Hepcidin correlates with interleukin-1β and interleukin-6 but not iron deficiency in children with Helicobacter pylori infection

Chen, Szu-Ta; Ni, Yen‐Hsuan; Li, Chuan-Chun; Liu, Shing‐Hwa

doi:10.1016/j.pedneo.2018.02.007

Cited by 10 publications

(8 citation statements)

References 33 publications

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“…In addition, the H. pylori seropositive children with low hepcidin levels were more likely to have iron deficiency than the seropositive children with high hepcidin levels. These results imply that not all children with infection show an increased serum hepcidin level, thus the association between in H. pylori infection and iron deficiency might be explained by other mechanisms than hepcidin production [34]. However, the serologic method used to detect H. pylori also can imply that some children may have had a prior inactive infection by H. pylori [35].…”

Section: Discussionmentioning

confidence: 99%

Association between Active H. pylori Infection and Iron Deficiency Assessed by Serum Hepcidin Levels in School-Age Children

et al. 2019

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Hepcidin regulates iron metabolism. Its synthesis increases in infection and decreases in iron deficiency. The aim of this study was to evaluate the relationship between H. pylori infection and iron deficiency by levels of hepcidin in children. A total of 350 school-age children participated in this cross-sectional study. Determinations of serum ferritin, hemoglobin, hepcidin, C-reactive protein, and α-1-acid-glycoprotein were done. Active H. pylori infection was performed with a 13C-urea breath test. In schoolchildren without H. pylori infection, hepcidin was lower in those with iron deficiency compared to children with normal iron status (5.5 ng/mL vs. 8.2 ng/mL, p = 0.017); while in schoolchildren with H. pylori infection the levels of hepcidin tended to be higher, regardless of the iron nutritional status. Using multivariate analysis, the association between H. pylori infection and iron deficiency was different by hepcidin levels. The association between H. pylori and iron deficiency was not significant for lower values of hepcidin (Odds Ratio = 0.17; 95% Confidence Interval [CI] 0.02–1.44), while the same association was significant for higher values of hepcidin (OR = 2.84; CI 95% 1.32–6.09). This joint effect is reflected in the adjusted probabilities for iron deficiency: Individuals with H. pylori infection and higher levels of hepcidin had a probability of 0.24 (CI 95% 0.14–0.34) for iron deficiency, and this probability was 0.24 (CI 95% 0.14–0.33) in children without H. pylori infection and lower levels of hepcidin. In children with H. pylori infection and iron deficiency, the hepcidin synthesis is upregulated. The stimulus to the synthesis of hepcidin due to H. pylori infection is greater than the iron deficiency stimulus.

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Section: Discussionmentioning

confidence: 99%

Association between Active H. pylori Infection and Iron Deficiency Assessed by Serum Hepcidin Levels in School-Age Children

et al. 2019

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“…Although IL-8 was initially considered to have a key role in triggering immuneinflammatory responses as a result of H. pylori infection, further studies questioned this hypothesis, revealing that the effect of this cytokine might vary and depends on both the host's immune response and bacterial peculiarities. These findings were recently supported by Chen et al, who found no correlation between IL-8 serum levels and hepcidin levels, which is a well-known regulator hormone of iron absorption, in children with H. pylori infection [49], suggesting once more that the role of this interleukin might not be the same as described initially.…”

Section: Interleukin (Il)-8mentioning

confidence: 53%

“…Thus, Jing et al recently concluded that IL-6 might represent a useful screening tool for the detection of early gastric cancer [72]. Similarly, a recent study performed on pediatric patients with H. pylori noted a strong association between IL-6 and increased hepcidin levels [49]. Another study that assessed H.-pylori-positive children indicated that innate immune players, such as toll-like receptor 2 (TLR) and TLR4, play key roles in the expression of IL-6 in H.-pylori-infected children [74,75] (Table 1).…”

