Helicobacter pylori evasion strategies of the host innate and adaptive immune responses to survive and develop gastrointestinal diseases

Karkhah, Ahmad; Ebrahimpour, Soheil; Rostamtabar, Maryam; Koppolu, Veerendra; Darvish, Sorena; Vasigala, Veneela Krishna Rekha; Validi, Majid; Nouri, Hamid Reza

doi:10.1016/j.micres.2018.09.011

Cited by 66 publications

(58 citation statements)

References 96 publications

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“…As such, it is beyond the scope of this perspective article to elaborate on them. Further information can be obtained from the following literature references for pathogenic bacteria (Finlay and McFadden, 2006; Flannagan et al, 2015; Thammavongsa et al, 2015; Fisher et al, 2017; Karkhah et al, 2019), endoparasites (Cooper and Eleftherianos, 2016; Gomes et al, 2016; Nakada-Tsukui and Nozaki, 2016; Stijlemans et al, 2016; Wahlgren et al, 2017; Martínez-López et al, 2018), viruses (Finlay and McFadden, 2006; Chan and Gack, 2016; Agrawal et al, 2017; Felix and Savvides, 2017; Hsu, 2018; Soto et al, 2018), and cancer cells (Bhatia and Kumar, 2014; Vinay et al, 2015; Goodman et al, 2017; Bates et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Potential Therapies for Infectious Diseases Based on Targeting Immune Evasion Mechanisms That Pathogens Have in Common With Cancer Cells

Wong

Choi

Liu

et al. 2019

Front. Cell. Infect. Microbiol.

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Many global infectious diseases are not well-controlled, underlining a critical need for new, more effective therapies. Pathogens and pathogen-infected host cells, like cancer cells, evade immune surveillance via immune evasion mechanisms. The present study indicates that pathogenic bacteria, endoparasites, and virus-infected host cells can have immune evasion mechanisms in common with cancers. These include entry into dormancy and metabolic reprogramming to aerobic glycolysis leading to excessive secretion of lactic acid and immobilization of local host immunity. The latter evasion tactic provides a therapeutic target for cancer, as shown by our recent finding that patient-derived cancer xenografts can be growth-arrested, without major host toxicity, by inhibiting their lactic acid secretion (as mediated by the MCT4 transporter)-with evidence of host immunity restoration. Accordingly, the multiplication of bacteria, endoparasites, and viruses that primarily depend on metabolic reprogramming to aerobic glycolysis for survival may be arrested using cancer treatment strategies that inhibit their lactic acid secretion. Immune evasion mechanisms shared by pathogens and cancer cells likely represent fundamental, evolutionarily-conserved mechanisms that may be particularly critical to their welfare. As such, their targeting may lead to novel therapies for infectious diseases.

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Section: Discussionmentioning

confidence: 99%

Potential Therapies for Infectious Diseases Based on Targeting Immune Evasion Mechanisms That Pathogens Have in Common With Cancer Cells

Wong

Choi

Liu

et al. 2019

Front. Cell. Infect. Microbiol.

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“…However, when the damage of the gastric mucosa cannot be completely repaired by the gastric mucosal immunity, H. pylori will smartly escape the immune response to cause further damage to the gastric mucosa, which is called immune escape. In this process, H. pylori escapes from immune response by activating inflammation and TLR cell signal pathways and changing surface molecules to avoid the recognition of innate immune receptors (such as TLRs and RIG-I of DCs) [38,42]. In addition, the infiltration of immune cells (Th1, Treg cells, etc.)…”

Section: The Pathophysiological Mechanism Of Gastric Mucosalmentioning

confidence: 99%

“…In the gastric mucosal innate immunity associated with H. pylori infection, TIFA complex acting as the core regulatory factor and human β -defensin acting as the main component of the innate immune defense mechanism both stimulate the occurrence of adaptive immune response [ 40 , 41 ]. In the gastric mucosal adaptive immunity associated with H. pylori infection, H. pylori initiates the immune response by recognizing pathogen-related molecular pattern through the pattern recognition receptor on gastric epithelial cells and innate immune cells [ 42 ] with the occurrence of Th1- and CD4 + T cell-related response (Th17 and Tregs response), the infiltration of corresponding immune cells and the participation of TNF- α signal pathway [ 32 , 38 , 43 ]. H. pylori can lead to the formation of gastric lymph follicles and the aggregation of lymphocytes in the lamina propria and induce the adaptive immune response by promoting the expression of T cells and B cells with the ability of adsorbing cell adhesion molecule-1 and attracting chemokines (CXCL10 and CCL28) [ 19 ].…”

