scholarly journals The Protective Effects of Helicobacter pylori Infection on Allergic Asthma

2020 ◽  
Vol 182 (1) ◽  
pp. 53-64
Author(s):  
Zhi Tong Zuo ◽  
Ya Ma ◽  
Yan Sun ◽  
Cui Qing Bai ◽  
Chun Hua Ling ◽  
...  
Keyword(s):  
T Cells ◽  
Helicobacter Pylori ◽  
Allergic Asthma ◽  
Allergic Diseases ◽  
Protective Role ◽  
Helper T Cells ◽  
Protective Effects ◽  
Immune Mediated ◽  
H Pylori ◽  
Allergies And Asthma

As an ancient Gram-negative bacterium, <i>Helicobacter pylori</i> has settled in human stomach. Eradicating <i>H. pylori</i> increases the morbidities of asthma and other allergic diseases. Therefore, <i>H. pylori</i> might play a protective role against asthma. The “disappearing microbiota” hypothesis suggests that the absence of certain types of the ancestral microbiota could change the development of immunology, metabolism, and cognitive ability in our early life, contributing to the development of some diseases. And the Hygiene Hypothesis links early environmental and microbial exposure to the prevalence of atopic allergies and asthma. Exposure to the environment and microbes can influence the growing immune system and protect subsequent immune-mediated diseases. <i>H. pylori</i> can inhibit allergic asthma by regulating the ratio of helper T cells 1/2 (Th1/Th2), Th17/regulatory T cells (Tregs), etc. <i>H. pylori</i> can also target dendritic cells to promote immune tolerance and enhance the protective effect on allergic asthma, and this effect relies on highly suppressed Tregs. The remote regulation of lung immune function by <i>H. pylori</i> is consistent with the gut-lung axis theory. Perhaps, <i>H. pylori</i> also protects against asthma by altering levels of stomach hormones, affecting the autonomic nervous system and lowering the expression of heat shock protein 70. Therapeutic products from <i>H. pylori</i> may be used to prevent and treat asthma. This paper reviews the possible protective influence of <i>H. pylori</i> on allergic asthma and the possible application of <i>H. pylori</i> in treating asthma.

scholarly journals Helicobacter pylori and Immune-mediated Disorders

2020 ◽  
Vol 20 (1) ◽  
pp. 29-37
Author(s):  
Jae Yong Park
Keyword(s):  
Helicobacter Pylori ◽  
Autoimmune Diseases ◽  
Allergic Diseases ◽  
Causative Factor ◽  
Autoimmune Disorders ◽  
Skin Disorders ◽  
Cross Sectional ◽  
Immune Mediated ◽  
H Pylori

Recently, many studies have reported the potential association of <i>Helicobacter pylori</i> (<i>H. pylori</i>) with various extragastric diseases. <i>H. pylori</i>, a major component of the gastric microbiota, is in symbiosis with humans. It is, therefore, assumed to potentially influence immune homeostasis in humans to some extent. There are several reports highlighting the possible association of <i>H. pylori</i> with allergic diseases. However, these were mainly based on cross-sectional or epidemiological studies. With a greater emphasis on the effects of human microbiota on host immunity and disease development, studies have attempted to explain the association between <i>H. pylori</i> infection and allergic diseases. Nevertheless, no concrete evidence for a causal relationship has been clearly demonstrated yet. The association of <i>H. pylori</i> infection with autoimmune disorders has also been reported in the literature. It has been hypothesized that environmental triggers act on genetically vulnerable hosts, leading to autoimmune disorders. The role of <i>H. pylori</i> infection as one of the triggers in autoimmune diseases has been explored previously. However, the results were conflicting and indistinct with respect to most autoimmune diseases. Similar findings were also detected in skin disorders where <i>H. pylori</i> infection was deemed to be a causative factor. The role of <i>H. pylori</i> in majority of the immune-mediated disorders or skin disorders remains controversial. In this review, the association of <i>H. pylori</i> with various immune-mediated disorders and skin disorders is discussed. The epidemiological, serological, and experimental evidences relevant to the aforementioned association are also addressed.