Section: Il-6mentioning

confidence: 96%

Old and New Aspects of H. pylori-Associated Inflammation and Gastric Cancer

Meliţ

Mărginean

2022

Children

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H. pylori is involved in the development of 80% of gastric cancers and 5.5% of all malignant conditions worldwide. Its persistence within the host’s stomach causes chronic inflammation, which is a well-known hallmark of carcinogenesis. A wide range of cytokines was reported to be involved in the initiation and long-term persistence of this local and systemic inflammation. IL-8 was among the first cytokines described to be increased in patients with H. pylori infection. Although, this cytokine was initially identified to exert a chemoattracting effect that represents a trigger for the activation of inflammatory cells within H.-pylori-infected mucosa, more recent studies failed in encountering any association between IL-8 and H. pylori infection. IL-6 is a multifunctional, pleiotropic and multipotent cytokine involved in mediating the interaction between innate and adaptive immunity with a dichotomous role acting as both a proinflammatory and an anti-inflammatory cytokine depending on the signaling pathway. IL-1α functions as a promoter of angiogenesis and vascular endothelial cell proliferation in gastric carcinoma since it is closely related to H.-pylori-induced inflammation in children. IL-1β is an essential trigger and enhancer of inflammation. The association between a low IL-1β level and an increased TNF-α level might be considered a risk factor for peptic ulcer disease in the setting of H. pylori infection. IL-10 downregulates both cytotoxic inflammatory responses and cell-mediated immune responses. H. pylori uses the immunosuppressive role of IL-10 to favor its escape from the host’s immune system. TGFβ is a continuous inflammatory mediator that promotes the adherence of H. pylori to the host’s cells and their subsequent colonization. The role of H.-pylori-induced inflammatory responses in the onset of gastric carcinogenesis seems to represent the missing puzzle piece for designing effective preventive and therapeutic strategies in patients with H.-pylori-associated gastric cancer.

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“…However, we found that only a small number of lymphocytes infiltrating the mucosa were hepcidin-positive, suggesting that H. pylori infection had a limited effect on hepcidin production in gastric mucosal lymphocytes, except for lymph follicles; therefore, the relationship between H. pylori and iron deficiency cannot always be explained by local hepcidin expression alone. Indeed, several reports [31][32][33] have revealed that hepcidin is not involved in the relationship between H. pylori and IDA.…”

Section: Discussionmentioning

confidence: 99%

Influence of Helicobacter Pylori Infection on Hepcidin Expression in the Gastric Mucosa

Nishigaki

Sato

et al. 2021

Kurume Med. J.

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Background: Hepcidin is an antimicrobial peptide and a key hormone involved in iron homeostasis. Hepcidin level is elevated in the serum during the course of Helicobacter pylori infection and hepcidin is considered to contribute to iron deficiency anemia. However, it is unclear whether H. pylori infection influences hepcidin expression in the gastric mucosa. Method: In this study, 15 patients with H. pylori-infected nodular gastritis, 43 patients with H. pylori-infected chronic gastritis, and 33 patients without H. pylori infection were enrolled. Endoscopic biopsy, and histological and immunohistochemical analysis were performed to evaluate the expression of hepcidin and its distribution in the gastric mucosa. Result: Hepcidin was strongly expressed in the lymph follicles of patients with nodular gastritis. The detection rates of gastric hepcidin-positive lymphocytes in patients with nodular gastritis and chronic gastritis were significantly higher than that without H. pylori infection. Moreover, regardless of the H. pylori infection status, hepcidin was expressed in the cytoplasm and intracellular canaliculi of gastric parietal cells. Conclusion:Hepcidin is expressed at a steady state in gastric parietal cells, and H. pylori infection may induce hepcidin expression in lymphocytes present in the gastric mucosal lymphoid follicles. This phenomenon may be associated with systemic hepcidin overexpression and iron deficiency anemia in patients with H. pylori-infected nodular gastritis.

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Hepcidin correlates with interleukin-1β and interleukin-6 but not iron deficiency in children with Helicobacter pylori infection

Abstract: Inflammatory cytokines IL-1β and IL-6, but not IL-8, might be associated with increased hepcidin levels among H. pylori-seropositive children. Further studies are needed to clarify the role of hepcidin.

Cited by 10 publications

References 33 publications

Association between Active H. pylori Infection and Iron Deficiency Assessed by Serum Hepcidin Levels in School-Age Children

Association between Active H. pylori Infection and Iron Deficiency Assessed by Serum Hepcidin Levels in School-Age Children

Old and New Aspects of H. pylori-Associated Inflammation and Gastric Cancer

Influence of Helicobacter Pylori Infection on Hepcidin Expression in the Gastric Mucosa

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