Potential Association of IL1B Polymorphism With Iron Deficiency Risk in Childhood Helicobacter pylori Infection
Szu-Ta Chen1,2,3,4, Yen-Hsuan Ni2, Shing-Hwa Liu2,3,5
1Department of Pediatrics, National Taiwan University Hospital Yun-Lin Branch.
Insights
This study found that specific gene variations in ABO and IL1B influence susceptibility to Helicobacter pylori infection in children. The IL1B gene also appears to increase the risk of iron deficiency in infected children.
Area of Science:
- Genetics
- Microbiology
- Pediatrics
Background:
- Helicobacter pylori infection is common in childhood and linked to gastric cancer.
- Host immune response gene polymorphisms affect H. pylori susceptibility and disease outcomes.
- The connection between H. pylori, host genetics, and iron deficiency (ID) is not fully understood.
Purpose of the Study:
- To investigate the relationship between host genetic polymorphisms and iron deficiency in children with H. pylori infection.
- To identify specific single nucleotide polymorphisms (SNPs) associated with H. pylori infection and iron status in adolescents.
Main Methods:
- 644 adolescents (10-18 years) were grouped into H. pylori seropositive and seronegative.
- Genotyping was performed for five SNPs in IL1B, IL8, IL10, and ABO genes.
- Iron status was compared between infected and uninfected groups and within the infected group based on genotype.
Main Results:
- H. pylori seroprevalence was 10.7%; infected subjects were older and had lower serum iron.
- The T allele of ABO (rs505922) was associated with higher H. pylori infection risk (OR=6.128).
- The T allele of IL1B (rs1143627) was associated with lower infection risk (OR=0.846) but higher ID risk in infected children (OR=3.156).
Conclusions:
- ABO (rs505922) and IL1B (rs1143627) polymorphisms may influence susceptibility to H. pylori infection.
- IL1B (rs1143627) may also play a role in the risk of developing iron deficiency in H. pylori-infected children.
Objective:
Helicobacter pylori infection occurs predominantly in childhood. Host immune response gene polymorphism is reported to affect the susceptibility to H pylori infection and the outcome of H pylori-related gastric cancer. Not all H pylori-infected patients, however, exhibit iron deficiency (ID). The relationship between host genetic polymorphisms and ID mediated by H pylori infection is not well understood.
Methods:
Subjects (n = 644) from the general population of age 10 to 18 years were divided into 2 groups based on serology testing for anti-H pylori IgG: seropositive study group; and seronegative control group. Five single nucleotide polymorphisms (SNPs) in IL1B (rs1143627 and rs16944), IL8 (rs4073), IL10 (rs1800896), and ABO (rs505922), were genotyped and the iron status of the 2 groups was compared.
Results:
The seroprevalence rate for H pylori was 10.7% in this study. Infected subjects were significantly older and had lower serum iron levels than uninfected subjects (P = 0.0195 and 0.0059, respectively). Multivariate analysis revealed a significantly higher frequency of the T allele of rs505922 (odds ratio [OR] = 6.128; P < 0.001) and lower frequency of the T allele of rs1143627 (OR = 0.846; P = 0.014) in seropositive subjects. Among 59 seropositive subjects, the T allele frequency of rs1143627 was significantly higher in those with ID (OR = 3.156; P = 0.043), compared with those without ID.
Conclusions:
ABO (rs505922) and IL1B (rs1143627) may affect H pylori infection susceptibility, and IL1B (rs1143627) may also influence ID risk in infected children.
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