritis,
which is a unique endoscopic characteristic in childhood (18,
24), and with peptic ulcer disease.
Patients.
A total of 40 H. pylori-positive
dyspeptic patients were enrolled in this study: 20 patients with
duodenal ulcer, 5 with gastric ulcer, and 15 with nodular gastritis
alone (Table 1). Diagnoses were
determined on the basis of findings by upper gastrointestinal endoscopy. Nodular gastritis, defined as endoscopically proven multiple
nodularity in the antrum with lymphoid follicles and inflammatory cell
infiltration in the lamina propria, is believed to be the major form of
H. pylori gastritis in childhood (18, 24). The
patients selected had no underlying diseases and were not taking
medications, including nonsteroidal anti-inflammatory drugs. H. pylori status was assessed by biopsy-based tests (rapid biopsy
urease test, histology, and culture) and testing for the presence of
serum anti-H. pylori IgG antibody with a commercial enzyme-linked immunosorbent assay (ELISA) kit (HM-CAP; Enteric Products, Inc., Westbury, N.Y.). In adults, because H. pylori is often difficult to isolate in culture, nonculture
techniques (histology, rapid biopsy urease test, serology, or urea
breath test) are performed for diagnosing H. pylori
infection (17). Our previous studies have demonstrated that
compared with biopsy tests, the sensitivity of anti-H.
pylori IgG and IgA antibodies were 88.2 and 91.2%, respectively
(22). Even when H. pylori has not been cultured,
the presence of the organism can be confirmed by a combination of these
techniques. As controls, 77 asymptomatic children with positive
anti-H. pylori IgG tests, who did not undergo endoscopy,
were enrolled into this study. All sera were stored at
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Copyright © 2000, American Society for Microbiology. All rights reserved.
CagA Antibodies in Japanese Children with Nodular
Gastritis or Peptic Ulcer Disease
ABSTRACT
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
INTRODUCTION
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
MATERIALS AND METHODS
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
20°C until
assay. Sixteen patients who received eradication therapy (proton pump
inhibitor-based dual or triple regimens) and had successful eradication
of H. pylori (23, 24) were studied at serial
intervals. In these patients, pretreatment and posttreatment levels of
H. pylori IgG antibodies were measured by using HM-CAP.
Serum samples were taken pretreatment and at 3, 6, and 12 months after
completion of eradication therapy. Informed consent was obtained from
patients or their parents in all cases.
TABLE 1.
Characteristics of 117 study patients
CagA antibodies.
Serum anti-CagA IgG antibody levels
were assayed as previously described (6). Briefly, a
recombinant protein fragment of CagA (ORV220; OraVax, Inc.,
Cambridge, Mass.) that was purified from Escherichia coli
cell lysates was used as an antigen and was fixed to a 96-well plate in
carbonate-bicarbonate buffer. After incubation of treated wells with
serum diluted 1:100, alkaline phosphatase-conjugated goat anti-human
IgG (1:1,000 dilution) was added. After addition of the phosphatase
substrate, absorbance was read at 405 nm. Based on results from
H. pylori-negative controls in adults, a value of 
0.2
ELISA unit (EU) of CagA IgG antibodies was considered to be positive
(21).
Statistical methods. The difference in CagA seropositivity between asymptomatic controls and patients with each of the three clinical diagnoses was analysed by Fisher's exact test. Differences between pretreatment and posttreatment levels of CagA and differences between posttreatment levels of CagA and H. pylori IgG antibodies were analyzed by the paired t test. A value of P < 0.05 was regarded as statistically significant. Values were presented as means ± standard deviations.
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RESULTS |
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Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
|
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CagA seropositivity.
