Helicobacter pylori infection and demyelinating disease of the central nervous system

研究成果: ジャーナルへの寄稿評論記事

抄録

Helicobacter pylori (H. pylori) colonize >50% of the entire human population. Generally, H. pylori infect the human stomach in infancy when parietal cells secreting gastric acids, which reduce the survival of H. pylori, are not well matured. Once acquired, the bacterium persists for life. Thus, H. pylori infection reflects sanitary conditions during childhood. >10 studies performed in various Eastern and Western countries as well as two meta-analyses collectively indicated the H. pylori infection rate is significantly lower in patients with multiple sclerosis (MS) than in healthy controls. Thus, the bacterium might be a protective factor for MS, especially in low prevalence countries and younger generations that grew up in the low prevalence era. The protective effects of H. pylori might be explained by the hygiene hypothesis—encountering generic infection early in life facilitates development of the immunoregulatory system, which suppresses overactivity of autoimmune T cells later in life. However, no influence of common childhood infections on MS risk was reported by large MS cohort studies. Direct attenuation of autoreactive Th1 and Th17 cells by H. pylori infection was found in experimental autoimmune encephalomyelitis, an animal model of MS. These observations may underscore the direct protective effects of H. pylori on MS rather than generic infection in childhood. By contrast, several studies reported that H. pylori infection rates are significantly higher in anti-aquaporin-4 (AQP4) antibody-positive neuromyelitis optica spectrum disorder (NMOSD) than in healthy controls. H. pylori strongly activate Th17 cells via the induction of IL-23, resulting in neutrophil mobilization and activation. H. pylori neutrophil-activating protein (NAP) is a major proinflammatory protein responsible for the pathology of H. pylori-related gastric inflammatory diseases. Anti-H. pylori-NAP antibody levels were positively correlated with final EDSS scores and myeloperoxidase levels in anti-AQP4 antibody-positive NMOSD patients. Given that spinal cord lesions of NMOSD are heavily infiltrated with myeloperoxidase-positive neutrophils, H. pylori-NAP, which can be absorbed and presented to the host immune system, may exacerbate NMOSD. Thus, H. pylori infection and its proinflammatory proteins, such as NAP, may contribute to the pathology of anti-AQP4 antibody-related neural damage, by activating neutrophils. It is interesting that two representative demyelinating diseases of the central nervous system are differentially modulated by chronic H. pylori infection. The direct effects of H. pylori infection on MS and NMOSD warrant future studies.

元の言語英語
ページ(範囲)14-19
ページ数6
ジャーナルJournal of Neuroimmunology
329
DOI
出版物ステータス出版済み - 4 15 2019

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Helicobacter Infections
Demyelinating Diseases
Helicobacter pylori
Central Nervous System
Neuromyelitis Optica
Multiple Sclerosis
Aquaporin 4
Th17 Cells
Neutrophils
Antibodies
Peroxidase
Infection
Pathology
Bacteria
Interleukin-23
Stomach Diseases
Neutrophil Activation
Th1 Cells
Proteins
Autoimmune Experimental Encephalomyelitis

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

これを引用

Helicobacter pylori infection and demyelinating disease of the central nervous system. / Kira, Jun-Ichi; Isobe, Noriko.

:: Journal of Neuroimmunology, 巻 329, 15.04.2019, p. 14-19.

研究成果: ジャーナルへの寄稿評論記事

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abstract = "Helicobacter pylori (H. pylori) colonize >50{\%} of the entire human population. Generally, H. pylori infect the human stomach in infancy when parietal cells secreting gastric acids, which reduce the survival of H. pylori, are not well matured. Once acquired, the bacterium persists for life. Thus, H. pylori infection reflects sanitary conditions during childhood. >10 studies performed in various Eastern and Western countries as well as two meta-analyses collectively indicated the H. pylori infection rate is significantly lower in patients with multiple sclerosis (MS) than in healthy controls. Thus, the bacterium might be a protective factor for MS, especially in low prevalence countries and younger generations that grew up in the low prevalence era. The protective effects of H. pylori might be explained by the hygiene hypothesis—encountering generic infection early in life facilitates development of the immunoregulatory system, which suppresses overactivity of autoimmune T cells later in life. However, no influence of common childhood infections on MS risk was reported by large MS cohort studies. Direct attenuation of autoreactive Th1 and Th17 cells by H. pylori infection was found in experimental autoimmune encephalomyelitis, an animal model of MS. These observations may underscore the direct protective effects of H. pylori on MS rather than generic infection in childhood. By contrast, several studies reported that H. pylori infection rates are significantly higher in anti-aquaporin-4 (AQP4) antibody-positive neuromyelitis optica spectrum disorder (NMOSD) than in healthy controls. H. pylori strongly activate Th17 cells via the induction of IL-23, resulting in neutrophil mobilization and activation. H. pylori neutrophil-activating protein (NAP) is a major proinflammatory protein responsible for the pathology of H. pylori-related gastric inflammatory diseases. Anti-H. pylori-NAP antibody levels were positively correlated with final EDSS scores and myeloperoxidase levels in anti-AQP4 antibody-positive NMOSD patients. Given that spinal cord lesions of NMOSD are heavily infiltrated with myeloperoxidase-positive neutrophils, H. pylori-NAP, which can be absorbed and presented to the host immune system, may exacerbate NMOSD. Thus, H. pylori infection and its proinflammatory proteins, such as NAP, may contribute to the pathology of anti-AQP4 antibody-related neural damage, by activating neutrophils. It is interesting that two representative demyelinating diseases of the central nervous system are differentially modulated by chronic H. pylori infection. The direct effects of H. pylori infection on MS and NMOSD warrant future studies.",
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AU - Kira, Jun-Ichi