scholarly journals Adoptive Transfer of CD4+ T Cells Specific for Subunit A of Helicobacter pylori Urease ReducesH. pylori Stomach Colonization in Mice in the Absence of Interleukin-4 (IL-4)/IL-13 Receptor Signaling

2001 ◽  
Vol 69 (3) ◽  
pp. 1714-1721 ◽  
Author(s):  
Bernadette Lucas ◽  
Dirk Bumann ◽  
Anna Walduck ◽  
Jan Koesling ◽  
Leyla Develioglu ◽  
...  
Keyword(s):  
T Cells ◽  
Helicobacter Pylori ◽  
Adoptive Transfer ◽  
Bacterial Load ◽  
Interleukin 4 ◽  
T Cell Epitopes ◽  
Necrosis Factor Alpha ◽  
Subunit A ◽  
Ifn Γ ◽  
H Pylori

ABSTRACT Protection in the murine model of Helicobacter pyloriinfection may be mediated by CD4+ T cells, but the mechanism remains unclear. To better understand how protection occurs in this model, we generated and characterized H. pyloriurease-specific CD4+ T cells from BALB/c mice immunized with Salmonella enterica serovar Typhimurium expressingH. pylori urease (subunits A and B). The CD4+ T cells were found to be specific for subunit A (UreA). Upon antigen-specific stimulation, expression of interleukin 4 (IL-4), IL-10, gamma interferon (IFN-γ), and tumor necrosis factor alpha was induced. Immunocytochemical analysis showed that the majority of cells produced IFN-γ and IL-10. Adoptive transfer of the UreA-specific CD4+ T cells into naive syngeneic recipients led to a threefold reduction in the number of bacteria in the recipient group when compared to that in the nonrecipient group. Stomach colonization was also reduced significantly after transfer of these cells into patently infected mice. Adoptive transfer of UreA-specific CD4+ T cells into IL-4 receptor α chain-deficient BALB/c mice indicated that IL-4 and IL-13 were not critical in the control of bacterial load. In addition, synthetic peptides were used to identify three functional T-cell epitopes present in subunit A which were recognized by the UreA-specific T cells. Analysis of H. pylori-specific cellular immune responses in recipient challenged and nonrecipient infected mice indicated a strong local restriction of the response in infected animals. The implications of these findings for the mechanism of protection and the development of peptide-based vaccination are discussed.

scholarly journals Mucosal FOXP3-Expressing CD4+ CD25high Regulatory T Cells in Helicobacter pylori-Infected Patients

2005 ◽  
Vol 73 (1) ◽  
pp. 523-531 ◽  
Author(s):  
Anna Lundgren ◽  
Erika Strömberg ◽  
Åsa Sjöling ◽  
Catharina Lindholm ◽  
Karin Enarsson ◽  
...  
Keyword(s):  
T Cells ◽  
Helicobacter Pylori ◽  
Regulatory T Cells ◽  
Gastric Adenocarcinoma ◽  
Cytotoxic T Lymphocyte ◽  
Duodenal Mucosa ◽  
Peptic Ulcers ◽  
Low Levels ◽  
H Pylori ◽  
And Function

ABSTRACT Helicobacter pylori chronically colonizes the stomach and duodenum and causes peptic ulcers or gastric adenocarcinoma in 10 to 20% of infected individuals. We hypothesize that the inability of patients to clear H. pylori infections is a consequence of active suppression of the immune response. Here we show that H. pylori-infected individuals have increased frequencies of CD4+ CD25high T cells in both the stomach and duodenal mucosa compared to uninfected controls. These cells have the phenotype of regulatory T cells, as they express FOXP3, a key gene for the development and function of regulatory T cells, as well as high levels of the cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) protein. In contrast, mucosal CD4+ CD25low and CD4+ CD25− cells express little FOXP3 mRNA and low levels of the CTLA-4 protein. Mucosal CD4+ CD25high T cells are present in individuals with asymptomatic H. pylori infections as well as in duodenal ulcer patients. The frequencies of CD4+ CD25high cells are also increased in the stomachs of H. pylori-infected patients with gastric adenocarcinoma, particularly in cancer-affected tissues. These findings suggest that regulatory T cells may suppress mucosal immune responses and thereby contribute to the persistence of H. pylori infections.

