The Experts below are selected from a list of 2055 Experts worldwide ranked by ideXlab platform
Steven J. Czinn - One of the best experts on this subject based on the ideXlab platform.
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Helicobacter Infection: pathogenesis.
Current Opinion in Gastroenterology, 2020Co-Authors: Thomas G Blanchard, Maureen L. Drakes, Steven J. CzinnAbstract:Purpose of reviewHelicobacter pylori remains one of the world's most prevalent bacterial pathogens, often causing gastritis, peptic ulcer disease, gastric mucosa-associated lymphatic tissue lymphoma, or gastric adenocarcinoma. Elucidation of H. pylori virulence mechanisms and characteristics of the
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Lack of genetic influence on the innate inflammatory response to Helicobacter Infection of the gastric mucosa
Frontiers in Immunology, 2012Co-Authors: J. Nedrud, Brandon M Zagorski, Steven J. Czinn, Raymond W Redline, Hua Ding, William S. Twaddell, Thomas G BlanchardAbstract:Helicobacter pylori (H. pylori) is a bacterial pathogen that resides at the gastric mucosa and has a world-wide prevalence of over 50%. Infection usually lasts for the life of the host, and although all infected individuals will develop histologic gastritis only a subset will develop symptomatic gastritis, peptic ulcer disease, gastric MALT lymphoma, or gastric adenocarcinoma. The bacterial and host factors that determine clinical outcome and influence the development of widely varying diseases have not been elucidated. We compared disease in Helicobacter-infected SCID mice on different genetic backgrounds with their corresponding immunocompetent partners to determine if the genetics of the host significantly impacts the innate inflammatory outcome, independent of variations in bacterial virulence factors. BALB/c SCID and C57BL/6 SCID mice developed equivalent histologic gastritis by eight weeks of Infection. Immunocompetent BALB/c mice and C57BL/6 mice developed significantly lower or higher degrees of inflammation respectively. Innate inflammation in immunodeficient mice on the C57BL/6 background remained low even in the absence of the regulatory cytokine IL-10. These results demonstrate that adaptive immunity is not required for the generation of low level inflammation in response to Helicobacter Infection and that the degree of inflammation is consistent among different genetic backgrounds. Additionally, this inflammation is limited even in the absence of regulatory T cells.
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protective anti Helicobacter immunity is induced with aluminum hydroxide or complete freund s adjuvant by systemic immunization
The Journal of Infectious Diseases, 2001Co-Authors: Judith M Gottwein, J. Nedrud, Magdalena Tarylehmann, Thomas G Blanchard, Oleg S Targoni, Julia C Eisenberg, Brandon M Zagorski, Paul V. Lehmann, Raymond W Redline, Steven J. CzinnAbstract:To determine whether systemic immunization against Helicobacter pylori could be achieved with an adjuvant approved for human use, the efficacy of vaccination with Helicobacter antigen in combination with aluminum hydroxide (AlOH) was evaluated in a murine model of Helicobacter Infection. Immunization with antigen and AlOH induced interleukin-5–secreting, antigen-specific T cells, and immunization with antigen and complete Freund’s adjuvant induced interferon-γ–secreting, antigen-specific T cells, as determined by ELISPOT assay. Both immune responses conferred protection after challenge with either H. pylori or H. felis, as confirmed by the complete absence of any bacteria, as assessed by both histology and culture of gastric biopsy samples. Protection was antibody independent, as demonstrated with antibody-deficient μMT mice (immunoglobulin-gene knockout mice), and CD4 + spleen T cells from immunized mice were sufficient to transfer protective immunity to otherwise immunodeficient rag1 −/− recipients. These results suggest an alternative and potentially more expeditious strategy for development of a human-use H. pylori vaccine.
