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| 1 | Host pathogen interactions in Helicobacter pylori related gastric cancer显示文摘Helicobacter pylori (H. pylori), discovered in 1982, is a microaerophilic, spiral-shaped gram-negative bacterium that is able to colonize the human stomach. Nearly half of the world's population is infected by this pathogen. Its ability to induce gastritis, peptic ulcers, gastric cancer and mucosa-associated lymphoid tissue lymphoma has been confirmed. The susceptibility of an individual to these clinical outcomes is multifactorial and depends on H. pylori virulence, environmental factors, the genetic susceptibility of the host and the reactivity of the host immune system. Despite the host immune response, H. pylori infection can be difficult to eradicate. H. pylori is categorized as a group?Ⅰ?carcinogen since this bacterium is responsible for the highest rate of cancerrelated deaths worldwide. Early detection of cancer can be lifesaving. The 5-year survival rate for gastric cancer patients diagnosed in the early stages is nearly 90%. Gastric cancer is asymptomatic in the early stages but always progresses over time and begins to cause symptoms when untreated. In 97% of stomach cancer cases, cancer cells metastasize to other organs. H. pylori infection is responsible for nearly 60% of the intestinaltype gastric cancer cases but also influences the development of diffuse gastric cancer. The host genetic susceptibility depends on polymorphisms of genes involved in H. pylori-related inflammation and the cytokine response of gastric epithelial and immune cells. H. pylori strains differ in their ability to induce a deleterious inflammatory response. H. pylori-driven cytokines accelerate the inflammatory response and promote malignancy. Chronic H. pylori infection induces genetic instability in gastric epithelial cells and affects the DNA damage repair systems. Therefore, H. pylori infection should always be considered a pro-cancerous factor. | Magdalena Chmiela Zuzanna Karwowska Weronika Gonciarz Bujana Allushi Pawel Staczek | 2017 | World Journal of Gastroenterology2017，23，9： | 37 |
| 2 | Helicobacter pylori vs coronary heart disease-searching for connections显示文摘In this review,we discussed the findings and concepts underlying the potential role of Helicobacter pylori(H.pylori) infections in the initiation,development or persistence of atherosclerosis and coronary heart disease(CHD).This Gram-negative bacterium was described by Marshall and Warren in 1984.The majority of infected subjects carries and transmits H.pylori with no symptoms; however,in some individuals these bacteria may cause peptic ulcers,and even gastric cancers.The widespread prevalence of H.pylori infections and the fact that frequently they remain asymptomatic may suggest that,similarly to intestinal microflora,H.pylori may deliver antigens that stimulate not only local,but also systemic inflammatory response.Recently,possible association between H.pylori infection and extragastric disorders has been suggested.Knowledge on the etiology of atherosclerosis together with current findings in the area of H.pylori infections constitute the background for the newly proposed hypothesis that those two processes may be related.Many research studies confirm the indirect association between the prevalence of H.pylori and the occurrence of CHD.According to majority of findings the involvement of H.pylori in this process is based on the chronic inflammation which might facilitate the CHDrelated pathologies.It needs to be elucidated,if the infection initiates or just accelerates the formation of atheromatous plaque. | Magdalena Chmiela Adrian Gajewski Karolina Rudnicka | 2015 | World Journal of Cardiology2015，7，4： | 33 |