AU - Isobe, Noriko

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N2 - Helicobacter pylori (H. pylori) colonize >50% of the entire human population. Generally, H. pylori infect the human stomach in infancy when parietal cells secreting gastric acids, which reduce the survival of H. pylori, are not well matured. Once acquired, the bacterium persists for life. Thus, H. pylori infection reflects sanitary conditions during childhood. >10 studies performed in various Eastern and Western countries as well as two meta-analyses collectively indicated the H. pylori infection rate is significantly lower in patients with multiple sclerosis (MS) than in healthy controls. Thus, the bacterium might be a protective factor for MS, especially in low prevalence countries and younger generations that grew up in the low prevalence era. The protective effects of H. pylori might be explained by the hygiene hypothesis—encountering generic infection early in life facilitates development of the immunoregulatory system, which suppresses overactivity of autoimmune T cells later in life. However, no influence of common childhood infections on MS risk was reported by large MS cohort studies. Direct attenuation of autoreactive Th1 and Th17 cells by H. pylori infection was found in experimental autoimmune encephalomyelitis, an animal model of MS. These observations may underscore the direct protective effects of H. pylori on MS rather than generic infection in childhood. By contrast, several studies reported that H. pylori infection rates are significantly higher in anti-aquaporin-4 (AQP4) antibody-positive neuromyelitis optica spectrum disorder (NMOSD) than in healthy controls. H. pylori strongly activate Th17 cells via the induction of IL-23, resulting in neutrophil mobilization and activation. H. pylori neutrophil-activating protein (NAP) is a major proinflammatory protein responsible for the pathology of H. pylori-related gastric inflammatory diseases. Anti-H. pylori-NAP antibody levels were positively correlated with final EDSS scores and myeloperoxidase levels in anti-AQP4 antibody-positive NMOSD patients. Given that spinal cord lesions of NMOSD are heavily infiltrated with myeloperoxidase-positive neutrophils, H. pylori-NAP, which can be absorbed and presented to the host immune system, may exacerbate NMOSD. Thus, H. pylori infection and its proinflammatory proteins, such as NAP, may contribute to the pathology of anti-AQP4 antibody-related neural damage, by activating neutrophils. It is interesting that two representative demyelinating diseases of the central nervous system are differentially modulated by chronic H. pylori infection. The direct effects of H. pylori infection on MS and NMOSD warrant future studies.

AB - Helicobacter pylori (H. pylori) colonize >50% of the entire human population. Generally, H. pylori infect the human stomach in infancy when parietal cells secreting gastric acids, which reduce the survival of H. pylori, are not well matured. Once acquired, the bacterium persists for life. Thus, H. pylori infection reflects sanitary conditions during childhood. >10 studies performed in various Eastern and Western countries as well as two meta-analyses collectively indicated the H. pylori infection rate is significantly lower in patients with multiple sclerosis (MS) than in healthy controls. Thus, the bacterium might be a protective factor for MS, especially in low prevalence countries and younger generations that grew up in the low prevalence era. The protective effects of H. pylori might be explained by the hygiene hypothesis—encountering generic infection early in life facilitates development of the immunoregulatory system, which suppresses overactivity of autoimmune T cells later in life. However, no influence of common childhood infections on MS risk was reported by large MS cohort studies. Direct attenuation of autoreactive Th1 and Th17 cells by H. pylori infection was found in experimental autoimmune encephalomyelitis, an animal model of MS. These observations may underscore the direct protective effects of H. pylori on MS rather than generic infection in childhood. By contrast, several studies reported that H. pylori infection rates are significantly higher in anti-aquaporin-4 (AQP4) antibody-positive neuromyelitis optica spectrum disorder (NMOSD) than in healthy controls. H. pylori strongly activate Th17 cells via the induction of IL-23, resulting in neutrophil mobilization and activation. H. pylori neutrophil-activating protein (NAP) is a major proinflammatory protein responsible for the pathology of H. pylori-related gastric inflammatory diseases. Anti-H. pylori-NAP antibody levels were positively correlated with final EDSS scores and myeloperoxidase levels in anti-AQP4 antibody-positive NMOSD patients. Given that spinal cord lesions of NMOSD are heavily infiltrated with myeloperoxidase-positive neutrophils, H. pylori-NAP, which can be absorbed and presented to the host immune system, may exacerbate NMOSD. Thus, H. pylori infection and its proinflammatory proteins, such as NAP, may contribute to the pathology of anti-AQP4 antibody-related neural damage, by activating neutrophils. It is interesting that two representative demyelinating diseases of the central nervous system are differentially modulated by chronic H. pylori infection. The direct effects of H. pylori infection on MS and NMOSD warrant future studies.

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