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Protective Anti‐Helicobacter Immunity Is Induced with Aluminum Hydroxide or Complete Freund’s Adjuvant by Systemic Immunization
The Journal of Infectious Diseases, 2001Co-Authors: Judith M Gottwein, J. Nedrud, Thomas G Blanchard, Oleg S Targoni, Julia C Eisenberg, Brandon M Zagorski, Paul V. Lehmann, Raymond W Redline, Magdalena Tary-lehmann, Steven J. CzinnAbstract:To determine whether systemic immunization against Helicobacter pylori could be achieved with an adjuvant approved for human use, the efficacy of vaccination with Helicobacter antigen in combination with aluminum hydroxide (AlOH) was evaluated in a murine model of Helicobacter Infection. Immunization with antigen and AlOH induced interleukin-5–secreting, antigen-specific T cells, and immunization with antigen and complete Freund’s adjuvant induced interferon-γ–secreting, antigen-specific T cells, as determined by ELISPOT assay. Both immune responses conferred protection after challenge with either H. pylori or H. felis, as confirmed by the complete absence of any bacteria, as assessed by both histology and culture of gastric biopsy samples. Protection was antibody independent, as demonstrated with antibody-deficient μMT mice (immunoglobulin-gene knockout mice), and CD4 + spleen T cells from immunized mice were sufficient to transfer protective immunity to otherwise immunodeficient rag1 −/− recipients. These results suggest an alternative and potentially more expeditious strategy for development of a human-use H. pylori vaccine.
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Antibody-independent protective mucosal immunity to gastric Helicobacter Infection in mice.
Cellular Immunology, 1999Co-Authors: Thomas G Blanchard, Steven J. Czinn, Raymond W Redline, N. Sigmund, Gregory Harriman, J. NedrudAbstract:Abstract Helicobacter pylori Infection of the gastric mucosa can result in gastritis and peptic ulcer disease. Although vaccination can induce protective immunity in animal models of Helicobacter Infection, the mechanism(s) of protective immunity has not been fully elucidated. This study was designed to determine whether humoral immune responses are required for protective Helicobacter immunity. IgA-deficient or immunoglobulin-deficient mice were orally immunized against Helicobacter felis and then challenged with live H. felis. Both groups were protected at levels comparable to that of wild-type mice. Additionally, inflammation was equivalent in extent and character between wild-type and antibody-deficient mice. Therefore antibody-independent mechanisms of immunity can protect mice against gastric Helicobacter Infection.
J. Nedrud - One of the best experts on this subject based on the ideXlab platform.
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Lack of genetic influence on the innate inflammatory response to Helicobacter Infection of the gastric mucosa
Frontiers in Immunology, 2012Co-Authors: J. Nedrud, Brandon M Zagorski, Steven J. Czinn, Raymond W Redline, Hua Ding, William S. Twaddell, Thomas G BlanchardAbstract:Helicobacter pylori (H. pylori) is a bacterial pathogen that resides at the gastric mucosa and has a world-wide prevalence of over 50%. Infection usually lasts for the life of the host, and although all infected individuals will develop histologic gastritis only a subset will develop symptomatic gastritis, peptic ulcer disease, gastric MALT lymphoma, or gastric adenocarcinoma. The bacterial and host factors that determine clinical outcome and influence the development of widely varying diseases have not been elucidated. We compared disease in Helicobacter-infected SCID mice on different genetic backgrounds with their corresponding immunocompetent partners to determine if the genetics of the host significantly impacts the innate inflammatory outcome, independent of variations in bacterial virulence factors. BALB/c SCID and C57BL/6 SCID mice developed equivalent histologic gastritis by eight weeks of Infection. Immunocompetent BALB/c mice and C57BL/6 mice developed significantly lower or higher degrees of inflammation respectively. Innate inflammation in immunodeficient mice on the C57BL/6 background remained low even in the absence of the regulatory cytokine IL-10. These results demonstrate that adaptive immunity is not required for the generation of low level inflammation in response to Helicobacter Infection and that the degree of inflammation is consistent among different genetic backgrounds. Additionally, this inflammation is limited even in the absence of regulatory T cells.
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protective anti Helicobacter immunity is induced with aluminum hydroxide or complete freund s adjuvant by systemic immunization
The Journal of Infectious Diseases, 2001Co-Authors: Judith M Gottwein, J. Nedrud, Magdalena Tarylehmann, Thomas G Blanchard, Oleg S Targoni, Julia C Eisenberg, Brandon M Zagorski, Paul V. Lehmann, Raymond W Redline, Steven J. CzinnAbstract:To determine whether systemic immunization against Helicobacter pylori could be achieved with an adjuvant approved for human use, the efficacy of vaccination with Helicobacter antigen in combination with aluminum hydroxide (AlOH) was evaluated in a murine model of Helicobacter Infection. Immunization with antigen and AlOH induced interleukin-5–secreting, antigen-specific T cells, and immunization with antigen and complete Freund’s adjuvant induced interferon-γ–secreting, antigen-specific T cells, as determined by ELISPOT assay. Both immune responses conferred protection after challenge with either H. pylori or H. felis, as confirmed by the complete absence of any bacteria, as assessed by both histology and culture of gastric biopsy samples. Protection was antibody independent, as demonstrated with antibody-deficient μMT mice (immunoglobulin-gene knockout mice), and CD4 + spleen T cells from immunized mice were sufficient to transfer protective immunity to otherwise immunodeficient rag1 −/− recipients. These results suggest an alternative and potentially more expeditious strategy for development of a human-use H. pylori vaccine.
