scholarly journals Antibody Responses to Helicobacter pylori and Risk of Developing Colorectal Cancer in a European Cohort

2020 ◽  
Vol 29 (7) ◽  
pp. 1475-1481
Author(s):  
Julia Butt ◽  
Mazda Jenab ◽  
Michael Pawlita ◽  
Anne Tjønneland ◽  
Cecilie Kyrø ◽  
...  
2020 ◽  
Vol 8 (11) ◽  
pp. 1698
Author(s):  
Meira Epplein ◽  
Loïc Le Marchand ◽  
Timothy L. Cover ◽  
Mingyang Song ◽  
William J. Blot ◽  
...  

Previously, we found that risk of colorectal cancer (CRC) is increased in individuals with serum antibody response to both Helicobacter pylori (HP) Vacuolating Cytotoxin (VacA) toxin or Streptococcus gallolyticus (SGG) pilus protein Gallo2178. In the present analysis, we tested the hypothesis that combined seropositivity to both antigens is a better indicator of CRC risk than seropositivity to single antigens. We used multiplex serologic assays to analyze pre-diagnostic serum for antibody responses from 4063 incident CRC cases and 4063 matched controls from 10 US cohorts. To examine whether combined SGG Gallo2178 and HP VacA sero-status was associated with CRC risk, we used conditional logistic regression models to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Compared to dual sero-negative individuals, there was no increased risk for individuals sero-positive to SGG Gallo2178 only (OR: 0.93; 95% CI: 0.66–1.31) or to HP VacA only (OR: 1.08; 95% CI: 0.98–1.19). However, dual sero-positive individuals had a >50% increased odds of developing CRC (OR: 1.54; 95% CI: 1.16–2.04), suggesting an interaction between antibody responses to these two pathogens and CRC risk (pinteraction = 0.06). In conclusion, this study suggests that dual sero-positivity to HP VacA and SGG Gallo2178 is an indicator of increased risk of CRC.


2013 ◽  
Vol 22 (11) ◽  
pp. 1964-1974 ◽  
Author(s):  
Meira Epplein ◽  
Michael Pawlita ◽  
Angelika Michel ◽  
Richard M. Peek ◽  
Qiuyin Cai ◽  
...  

2018 ◽  
Vol 27 (10) ◽  
pp. 1186-1194 ◽  
Author(s):  
Julia Butt ◽  
William J. Blot ◽  
Lauren R. Teras ◽  
Kala Visvanathan ◽  
Loïc Le Marchand ◽  
...  

2000 ◽  
Vol 68 (1) ◽  
pp. 100-106 ◽  
Author(s):  
Chikashi Oshima ◽  
Kazuichi Okazaki ◽  
Yumi Matsushima ◽  
Mitsutaka Sawada ◽  
Tsutomu Chiba ◽  
...  

ABSTRACT Helicobacter pylori is the major causative agent of chronic antral gastritis and is thought to be involved in the pathogenesis of mucosa-associated lymphoid tissue lymphoma (MALToma) developing in the human stomach. The aim of this study was to clarify whether corporal autoimmune gastritis (AIG), which is known to decrease acidity due to destruction of parietal cells, predisposes mice toH. pylori infection, thereby leading to MALToma-like pathology. BALB/c mice in which AIG had been induced by thymectomy 3 days after birth (AIG mice) were used. The AIG mice were orally administered mouse-adapted H. pylori at the age of 6 weeks and were examined histologically and serologically after 2 to 12 months. The results were compared with those obtained from uninfected AIG mice and infected normal mice. Germinal centers were induced in the corpus in 57% of the H. pylori-infected AIG mice, which elicited anti-H. pylori antibody responses in association with upregulation of interleukin-4 (IL-4) mRNA. In these mice, parietal cells remained in the corpus mucosa. These findings were in contrast to those with the uninfected AIG mice: fundic gland atrophy due to disappearance of parietal cells associated with upregulation of gamma interferon, but not IL-4, mRNA and no germinal center formation in the corpus. These observations suggest that AIG alters the infectivity ofH. pylori, leading to MALToma-like follicular gastritis, at an early stage after H. pylori infection.


2013 ◽  
Vol 23 (2) ◽  
pp. 365-365 ◽  
Author(s):  
Jannis Kountouras ◽  
Nikolaos Kapetanakis ◽  
Christos Zavos ◽  
Stergios A. Polyzos ◽  
Elisabeth Vardaka ◽  
...  

2001 ◽  
Vol 16 (4) ◽  
pp. 202-210 ◽  
Author(s):  
A. Hartwich ◽  
S.J. Konturek ◽  
P. Pierzchalski ◽  
M. Zuchowicz ◽  
H. Labza ◽  
...  

1998 ◽  
Vol 5 (3) ◽  
pp. 288-293 ◽  
Author(s):  
A. Mattsson ◽  
A. Tinnert ◽  
A. Hamlet ◽  
H. Lönroth ◽  
I. Bölin ◽  
...  

ABSTRACT In this study we have determined systemic and local antibody responses against different Helicobacter pylori antigens inH. pylori-infected and noninfected subjects. In addition, we studied whether differences in antibody responses between patients with duodenal ulcers and asymptomatic H. pylori carriers might explain the different outcomes of infection. Sera and in most instances gastric aspirates were collected from 19 duodenal ulcer patients, 15 asymptomatic H. pylori carriers, and 20 noninfected subjects and assayed for specific antibodies against different H. pylori antigens, i.e., whole membrane proteins (MP), lipopolysaccharides, flagellin, urease, the neuraminyllactose binding hemagglutinin HpaA, and a 26-kDa protein, by enzyme-linked immunosorbent assay. The H. pylori-infected subjects had significantly higher antibody titers against MP, flagellin, and urease in both sera and gastric aspirates compared with the noninfected subjects. Furthermore, the antibody titers against HpaA were significantly elevated in sera but not in gastric aspirates from the infected subjects. However, no differences in antibody titers against any of the tested antigens could be detected between the duodenal ulcer patients and the asymptomatic H. pyloricarriers, either in sera or in gastric aspirates.


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