scholarly journals Role of Transcription Factor T-bet Expression by CD4+ Cells in Gastritis Due to Helicobacter pylori in Mice

2006 ◽  
Vol 74 (8) ◽  
pp. 4673-4684 ◽  
Author(s):  
Kathryn A. Eaton ◽  
Lucy H. Benson ◽  
Jennifer Haeger ◽  
Brian M. Gray
Keyword(s):  
T Cells ◽  
Helicobacter Pylori ◽  
Transcription Factor ◽  
Scid Mice ◽  
Delayed Type Hypersensitivity ◽  
Necrosis Factor Alpha ◽  
Ifn Γ ◽  
H Pylori ◽  
Cd4 Cell

ABSTRACT Gastritis due to Helicobacter pylori is induced by a Th1-mediated response that is CD4 cell and gamma interferon (IFN-γ) dependent. T-bet is a transcription factor that directs differentiation of and IFN-γ secretion by CD4+ Th1 T cells. The goal of this study was to use two mouse models to elucidate the role of T-bet in gastritis due to H. pylori. C57BL/6J mice, congenic T-bet knockout (KO) mutants, or congenic SCID (severe, combined immunodeficient) mutants were given live H. pylori by oral inoculation. SCID mice were given CD4+ splenocytes from C57BL/6J or T-bet KO mice by intraperitoneal injection. Twelve or 24 weeks after bacterial inoculation, C57BL/6J mice developed moderate gastritis but T-bet KO mice and SCID mice did not. In contrast, SCID recipients of either C57BL/6J T cells or T-bet KO T cells developed gastritis 4 or 8 weeks after adoptive transfer. In recipients of C57BL/6J CD4+ cells but not recipients of T-bet KO cells, gastritis was associated with a delayed-type hypersensitivity response to H. pylori antigen and elevated gastric and serum IFN-γ, interleukin 6, and tumor necrosis factor alpha. In spite of the absence of IFN-γ expression, indicating failure of Th1 differentiation, CD4+ T cells from T-bet KO mice induce gastritis in H. pylori-infected recipient SCID mice. This indicates that Th1-independent mechanisms can cause gastric inflammation and disease due to H. pylori.

TLR7 ligand prevents allergen-induced airway hyperresponsiveness and eosinophilia in allergic asthma by a MYD88-dependent and MK2-independent pathway

2006 ◽  
Vol 290 (5) ◽  
pp. L987-L995 ◽  
Author(s):  
J. Moisan ◽  
P. Camateros ◽  
T. Thuraisingam ◽  
D. Marion ◽  
H. Koohsari ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
Allergic Diseases ◽  
Bronchial Tree ◽  
Protective Effects ◽  
Toll Like Receptor ◽  
Asthma Model ◽  
Ifn Γ ◽  
Clinical Potential ◽  
Tlr7 Ligand ◽  
Inflammatory Effect