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Protective Anti‐Helicobacter Immunity Is Induced with Aluminum Hydroxide or Complete Freund’s Adjuvant by Systemic Immunization
The Journal of Infectious Diseases, 2001Co-Authors: Judith M Gottwein, J. Nedrud, Thomas G Blanchard, Oleg S Targoni, Julia C Eisenberg, Brandon M Zagorski, Paul V. Lehmann, Raymond W Redline, Magdalena Tary-lehmann, Steven J. CzinnAbstract:To determine whether systemic immunization against Helicobacter pylori could be achieved with an adjuvant approved for human use, the efficacy of vaccination with Helicobacter antigen in combination with aluminum hydroxide (AlOH) was evaluated in a murine model of Helicobacter Infection. Immunization with antigen and AlOH induced interleukin-5–secreting, antigen-specific T cells, and immunization with antigen and complete Freund’s adjuvant induced interferon-γ–secreting, antigen-specific T cells, as determined by ELISPOT assay. Both immune responses conferred protection after challenge with either H. pylori or H. felis, as confirmed by the complete absence of any bacteria, as assessed by both histology and culture of gastric biopsy samples. Protection was antibody independent, as demonstrated with antibody-deficient μMT mice (immunoglobulin-gene knockout mice), and CD4 + spleen T cells from immunized mice were sufficient to transfer protective immunity to otherwise immunodeficient rag1 −/− recipients. These results suggest an alternative and potentially more expeditious strategy for development of a human-use H. pylori vaccine.
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Antibody-independent protective mucosal immunity to gastric Helicobacter Infection in mice.
Cellular Immunology, 1999Co-Authors: Thomas G Blanchard, Steven J. Czinn, Raymond W Redline, N. Sigmund, Gregory Harriman, J. NedrudAbstract:Abstract Helicobacter pylori Infection of the gastric mucosa can result in gastritis and peptic ulcer disease. Although vaccination can induce protective immunity in animal models of Helicobacter Infection, the mechanism(s) of protective immunity has not been fully elucidated. This study was designed to determine whether humoral immune responses are required for protective Helicobacter immunity. IgA-deficient or immunoglobulin-deficient mice were orally immunized against Helicobacter felis and then challenged with live H. felis. Both groups were protected at levels comparable to that of wild-type mice. Additionally, inflammation was equivalent in extent and character between wild-type and antibody-deficient mice. Therefore antibody-independent mechanisms of immunity can protect mice against gastric Helicobacter Infection.
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Murine CD4 T-cell response to Helicobacter Infection: TH1 cells enhance gastritis and TH2 cells reduce bacterial load.
Gastroenterology, 1997Co-Authors: M Mohammadi, J. Nedrud, Nils Lycke, Raymond W Redline, Steven J. CzinnAbstract:Abstract BACKGROUND & AIMS: Previous findings suggest that TH1 cellular immune responses contribute to Helicobacter-associated gastritis. To further investigate this issue, interleukin 4 gene targeted mice were infected with Helicobacter felis, and a series of adoptive transfer experiments was performed to evaluate the role of both TH1 and TH2 cells. METHODS: Antigen-specific spleen cells from immunized/challenged or nonimmunized/infected mice or CD4+ T-cell lines were transferred adoptively into naive recipients before live bacterial challenge. RESULTS: Transfer of cells from both groups of donors as well as TH1 or TH2 cell lines exacerbated gastric inflammation in the recipients. No effect on bacterial load was observed in recipients of bulk spleen cells from infected mice or recipients of TH1 cell lines. In contrast, when either a TH2 cell line or bulk cells from immunized challenged mice were transferred adoptively, recipients showed a dramatic reduction in bacterial load. Increased numbers of bacteria were also noted in interleukin 4-deficient mice. CONCLUSIONS: These data suggest a differential contribution of TH1 and TH2 cell-mediated immune responses in Helicobacter Infection: one associated with the pathogenesis of disease (TH1 phenotype) and the other associated with protection from or control of Infection (TH2 phenotype). (Gastroenterology 1997 Dec;113(6):1848-57)
M Mohammadi - One of the best experts on this subject based on the ideXlab platform.