Section: Gastric Mucosal Immunity and Gastric Diseasesmentioning

confidence: 99%

“…and the expression of corresponding cytokines (such as CCR6 ligand, chemokine CCL20, IFN- γ , and tumor necrosis factor- α ) increase. Chemical gradients produced by cytokines can regulate the expression of cell adhesion receptor-ligand pairs and promote the recruitment of leukocytes to the site of injury, which is beneficial for H. pylori to escape from the host's immune defense, causing chronic inflammation and even gastric cancer [ 19 , 42 , 46 – 48 ].…”

Section: Gastric Mucosal Immunity and Gastric Diseasesmentioning

confidence: 99%

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The Role of Gastric Mucosal Immunity in Gastric Diseases

Nie

Yuan

2020

Journal of Immunology Research

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Gastric mucosa plays its immune function through innate and adaptive immunity by recruiting immune cells and releasing corresponding cytokines, which have an inseparable relationship with gastric diseases. Whether infective gastric diseases caused by Helicobacter pylori, Epstein-Barr virus or other microbe, noninfective gastric diseases, or gastric cancer, gastric mucosal immunity plays an important role in the occurrence and development of the disease. Understanding the unique immune-related tissue structure of the gastric mucosa and its role in immune responses can help prevent gastric diseases or treat them through immunotherapy. In this review, we summarize the basic feature of gastric mucosal immunity and its relationship with gastric diseases to track the latest progress of gastric mucosal immunity, update relevant knowledge and provide theoretical reference for the prevention and treatment of gastric diseases based on the gastric mucosal immunity.

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“…Behaving as microbiota, Hp and its virulent products induce lasting chronic gastrointestinal inflammatory processes and systemic inflammatory reactions by orchestrating and modifying the character of immune system responses. Therefore, it contributes to the pathophysiology of gastrointestinal and systemic disorders …”

Section: Hp In No‐related Glaucoma Pathophysiologymentioning

confidence: 99%

Impact of nitric oxide's bidirectional role on glaucoma: focus onHelicobacter pylori–related nitrosative stress

Papaefthymiou

Doulberis

Katsinelos

et al. 2019

Annals of the New York Academy of Sciences

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Nitric oxide (NO), a small molecule generated ubiquitously, targets a plethora of tissues to regulate both physiological and pathophysiological functions. NO overproduction, stimulated by microenvironmental conditions, is the main component that dysregulates the tight balance between its beneficial and damaging roles in ocular homeostasis. Considering the protective functions of NO against glaucoma, its endogenous release facilitates aqueous humor drainage and regulates ocular blood flow, maintaining a normal intraocular pressure. NO overproduction generates free radicals, such as peroxynitrite, which induce a vicious circle of vascular disharmony and dysregulation, transient ischemia, nitrosative stress, neuronal degeneration, and permanent glaucomatic injury. Helicobacter pylori (Hp) is considered a burdening factor of glaucoma. NO overproduction and possible systematic dispersion in Hp infection (Hp‐I) could suggest a potential pathophysiological bridge between these conditions. In this review, we aim to elucidate the role of NO in glaucoma with respect to Hp‐I, with the aim to stimulate further studies.

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Helicobacter pylori evasion strategies of the host innate and adaptive immune responses to survive and develop gastrointestinal diseases

Cited by 66 publications

References 96 publications

Potential Therapies for Infectious Diseases Based on Targeting Immune Evasion Mechanisms That Pathogens Have in Common With Cancer Cells

Potential Therapies for Infectious Diseases Based on Targeting Immune Evasion Mechanisms That Pathogens Have in Common With Cancer Cells

The Role of Gastric Mucosal Immunity in Gastric Diseases

Impact of nitric oxide's bidirectional role on glaucoma: focus onHelicobacter pylori–related nitrosative stress

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