Soluble adhesion molecules ICAM-1, VCAM-1, P-selectin in children with<i>Helicobacter pylori</i>infection

Maciorkowska, Elżbieta; Kaczmarski, Maciej; Panasiuk, Anatol; Kondej-Muszyńska, K; Kemonai, Andrzej

doi:10.3748/wjg.v11.i43.6745

Cited by 14 publications

(15 citation statements)

References 19 publications

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“…Maciorkowska et al. [45] evaluated the role of adhesion molecules ICAM‐1, VACAM‐1, and P‐selectin levels in H. pylori ‐infected children showing that in these children with gastritis, the VCAM‐1 reached the highest levels, whereas ICAM and P‐selectin did not differ in the H. pylori ‐positive and H. pylori ‐negative groups. According to Chan [46], a family of adhesion glycoproteins such as cadherins, act not only as adhesive molecules but may be also responsible for the growth development and carcinogenesis.…”

Section: Pathomechanism Of H Pylori Infectionmentioning

confidence: 99%

Pathogenesis of Helicobacter pylori Infection

Hatakeyama

Brzozowski

2006

Helicobacter

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Much interest has been shown in the relationship between Helicobacter pylori infection and gastric carcinogenesis. It is becoming clearer that H. pylori strains carrying a functional cag pathogenicity island (cagPAI), which encodes the type IV secretion system (TFSS) and its effector CagA, play an important role in the development of gastric carcinoma. Furthermore, genetic polymorphism present in the cagA gene appears to influence the degree of an individual cagPAI-positive H. pylori to elicit gastric mucosal lesions, and this process is significantly affected by host genetic polymorphisms such as proinflammatory cytokine gene polymorphisms. Pathomechanism of gastric carcinogenesis associated with H. pylori includes bacteria-host interaction leading to morphologic alterations such as atrophic gastritis and gastrointestinal metaplasia mediated by COX-2 overexpression, cancer cell invasion, and neo-angiogenesis via TLR2/TLR9 system and transcription factors (e.g., NF-kappaB) activation. In addition, H. pylori infection triggers adhesion molecule expression and activity and produces an enhancement in oxidative stress interacting with gastric production of appetite hormone ghrelin and nonsteroidal anti-inflammatory drugs.

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Section: Pathomechanism Of H Pylori Infectionmentioning

confidence: 99%

Pathogenesis of Helicobacter pylori Infection

Hatakeyama

Brzozowski

2006

Helicobacter

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“…Pepsinogen II $ 8 (Fukuda et al, 2003;Rogers et al, 2003;Lopes et al, 2006;De Angelis et al, 2007;Koivusalo et al, 2007;Guariso et al, 2009;Kassem et al, 2017;Nakayama et al, 2017) Extracellular secreted protein GC biomarker PIM2 (Maciorkowska et al, 2005) Cell adhesion protein Oncogenic *1 study shows no significant mRNA upregulation in infected children. (Haruna et al, 2008).…”

Section: Transcription Factorsmentioning

confidence: 99%

“…Thirty-seven studies from 14 different countries were finally selected, involving children and adolescents from 3 months to 19 years of age. Only 1 study included patients older than 18 years (Maciorkowska et al, 2005), but median age were 10-13 years in different groups, so it was no excluded. Most studied children were symptomatic, with only 3/37 studies including asymptomatic children (Supplementary Tables S1, S2).…”

Section: Oncogenic and Gastric Damage-related Biomarkers Identified Imentioning

confidence: 99%

“…VCAM-1 (Vascular Cell Adhesion Molecule 1) overexpression is related to angiogenesis and metastasis in cancer, including GC (Kong et al, 2018); in which both local expression in gastric tissue and serum levels are directly associated with poor prognosis (Velikova et al, 1997;Ding et al, 2003). In children, Maciorkowska et al, described that serum concentrations of VCAM-1 were higher in symptomatic children with H. pyloriassociated gastritis compared to non-infected children; they also compared children with positive IgG against H. pylori but with no active gastric infection (Maciorkowska et al, 2005), showing that serum levels of VCAM-1 correlate with H. pylori-induced gastric inflammation and damage.…”