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Murine CD4 T-cell response to Helicobacter Infection: TH1 cells enhance gastritis and TH2 cells reduce bacterial load.
Gastroenterology, 1997Co-Authors: M Mohammadi, J. Nedrud, Nils Lycke, Raymond W Redline, Steven J. CzinnAbstract:Abstract BACKGROUND & AIMS: Previous findings suggest that TH1 cellular immune responses contribute to Helicobacter-associated gastritis. To further investigate this issue, interleukin 4 gene targeted mice were infected with Helicobacter felis, and a series of adoptive transfer experiments was performed to evaluate the role of both TH1 and TH2 cells. METHODS: Antigen-specific spleen cells from immunized/challenged or nonimmunized/infected mice or CD4+ T-cell lines were transferred adoptively into naive recipients before live bacterial challenge. RESULTS: Transfer of cells from both groups of donors as well as TH1 or TH2 cell lines exacerbated gastric inflammation in the recipients. No effect on bacterial load was observed in recipients of bulk spleen cells from infected mice or recipients of TH1 cell lines. In contrast, when either a TH2 cell line or bulk cells from immunized challenged mice were transferred adoptively, recipients showed a dramatic reduction in bacterial load. Increased numbers of bacteria were also noted in interleukin 4-deficient mice. CONCLUSIONS: These data suggest a differential contribution of TH1 and TH2 cell-mediated immune responses in Helicobacter Infection: one associated with the pathogenesis of disease (TH1 phenotype) and the other associated with protection from or control of Infection (TH2 phenotype). (Gastroenterology 1997 Dec;113(6):1848-57)
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Murine CD4 T-cell response to Helicobacter Infection: TH1 cells enhance gastritis and TH2 cells reduce bacterial load
Gastroenterology, 1997Co-Authors: M Mohammadi, J. Nedrud, Nils Lycke, Raymond Redline, Steven J. CzinnAbstract:Background and Aims: Previous findings suggest that TH1 cellular immune responses contribute to Helicobacter-associated gastritis. To further investigate this issue, interleukin 4 gene targeted mice were infected with Helicobacter felis, and a series of adoptive transfer experiments was performed to evaluate the role of both TH1 and TH2 cells. Methods: Antigen- specific spleen cells from immunized/challenged or nonimmunized/infected mice or CD4+T-cell lines were transferred adoptively into naive recipients before live bacterial challenge. Results: Transfer of cells from both groups of donors as well as TH1 or TH2 cell lines exacerbated gastric inflammation in the recipients. No effect on bacterial load was observed in recipients of bulk spleen cells from infected mice or recipients of TH1 cell lines. In contrast, when either a TH2 cell line or bulk cells from immunized challenged mice were transferred adoptively, recipients showed a dramatic reduction in bacterial load. Increased numbers of bacteria were also noted in interleukin 4-deficient mice. Conclusions: These data suggest a differential contribution of TH1 and TH2 cell-mediated immune responses in Helicobacter Infection: One associated with the pathogenesis of disease (TH1 phenotype) and the other associated with protection from or control of Infection (TH2 phenotype).
Jeanmarie Houghton - One of the best experts on this subject based on the ideXlab platform.
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Green Tea and Protection against Helicobacter Infection
Tea in Health and Disease Prevention, 2020Co-Authors: Calin Stoicov, Jeanmarie HoughtonAbstract:Helicobacter Infection is associated with chronic gastritis, ulceration and gastric malignancy. The main treatment for such Infection is antibiotic eradication, but widespread antibiotic use has many drawbacks, including antibiotic resistance, and untoward effects on the host, such as allergic reactions and Clostridium difficile colitis. Because of these limitations, natural agents that can impact bacterial growth and disease progression are attractive. Epidemiological evidence suggests that diet and added dietary compounds can impact both Infection rates and disease outcomes, therefore we examined the in vitro and in vivo effects of green tea on the viability of Helicobacter organisms, and using a mouse model of Infection, demonstrated that green tea consumption can prevent and/or attenuate the mucosal reaction to the bacterium. These findings support a role for green tea as a means of modulating Helicobacter Infection, and encourage investigation into the components of green tea which may be exploited therapeutically for treatment of Infection.