Among the H. pylori-positive
children in this study, a high percentage in each group were
seropositive for anti-CagA IgG antibodies (Table
2). There were no significant differences
in seropositivity rates and levels of CagA antibodies between
asymptomatic controls and patients with ulcer disease or nodular
gastritis.
|
Effect of treatment on CagA antibody levels. All 16 patients who had successful eradication were seropositive for CagA antibodies before therapy. In these patients, the mean pretreatment level of anti-CagA antibodies was 1.0 ± 0.6 EU. Posttreatment levels were significantly decreased at 3 months (0.7 ± 0.5 EU; P < 0.001), at 6 months (0.6 ± 0.4 EU; P < 0.001), and at 12 months (0.5 ± 0.3 EU; P < 0.01), compared with the pretreatment levels (Fig. 1). Nevertheless, by using the threshold of 0.2 EU as the indicator of seropositivity, 8 (64%) of 11 patients studied remained seropositive even at 12 months after therapy. At 3 months posttreatment, the percent decrease in CagA antibody levels was greater than that in H. pylori IgG levels (P < 0.05).
|
,
P < 0.05, comparing anti-H. pylori and
anti-CagA antibodies.
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DISCUSSION |
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Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
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In Western countries, patients with duodenal ulcer are more likely to be colonized by cagA+ H. pylori strains than patients with gastritis alone (10, 11, 15). In the West, H. pylori strains that are cagA+ also are associated with more-substantial gastric tissue involvement with increased neutrophil infiltration, in adults (10, 15) and in children (20). Similarly, in gastric mucosa from persons colonized with cagA+ strains, increased gastric epithelial cell interleukin-8 (IL-8) mRNA (38) and IL-8 secretion (14, 31) have been observed. However, similarly close correlations have not been universally observed (19). In addition, among Swedish children and adolescents, there was no significant correlation between degree of gastric inflammation and H. pylori cytotoxin production (8).
In Western patients, CagA seropositivity has been shown to be higher in those who have atrophic gastritis, which is a precursor to gastric cancer (3, 26). Although cagA+ strains may play a role in the development of gastric cancer, they are neither necessary nor sufficient for this process (6). In Japan, high CagA seropositivity rates have been observed in asymptomatic adults, reinforcing the insufficiency of carriage of a cagA+ strain for gastric cancer development (21). CagA seroprevalence varies geographically (1, 29, 37). The frequency of cagA+ strains observed in asymptomatic children has ranged from 76% in Mexico (7) to 40% in France (20). In Japan, cagA+ H. pylori strains are common in persons of all ages. Thus, available evidence from this and previous studies (1, 28, 29, 37) suggests that cagA+ strains are not significant as disease-specific pathogenetic markers.
Allelic differences within cagA that distinguish Western and East Asian cagA+ H. pylori strains have been reported (28, 36). These differences may reflect variation in other parts of the cag pathogenicity island, which has been considered to encode potential virulence-related genes. It is possible that Asian cagA+ H. pylori strains do not induce the accentuated tissue damage caused by Western cagA+ strains. In any event, both host and bacterial factors should be considered in order to understand the pathogenesis of H. pylori-associated diseases.
As a noninvasive assay, determination of serum CagA IgG antibody levels may be useful in the assessment of eradicative therapy, as is evaluation of H. pylori IgG antibody levels (25, 30). In this study, levels of serum CagA IgG antibodies decreased significantly after eradication of H. pylori using antimicrobial therapy. However, most successfully treated patients remained CagA seropositive for months during the follow-up period. Similarly, seroconversion to negativity for H. pylori IgG and IgA antibodies requires about 12 months after successful eradication (22). Thus, the humoral immune responses, not only to H. pylori group antigens but also to the CagA protein, do not quickly disappear after the organism is eliminated. Assessing anti-CagA antibodies as a marker for eradication does not appear to offer any direct benefit over use of anti-H. pylori antibodies alone.
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ACKNOWLEDGMENTS |
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We thank Takuji Fujisawa (Kurume, Japan), Hitoshi Tajiri (Osaka, Japan), Mutsuko Konno (Sapporo, Japan), and Shun-ichi Maisawa (Morioka, Japan) for providing the sera of patients and controls.
This work was supported in part by the Medical Research Service of the Department of Veterans Affairs.
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FOOTNOTES |
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* Corresponding author. Mailing address: Department of Pediatrics, Tohoku University School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan. Phone: 81-22-717-7287. Fax: 81-22-717-7290. E-mail: skato{at}ped.med.tohoku.ac.jp.
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References
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Journal of Clinical Microbiology, January 2000, p. 68-70, Vol. 38, No. 1
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Copyright © 2000, American Society for Microbiology. All rights reserved.
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