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| 1 | Potential implications of Helicobacter pylori-related neutrophil-activating protein显示文摘Helicobacter pylori (H.pylori) virulence factors promote the release of various chemoattractants/inflammatory mediators,including mainly the neutrophilattractant chemokine interleukin-8 and neutrophilactivating protein (NAP),involved in H.pylori-induced gastric pathologies.Co-administration of Chios mastic gum (CMG),which inhibits H.pylori NAP,with an H.pylori eradication regimen might add clinical benefits against H.pylori-related gastric pathologies,but possibly not CMG as main therapy.Although H.pylori NAP and other H.pylori-related cytotoxins [i.e.,vaculating cytotoxin (VacA)] appear to play a major role in generating and maintaining the H.pylori-associated gastric inflammatory response and H.pylori NAP is a promising vaccine candidate against H.pylori infection (H.pylori-I),concerns regarding its potential drawbacks,particularly neurogenic ones,due to possible crossmimicry,should be considered.Possible cross-mimicry between H.pylori NAP and/or bacterial aquaporin (AQP) and neural tissues may be associated with the anti-AQP-4 antibody-related neural damage in multiple sclerosis (MS)/neuromyelitis optica patients.Moreover,the sequence homology found between H.pylori VacA and human Na+/K+-ATPase A subunit suggests that antibodies to VacA involve ion channels in abaxonal Schwann cell plasmalemma resulting in demyelination in some patients.A series of factors have been implicated in inducing blood-brain barrier (BBB) disruption,including inflammatory mediators (e.g.,cytokines and chemokines induced by H.pylori-I) and oxidative stress.BBB disruption permits access of AQP4-specific antibodies and T lymphocytes to the central nervous system,thereby playing a major role in multiple sclerosis pathogenesis.Relative studies show a strong association between H.pylori-I and MS.H.pylori-I induces humoral and cellular immune responses that,owing to the sharing of homologous epitopes (molecular mimicry),cross-react with components of nerves,thereby contributing and perpetuating neural tissue damage.Finally,H.pylori NAP also plays a possible pathogenetic role in both gastric and colon oncogenesis. | Jannis Kountouras Christos Zavos Georgia Deretzi Emmanuel Gavalas Dimitrios Chatzopoulos Panagiotis Katsinelos Elena Tsiaousi Stergios Gagalis Stergios A Polyzos Ioannis Venizelos | 2012 | World Journal of Gastroenterology2012，18，5： | 5 |
| 2 | Comment on “Effect of biofilm formation by clinical isolates of Helicobacter pylori on the efflux-mediated resistance to commonly used antibiotics”显示文摘Attaran et al[1] have recently shown that decreased susceptibility of established Helicobacter pylori(H. pylori) biofilms to specific antibiotics,was associated with the overtly enhanced transcription of two efflux pump genes,hp1165 and hef A,involved in specific resistance to tetracycline and multiple antibiotics,respectively. Apart from antibiotic exposure,secretion of multiple antimicrobial peptides,such as human β-defensins(hβDs),by the gastric epithelium upon Hp challenge,may act as early triggering events that positively impact biofilm formation and thus,antibiotic resistance. In this regard,we undertook genomic transcriptional studies using Hp 26695 strain following exposure to sublethal,similar to those present in the gastric niche,concentrations of hβDs in an attempt to provide preliminary data regarding possible mechanisms of immune evasion and selective sensitivity of Hp. Our preliminary results indicate that hβD exposure ignites a rapid response that is largely due to the activation of several,possibly interconnected transcriptional regulatory networks – origons-that ultimately coordinate cellular processes needed to maintain homeostasis and successful adaptation of the bacterium in the gastric environment. In addition,we have shown that both antibiotic and hβD resistance are mediated by dedicated periplasmic transporters,including the aforementioned efflux pump genes hp1165 and hef A,involved in active export of antibiotics from the cell membrane and/or,as recently suggested,substrate sensing and signalling. Furthermore,itappears that sublethal doses of hβDs may enhance biofilm formation by the sustained expression of,mainly,quorum sensing-related genes. In conclusion,we provide additional data regarding the role of specific innate immune molecules in antibiotic cross-resistance mechanisms that may deepen our understanding in the context of the development of novel eradication regimens. | Evangelos I Kazakos Nick Dorrell Stergios A Polyzos Georgia Deretzi Jannis Kountouras | 2017 | World Journal of Gastroenterology2017，23，33： | 3 |
| 3 | Role of autophagy in gastric carcinogenesis显示文摘Gastric cancer represents a common and highly fatal malignancy,and thus a pathophysiology-based reconsideration is necessary,given the absence of efficient therapeutic regimens.In this regard,emerging data reveal a significant role of autophagy in gastric oncogenesis,progression,metastasis and chemoresistance.Although autophagy comprises a normal primordial process,ensuring cellular homeostasis under energy depletion and stress conditions,alterations at any stage of the complex regulatory system could stimulate a tumorigenic and promoting cascade.Among others,Helicobacter pylori infection induces a variety of signaling molecules modifying autophagy,during acute infection or after chronic autophagy degeneration.Subsequently,defective autophagy allows malignant transformation and upon cancer establishment,an overactive autophagy is stimulated.This overexpressed autophagy provides energy supplies and resistance mechanisms to gastric cancer cells against hosts defenses and anticancer treatment.This review interprets the implicated autophagic pathways in normal cells and in gastric cancer to illuminate the potential preventive,therapeutic and prognostic benefits of understanding and intervening autophagy. | Apostolis Papaefthymiou Gregory Christodoulidis Apostolos Koffas Michael Doulberis Stergios A Polyzos Anastasios Manolakis Spyros Potamianos Andreas Kapsoritakis Jannis Kountouras | 2021 | World Journal of Gastrointestinal Oncology2021，13，10： | 2 |
| 4 | Wnt/beta-catenin signaling inhibitors and nonalcoholic fatty liver disease:Potential therapeutic implications显示文摘To the Editor:We read with considerable interest the paper of Shree Harini and Ezhilarasan,summarizing the possible pathophysiological connections between the modulators of canonical Wnt/β-catenin pathway and nonalcoholic fatty liver disease(NAFLD)[1].The au-thors supported with evidence that Wnt/β-catenin signaling contributes to hepatic homeostasis by regulating hepatic development,regeneration and metabolism.They also supported that dysregula-tion of modulators of Wnt/β-catenin signaling is not only impli-cated in the development of NAFLD,but also in its progression to nonalcoholic steatohepatitis(NASH),hepatic fibrosis and hepato-cellular carcinoma(HCC). | Stergios A Polyzos Jannis Kountouras Athanasios D Anastasilakis Evangelos Terpos | 2023 | Hepatobiliary & Pancreatic Diseases International2023，22，4： | 0 |
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