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Helicobacter Infection: Infection, Immunity and the Progression of Lesions to Invasive Gastric Cancer
Pre-Invasive Disease: Pathogenesis and Clinical Management, 2010Co-Authors: Evelyn Kurt-jones, Jeanmarie HoughtonAbstract:Many malignancies that arise in areas of inflammation progress through a series of architectural changes prior to becoming frankly malignant. These changes are often times linked to the acquisition of distinct genetic defects, and predictably the appearance of distinctive lesions depends upon these changes. Gastric cancer arising from Helicobacter Infection is associated with architectural changes similar to those seen in other inflammatory driven malignancies. Tissue progresses from chronic active inflammation to atrophy. Within atrophic mucosa, metaplastic cell types begin to appear, and with long standing disease, adenocarcinoma can result. While temporally associated, it is not clear if the progression of changes from “premalignant” to malignant are causally related. Here we describe the sequence of events leading to the mucosal changes seen, and explore the data which relates these changes to the eventual appearance of gastric adenocarcinoma.
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carcinogenesis of Helicobacter pylori
Gastroenterology, 2007Co-Authors: Pelayo Correa, Jeanmarie HoughtonAbstract:Helicobacter Infection is the leading cause of gastric cancer worldwide. Infection with this ubiquitous bacterium incites a chronic active immune response that persists for the life of the host, in the absence of antibiotic-induced eradication. It is the combination of bacterial factors, environmental insults, and the host immune response that drives the initiation and progression of mucosal atrophy, metaplasia, and dysplasia toward gastric cancer. Although it may seem intuitively obvious that removing the offending organism would negate the cancer risk, this approach is neither feasible (half of the world harbors this Infection) nor is it straightforward. Most patients are infected in childhood, and present with various degrees of mucosal damage before any therapy. This review outlines the histologic progression of human Helicobacter Infection from the early stages of inflammation through the development of metaplasia, dysplasia, and, finally, cancer. The effects of dietary and bacterial eradication therapy on disease progression and lesion reversibility are reviewed within the context of population studies and compared between study designs and populations tested. Eradication studies in the mouse model of Infection prevents the formation of gastric cancer, and allows regression of established lesions, providing a useful model to study interaction between bacterium, environment, and host, without the difficulties inherent in human population studies. Recent advances in identifying the bone marrow-derived stem cell as the cell of origin of Helicobacter -induced gastric cancer in the murine model are discussed and interpreted in the context of human disease, and implications for future treatment are discussed.
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Helicobacter and gastric cancer disease mechanisms: Host response and disease susceptibility
Current Gastroenterology Reports, 2003Co-Authors: Hanchen Li, Timothy C. Wang, Calin Stoicov, Jeanmarie HoughtonAbstract:Helicobacter Infection is the single most common cause of gastric cancer worldwide. Although Infection prevention and eradication of established Infection offer the potential for cure, these strategies are neither feasible nor practical for widespread implementation. Patients most at risk need to be identified and targeted for treatment. For disease to occur, bacterial, environmental, and nutritional factors require a genetically susceptible host. Consequently, it is important to understand how the organism interacts with the host to cause disease. Only through an understanding of what places a patient at risk can we hope to identify susceptible patients early enough in disease to have an impact on their outcome. The immune response is the single most important determinant of disease. Single nucleotide polymorphisms within the promoter region of several critical proinflammatory genes dramatically increase the risk of Helicobacter -associated gastric cancer. Additionally, environmental and dietary factors may modulate the immune response or directly influence key apoptotic and proliferative signaling cascades to alter disease presentation. Lastly, concurrent disease states may have a dramatic impact on the host response to Helicobacter Infection and influence disease. An understanding of the immune signaling pathways responsible for disease and the ways in which environmental risk factors influence these pathways will allow identification of populations that are most at risk and targeted prevention and treatment strategies.