Asthma is one of the leading causes of childhood hospitalization, and its incidence is on the rise throughout the world. Currently, the standard treatment for asthma is the use of corticosteroids to try to suppress the inflammatory reaction taking place in the bronchial tree. Using a murine model of atopic allergic asthma employing a methacholine-hyperresponsive (A/J) as well as a hyporesponsive (C57BL/6) strain of mice sensitized and challenged with ovalbumin, we show that treatment with a synthetic Toll-like receptor 7 (TLR7) ligand (S-28463, a member of the imidazoquinoline family) prevents development of the asthmatic phenotype. Treatment with S-28463 resulted in a reduction of airway resistance and elastance following ovalbumin sensitization and challenge. This was accompanied by a dramatic reduction in infiltration of leukocytes, especially eosinophils, into the lungs of both C57BL/6 and A/J mice following OVA challenge. Treatment with S-28463 also abolished both the elevation in serum IgE level as well as the induction of IL-4, IL-5, and IL-13 by OVA challenge. The protective effects of S-28463 were also observed in MK2 knockout, but not MYD88 knockout, mice. We did not observe a switch in cytokine profile from TH2 to TH1, as both IL-12p70 and IFN-γ levels were reduced following S-28463 treatment. These results clearly demonstrate the anti-inflammatory effect of imidazoquinolines in an allergic asthma model as well as the clinical potential of TLR7 ligands in the treatment of allergic diseases.

scholarly journals Helicobacter pylori infection prevents allergic asthma in mouse models through the induction of regulatory T cells

2011 ◽  
Vol 121 (8) ◽  
pp. 3088-3093 ◽  
Author(s):  
Isabelle C. Arnold ◽  
Nina Dehzad ◽  
Sebastian Reuter ◽  
Helen Martin ◽  
Burkhard Becher ◽  
...  
Keyword(s):  
T Cells ◽  
Helicobacter Pylori ◽  
Regulatory T Cells ◽  
Allergic Asthma ◽  
Mouse Models ◽  
Helicobacter Pylori Infection

scholarly journals GITR Promotes the Polarization of TFH-Like Cells in Helicobacter pylori-Positive Gastritis

2021 ◽  
Vol 12 ◽  
Author(s):  
Siqi Ming ◽  
Huan Yin ◽  
Xingyu Li ◽  
Sitang Gong ◽  
Guoliang Zhang ◽  
...  
Keyword(s):  
T Cells ◽  
Helicobacter Pylori ◽  
T Cell ◽  
Tumor Necrosis Factor Receptor ◽  
Cell Subset ◽  
Mucosal Inflammation ◽  
T Cell Subset ◽  
Important Regulator ◽  
H Pylori ◽  
Necrosis Factor

Gastric CD4+T cells contribute to Helicobacter pylori (H. pylori)-induced gastritis by amplifying mucosal inflammation and exacerbating mucosal injuries. However, the pathogenic CD4+ T cell subset involved in gastritis and the potential regulators are still unclear. Here we identified an IL-21-producing gastric CD4+T cell subset, which exhibited tissue-resident CXCR5−BTLA−PD-1hi TFH-like phenotype in H. pylori-positive gastritis patients. Meanwhile, we identified glucocorticoid-induced tumor necrosis factor receptor (GITR) as an important regulator to facilitate IL-21 production by CD4+T cells and accelerate mucosal inflammation in gastritis patients with H. pylori infection. Moreover, GITR expression was increased in gastric CD4+T cells of gastritis patients compared to healthy controls, along with the upregulated expression of its ligand GITRL in mucosal macrophages (Mϕ) of gastritis patients. Further observations showed that the activation of GITR/GITRL signal promoted the IL-21 production of CD4+T cells via the STAT3 pathway. Besides this, IL-21 from CD4+T cells induced the proliferation of B cell and promoted the production of inflammatory cytokines IL-1β and IL-6 and chemokines MIP-3α and CCL-25 as well as matrix metalloproteinase (MMP)-3 and MMP-9 by human gastric epithelial cells, suggesting the facilitating effect of IL-21-producing CD4+T cells on mucosal inflammation and injuries. Taking these data together, we revealed that GITR/GITRL signal promoted the polarization of mucosal IL-21-producing CD4+T cells in H. pylori-positive gastritis, which may provide therapeutic strategies for the clinical treatment of H. pylori-induced gastritis.

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