<i>Helicobacter pylori</i> heat shock protein B (HspB) localizes in vivo in the gastric mucosa and MALT lymphoma

Luca, Antonio De; Falco, Maria De; Manente, Lucrezia; Dattilo, D; Lucariello, Angela; Esposito, Vincenzo; Gnarini, Mariarosaria; Citro, Gennaro; Baldi, Alfonso; Tufano, Maria Antonietta; Iaquinto, Gaetano

doi:10.1002/jcp.21376

Cited by 8 publications

(7 citation statements)

References 48 publications

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“…As for the relationship between MALT lymphoma and H. pylori factors, the presence of anti‐CagA IgG antibodies were confirmed to be a risk factor for lymphoid follicle development in patients with gastritis [48]. Immunohistochemistry analyses showed that cytoplasmic heat shock protein B (HspB) immunostaining was observed in groups of neoplastic cells of MALT lymphoma [49]. HspB is one of the dominant proteins of H. pylori and is being considered as a potential candidate for subunit vaccines, and the data suggest a possible involvement of HspB in the pathogenesis of H. pylori ‐related development of MALT lymphoma.…”

Section: Gastric Carcinomamentioning

confidence: 99%

Helicobacter and Gastric Malignancies

et al. 2008

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Individuals infected with Helicobacter pylori, a stomach colonizing bacteria, have an increased risk of developing gastric malignancies. The risk for developing cancer relates to the physiologic and histologic changes that H. pylori infection induces in the stomach. In the last year numerous studies have been conducted in order to characterize the association between H. pylori infection and gastric cancer. These studies range from epidemiologic approaches aiming at the identification of environmental, host genetic, and bacterial factors associated with risk of gastric cancer, to molecular and cell biology approaches aiming at understanding the interaction between H. pylori and the transforming epithelial cell. In this review an account of the last year’s research activity on the relationship between H. pylori and gastric cancer will be given.

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Section: Gastric Carcinomamentioning

confidence: 99%

Helicobacter and Gastric Malignancies

et al. 2008

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“… 34 Heat shock proteins are essential stress-induced molecular chaperones that facilitate protein folding and remodeling critical for virtually all main cellular processes, 35 with evidence of intracellular localization in the cytosol of infected gastric mucosa cells. 36 Proteomic studies showed that H. pylori cysteine-rich proteins can interact directly and indirectly in complex formation with human heat shock protein members and other intracellular proteins important in the response to viral and bacterial infection. 37 HspA by itself is a strong promoter of an inflammatory-type cytokine response via the Toll-like receptor-4-mediated signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Live Attenuated Measles Virus Vaccine Expressing Helicobacter pylori Heat Shock Protein A

Iankov

Kurokawa

Viker

et al. 2020

Molecular Therapy - Oncolytics

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Measles virus (MV) Edmonston derivative strains are attractive vector platforms in vaccine development and oncolytic virotherapy. Helicobacter pylori heat shock protein A (HspA) is a bacterial heat shock chaperone with essential function as a Ni-ion scavenging protein. We generated and characterized the immunogenicity of an attenuated MV strain encoding the HspA transgene (MV-HspA). MV-HspA showed faster replication within 48 h of infection with >10-fold higher titers and faster accumulation of the MV proteins. It also demonstrated a superior tumor-killing effect in vitro against a variety of human solid tumor cell lines, including sarcoma, ovarian and breast cancer. Two intraperitoneal (i.p.) doses of 10 6 50% tissue culture infectious dose (TCID 50 ) MV-HspA significantly improved survival in an ovarian cancer xenograft model: 63.5 days versus 27 days for the control group. The HspA transgene induced a humoral immune response in measles-permissive Ifnarko-CD46Ge transgenic mice. Eight of nine animals developed a long-term anti-HspA antibody response with titers of 1:400 to 1:12,800 without any negative impact on development of protective anti-MV immune memory. MV-HspA triggered an immunogenic cytopathic effect as measured by an HMGB1 assay. The absence of significant elevation of PD-L1 expression indicated that vector-encoded HspA could act as an immunomodulator on the immune check point axis. These data demonstrate that MV-HspA is a potent oncolytic agent and vaccine candidate for clinical translation in cancer treatment and immunoprophylaxis against H. pylori .

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“…Consequently, H. pylori ‐infected cells are impeded to activate the antioxidant response (Buommino et al, ). Moreover, co‐expression of CagA and HspB in AGS cells is able to induce cell cycle proliferation through an increase of rate of transit between the S/G2‐M phase of the cell cycle associated with a specific increase in cyclin D3 and Retinoblastoma gene product, Rb, in its phosphorylated form (De Luca et al, 2003, 2008). Hence, HspB deserves great attention since it has been demonstrated that its activity increases the risk of gastric carcinoma (Iaquinto et al, ).…”

Section: Molecular Mechanism Of H Pylori Pathogenesismentioning

confidence: 99%

Molecular Mechanisms ofHelicobacter pyloriPathogenesis

et al. 2015

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Helicobacter pylori infects 50% of mankind. The vast majority of H. pylori infection occurs in the developing countries where up to 80% of the middle-aged adults may be infected. Bacterial infection causes an inflammatory response that proceeds through a series of intermediated stages of precancerous lesions (gastritis, atrophy, intestinal metaplasia, and dysplasia). Among infected individuals, approximately 10% develops severe gastric lesions such as peptic ulcer disease, 1-3% progresses to gastric cancer (GC) with a low 5-year survival rate, and 0.1% develops mucosa-associated lymphoid tissue (MALT). GC is one of the most common cancer and the third leading cause of cancer-related deaths worldwide. In this review, we have summarized the most recent papers about molecular mechanisms of H. pylori pathogenesis. The main important steps of H. pylori infection such as adhesion, entry in epithelial gastric cells, activation of intracellular pathways until epigenetic modifications have been described.

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Helicobacter pylori heat shock protein B (HspB) localizes in vivo in the gastric mucosa and MALT lymphoma

Cited by 8 publications

References 48 publications

Helicobacter and Gastric Malignancies

Helicobacter and Gastric Malignancies

Live Attenuated Measles Virus Vaccine Expressing Helicobacter pylori Heat Shock Protein A

Molecular Mechanisms ofHelicobacter pyloriPathogenesis

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