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In Vivo Disruption of the Fas Pathway Abrogates Gastric Growth Alterations Secondary to Helicobactev Infection
The Journal of Infectious Diseases, 2000Co-Authors: Jeanmarie Houghton, Lisa Macera Bloch, Marsha M. Goldstein, Stanley Von Hagen, Reju KorahAbstract:: Helicobacter Infection is associated with gastric cell growth alterations, plausibly predisposing to ulcer disease and gastric adenocarcinoma. Previous investigations from our laboratory have implicated the involvement of the Fas pathway in Helicobacter-induced apoptotic signaling in vitro. In this report we use C57BL/6J00064 mice to examine the direct role of Fas signaling in Helicobacter-mediated growth alterations in vivo. Helicobacter Infection up-regulated gastric cell Fas antigen (Fas Ag) mRNA and increased surface receptor expression, along with concomitant altered apoptotic and proliferative response, measured by terminal deoxytransferase-deoxyuridine 5'-triphosphate nick end labeling and 5-bromo-2'-deoxuridine immunohistochemistry, respectively. In addition, histopathological alterations, including parietal cell loss and gastric atrophy, were noted. In contrast, Infection in B6. MRL-FAS(lpr), a Fas Ag knockout mouse in the C57BL/6 background, did not result in increased apoptosis, proliferation, or histological alterations, a finding that argues strongly for the role of Fas-signaling pathway in orchestrating diverse growth responses to Helicobacter Infection.
Nils Lycke - One of the best experts on this subject based on the ideXlab platform.
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Murine CD4 T-cell response to Helicobacter Infection: TH1 cells enhance gastritis and TH2 cells reduce bacterial load.
Gastroenterology, 1997Co-Authors: M Mohammadi, J. Nedrud, Nils Lycke, Raymond W Redline, Steven J. CzinnAbstract:Abstract BACKGROUND & AIMS: Previous findings suggest that TH1 cellular immune responses contribute to Helicobacter-associated gastritis. To further investigate this issue, interleukin 4 gene targeted mice were infected with Helicobacter felis, and a series of adoptive transfer experiments was performed to evaluate the role of both TH1 and TH2 cells. METHODS: Antigen-specific spleen cells from immunized/challenged or nonimmunized/infected mice or CD4+ T-cell lines were transferred adoptively into naive recipients before live bacterial challenge. RESULTS: Transfer of cells from both groups of donors as well as TH1 or TH2 cell lines exacerbated gastric inflammation in the recipients. No effect on bacterial load was observed in recipients of bulk spleen cells from infected mice or recipients of TH1 cell lines. In contrast, when either a TH2 cell line or bulk cells from immunized challenged mice were transferred adoptively, recipients showed a dramatic reduction in bacterial load. Increased numbers of bacteria were also noted in interleukin 4-deficient mice. CONCLUSIONS: These data suggest a differential contribution of TH1 and TH2 cell-mediated immune responses in Helicobacter Infection: one associated with the pathogenesis of disease (TH1 phenotype) and the other associated with protection from or control of Infection (TH2 phenotype). (Gastroenterology 1997 Dec;113(6):1848-57)
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Murine CD4 T-cell response to Helicobacter Infection: TH1 cells enhance gastritis and TH2 cells reduce bacterial load
Gastroenterology, 1997Co-Authors: M Mohammadi, J. Nedrud, Nils Lycke, Raymond Redline, Steven J. CzinnAbstract:Background and Aims: Previous findings suggest that TH1 cellular immune responses contribute to Helicobacter-associated gastritis. To further investigate this issue, interleukin 4 gene targeted mice were infected with Helicobacter felis, and a series of adoptive transfer experiments was performed to evaluate the role of both TH1 and TH2 cells. Methods: Antigen- specific spleen cells from immunized/challenged or nonimmunized/infected mice or CD4+T-cell lines were transferred adoptively into naive recipients before live bacterial challenge. Results: Transfer of cells from both groups of donors as well as TH1 or TH2 cell lines exacerbated gastric inflammation in the recipients. No effect on bacterial load was observed in recipients of bulk spleen cells from infected mice or recipients of TH1 cell lines. In contrast, when either a TH2 cell line or bulk cells from immunized challenged mice were transferred adoptively, recipients showed a dramatic reduction in bacterial load. Increased numbers of bacteria were also noted in interleukin 4-deficient mice. Conclusions: These data suggest a differential contribution of TH1 and TH2 cell-mediated immune responses in Helicobacter Infection: One associated with the pathogenesis of disease (TH1 phenotype) and the other associated with protection from or control of Infection (TH2 phenotype).