| 3 | Molecular mimicry in Helicobacter pylori infections显示文摘Gram-negative bacteria Helicobacter pylori(H. pylori) colonize gastric mucosa in humans and increase the risk of serious diseases such as gastric and duodenal ulcers, stomach cancers and mucosa associated lymphoid tissue lymphoma. The role of H. pylori infection in the pathogenesis of several extragastric diseases has been suggested including immune thrombocytopenic purpura, iron deficiency anemia, vitamin D deficiency, cardiovascular diseases,diabetes mellitus and dermatological disorders. Also neurological diseases and even lung cancer have attracted researchers concern. The relation between H. pylori infection and a growth retardation in children has also been suggested. Many mechanisms of molecular mimicry between H. pylori and the host have been proposed as a pathogen strategy to manipulate the immune system of the host in order to remain unrecognized and avoid eradication. A lot of effort has been put into the demonstration of homologous sequences between H. pylori and host compounds. However, knowledge about how often autoantibodies or autoreactive T lymphocytes induced during H. pylori infections cause pathological disorders is insufficient. This review provides data on H. pylori antigenic mimicry and possible deleterious effects due to the induction of immune response to the components common to these bacteria and the host. | magdalena chmiela weronika gonciarz | 2017 | World Journal of Gastroenterology2017，23，22： | 24 |
| 4 | Structural modifications of Helicobacter pylori lipopolysaccharide:An idea for how to live in peace显示文摘In this review,we discuss the findings and concepts underlying the'persistence mechanisms'of Helicobacter pylori(H.pylori),a spiral-shaped,Gram-negative rod bacterium that was discovered as a gastric pathogen by Marshall and Warren in 1984.H.pylori colonizes the gastric mucosa of nearly half of the human population.Infections appear in early childhood and,if not treated,persist for life.The presence or absence of symptoms and their severity depend on multiple bacterial components,host susceptibility and environmental factors,which allow H.pylori to switch between pathogenicity and commensalism.Many studies have shown that H.pylori components may facilitate the colonization process and the immune response of the host during the course of H.pylori infection.These H.pylori-driven interactions might result from positive or negative modulation.Among the negative immunomodulators,a prominent position is occupied by a vacuolating toxin A(VacA)and cytotoxin-associated gene A(CagA)protein.However,in light of the recent studies that are presented in this review,it is necessary to enrich this panel with H.pylori lipopolysaccharide(LPS).Together with CagA and VacA,LPS suppresses the elimination of H.pylori bacteria from the gastric mucosa by interfering with the activity of innate and adaptive immune cells,diminishing the inflammatory response,and affecting the adaptive T lymphocyte response,thus facilitating the development of chronic infections.The complex strategy of H.pylori bacteria for survival in the gastric mucosa of the host involves both structural modifications of LPS lipid A to diminish its endotoxic properties and the expression and variation of Lewis determinants,arranged in O-specific chains of H.pylori LPS.By mimicking host components,this phenomenon leaves these bacteria'invisible'to immune cells.Together,these mechanisms allow H.pylori to survive and live for many years within their hosts. | Magdalena Chmiela Karolina Rudnicka Eliza Miszczyk | 2014 | World Journal of Gastroenterology2014，20，29： | 15 |
| 5 | Impact of Helicobacter pylori on the healing process of the gastric barrier显示文摘AIM To determine the impact of selected well defined Helicobacter pylori(H. pylori) antigens on gastric barrier cell turnover.METHODS In this study,using two cellular models of gastric epithelial cells and fibroblasts,we have focused on exploring the effects of well defined H. pylori soluble components such as glycine acid extract antigenic complex(GE),subunit A of urease(Ure A),cytotoxin associated gene A protein(Cag A) and lipopolysaccharide(LPS) on cell turnover by comparing the wound healing capacity of the cells in terms of their proliferative and metabolic activity as well as cell cycle distribution. Toxic effects of H. pylori components have been assessed in an association with damage to cell nuclei and inhibition of signal transducer and activator of transcription 3(STAT3) phosphorylation. RESULTS We showed that H. pylori GE,Cag A and Ure A promoted regeneration of epithelial cells and fibroblasts,which is necessary for effective tissue healing. However,in vivo increased proliferative activity of these cells