Section: Cell-adhesion Proteinsmentioning

confidence: 99%

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Gastric Damage and Cancer-Associated Biomarkers in Helicobacter pylori-Infected Children

et al. 2020

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Helicobacter pylori (H. pylori) is well-known to be involved in gastric carcinogenesis, associated with deregulation of cell proliferation and epigenetic changes in cancerrelated genes. H. pylori infection is largely acquired during childhood, persisting long-term in about half of infected individuals, a subset of whom will go on to develop peptic ulcer disease and eventually gastric cancer, however, the sequence of events leading to disease is not completely understood. Knowledge on carcinogenesis and gastric damage-related biomarkers is abundant in adult populations, but scarce in children. We performed an extensive literature review focusing on gastric cancer related biomarkers identified in adult populations, which have been detected in children infected with H. pylori. Biomarkers were related to expression levels (RNA or protein) and/or methylation levels (DNA) in gastric tissue or blood of infected children as compared to non-infected controls. In this review, we identified 37 biomarkers of which 24 are over expressed, three are under expressed, and ten genes are significantly hypermethylated in H. pylori-infected children compared to healthy controls in at least 1 study. Only four of these biomarkers (pepsinogen I, pepsinogen II, gastrin, and SLC5A8) have been studied in asymptomatically infected children. Importantly, 13 of these biomarkers (β-catenin, C-MYC, GATA-4, DAPK1, CXCL13, DC-SIGN, TIMP3, EGFR, GRIN2B, PIM2, SLC5A8, CDH1, and VCAM-1.) are consistently deregulated in infected children and in adults with gastric cancer. Future studies should be designed to determine the clinical significance of these changes in infection-associated biomarkers in children and their persistence over time. The effect of eradication therapy over these biomarkers in children if proven significant, could lead to modifications in treatment guidelines for younger populations, and eventually promote the development of preventive strategies, such as vaccination, in the near future.

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“…These higher TNF‐a titers fell significantly after successful eradication, reaching levels observed in H. pylori ‐negative patients [90]. The assessment of adhesive molecules in the sera of children with active H. pylori infection has shown the presence of higher soluble vascular cell adhesion molecule‐1 (sVCAM‐1) levels [91], which has been shown to correlate to the presence and severity of IHD [92].…”

Section: Studies With Focus On Markers Of Inflammationmentioning

confidence: 99%

A Review of the Postulated Mechanisms Concerning the Association of Helicobacter pylori with Ischemic Heart Disease

2007

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Since its discovery, Helicobacter pylori has been implicated in the pathogenesis of several diseases, both digestive and extradigestive. Interestingly, the majority of the extradigestive-related literature is focused on two vascular manifestations: stroke and ischemic heart disease. Potential mechanisms for the establishment of a H. pylori-induced ischemic heart disease have been proposed with regard to chronic inflammation, molecular mimicry, oxidative modifications, endothelial dysfunction, direct effect of the microorganism on atherosclerotic plaques as well as changes regarding traditional or novel risk factors for ischemic heart disease or even platelet-H. pylori interactions. A positive link between H. pylori infection and ischemic heart disease has been suggested by a series of studies focusing on epidemiologic evidence, dyslipidemic alterations, upregulation of inflammatory markers or homocysteine levels, induction of hypercoagulability, oxidation of low-density lipoprotein, causation of impaired endothelial function, detection of H. pylori DNA in atherosclerotic plaques, and participation of certain antigens and antibodies in a cross-reactivity model. There are studies, however, which investigated the relationship between H. pylori and ischemic heart disease with regard to the same parameters and failed to confirm the suggested positive association. Further studies in the direction of interaction between H. pylori and the host's genotype as well as a quest for evidence towards novel risk factors for ischemic heart disease such as oxidative stress, vascular remodeling, vascular calcification, or vasomotor activity, may reveal a field of great interest, thus contributing to the determination of new potential mechanisms.

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Soluble adhesion molecules ICAM-1, VCAM-1, P-selectin in children withHelicobacter pyloriinfection

Cited by 14 publications

References 19 publications

Pathogenesis of Helicobacter pylori Infection

Pathogenesis of Helicobacter pylori Infection

Gastric Damage and Cancer-Associated Biomarkers in Helicobacter pylori-Infected Children

A Review of the Postulated Mechanisms Concerning the Association of Helicobacter pylori with Ischemic Heart Disease

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