may constitute an increased risk of gastric neoplasia. In contrast,H. pylori LPS showed a dose-dependent influence on the process of wound healing. At a low concentration(1 ng/m L) H. pylori LPS accelerated of healing epithelial cells,which was linked to significantly enhanced cell proliferation and MTT reduction as well as lack of alterations in cell cycle and downregulation of epidermal growth factor(EGF) production as well as cell nuclei destruction. By comparison,H. pylori LPS at a high concentration(25 ng/m L) inhibited the process of wound repair,which was related to diminished proliferative activity of the cells,cell cycle arrest,destruction of cell nuclei and downregulation of the EGF/STAT3 signalling pathway.CONCLUSION In vivo H. pylori LPS driven effects might lead to the maintenance of chronic inflammatory response and pathological disorders on the level of the gastric mucosal barrier. | Eliza Mnich Magdalena Kowalewicz-Kulbat Paulina Sicińska Krzysztof Hinc Michal Obuchowski Adrian Gajewski Anthony P Moran Magdalena Chmiela | 2016 | World Journal of Gastroenterology2016，22，33： | 4 |
| 6 | Immunophenotype of peripheral blood natural killer cells and IL ‐10 serum levels in relation to Helicobacter pylori status显示文摘 | Karolina Rudnicka Agnieszka Matusiak Eliza Miszczyk Wies?awa Rudnicka Micha? Tenderenda Magdalena Chmiela | 2013 | APMIS2013，，9： | 2 |
| 7 | The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages显示文摘 | Chmiela M Paziak-Domanska B Rudnicka W | 1995 | APMIS1995，103，6： | 1 |
| 8 | Level of mannoge-binding lectin(MBL) in patients with tuberculosis显示文摘 | Bonar A Chmiela M Rzlska B | 2004 | Pneumonol Alergol Pol2004，72，： | 1 |
| 9 | Mannose-binding lectin enhances the attachment and phagocytosis of mycobacteria in vitro显示文摘 | Agnieszka Bonar Magdalena Chmiela Wieslawa Rudnicka | 2005 | Arch Immunol Ther Exp2005，53，： | 1 |
| 10 | Circulating total and active metalloproteinase-9 and tissue inhibitor of metalloproteinases-1 in patients with systemic lupus erythomatosus显示文摘 | Robak E Wierzbowska A Chmiela M | 2006 | Mediators Inflamm2006，2006，1： | 1 |
| 11 | Circulating total and active metalloproteinase-9 and tissue inhibitor of metalloproteinases-1 in patients with systemic lupus erythomatosus 显示文摘 | Robak E Wierzbowska A Chmiela M | 2006 | Mediators Inflamm2006，，17： | 1 |
| 12 | Inflammation,immunity, vaceines for Helicobacter infection显示文摘 | Chmiela M Michetti P | 2006 | Helicobacter2006，11，1： | 1 |
| 13 | Mannose-binding lectin enhances the attachment and phagocytosis of mycobacteria in vitro 显示文摘 | Bonar A Chmiela M Rudnicka W | 2005 | Arch Immunol Ther Exp (Warsz)2005，53，5： | 1 |
| 14 | Level of mannose-binding lectin (MBL)in patients with tuberculosis显示文摘 | Bonar A Chmiela M Rzlska B | 2004 | Pneumonol Alergol Pol2004，72，： | 1 |
| 15 | 波兰矿山救护的组织结构与任务显示文摘介绍了波兰矿山救护组织的组织结构及任务。矿山救护为三级系统的准军事化组织。波兰救护行动是以国家法律为依据的。 | 窦林名 Andrzej CHMIELA Jan PECIAK | 2000 | 矿业安全与环保2000，27，6： | 1 |
| 16 | Networks of companies and branches in Poland显示文摘 | CHMIELA A M SIENKIEWICZA J SUCHECKIA K HOLYST J A | 2007 | Physica A: Statistical Mechanics and Its Applications2007，383，1： | 1 |
| 17 | Circulating total and active metalioproteinase-9 and tissue inhibitor of metalloproteinases-1 in patients with systemic lupus erythomatosus显示文摘 | Robak E Wierzbowska A Chmiela M | 2006 | Mediators Inflamm2006，1，17： | 1 |
| 18 | Detection of Specific Helicobacter pylori DNA and Antigens in Stool Samples in Dyspeptic Patients and Healthy Subjects显示文摘 | Monika Wi?niewska Hans Olof Nilsson Leokadia B?lk‐Romaniszyn Tomasz Rechciński W?adys?aw Bielański Izabela P?aneta‐Ma?ecka Ma?gorzata P?onka Stanis?aw Konturek Torkel Wadstr?m Wies?awa Rudnicka Magdalena Chmiela | 2002 | Microbiology and Immunology2002，，10： | 1 |
| 19 | Potential role of CagA in the inhibition of T cell reactivity in Helicobacter pylori infections 显示文摘 | Paziak Domanska B Chmiela M Jarosinska A | 2000 | Cell Immunol2000，202，： | 1 |
| 20 | Serological Indicators of Helicobacter pylori Infection in Adult Dyspeptic Patients and Healthy Blood Donors显示文摘 | Tomasz Rechciński Magdalena Chmiela Ewa Matecka‐Panas Izabela P?aneta‐Ma?secka Wies?awa Rudnicka | 1997 | Microbiology and Immunology1997，，5： | 1 |
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