The relationship between persistent secretion of RANTES and residual infiltration of eosinophils and memory T lymphocytes afterHelicobacter pylori eradication

Kikuchi, Tohru; Kato, Kanefusa; Ohara, Shuichi; Sekine, Hitoshi; Arikawa, Takashi; Suzuki, Toshimitsu; Noguchi, Kenji; Saito, Mizuki; Saito, Yasutoshi; Nishimura, Hiroshi; Toyota, Takayoshi; Shimosegawa, Tooru

doi:10.1002/1096-9896(2000)9999:9999<::aid-path688>3.0.co;2-d

Cited by 38 publications

(31 citation statements)

References 34 publications

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“…Clinical studies suggest that decreased severity of gastritis, and not H. pylori eradication per se, is associated with improvement of dyspeptic symptoms (35). In our study, chronic gastritis improved after H. pylori eradication, but did not resolve, mainly due to persistently increased CD3 ϩ lymphocyte counts, a finding that has also been reported in humans (14). We hypothesize that the residual chronic gut inflammation may result from increased H. pyloriinduced intestinal permeability, which persists after bacterial eradication (36).…”

Section: Discussionmentioning

confidence: 99%

Role of gut-brain axis in persistent abnormal feeding behavior in mice following eradication of Helicobacter pylori infection

Berčík

Verdú²,

Foster³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Here, we investigate the role of the gut-brain axis in gastric dysfunction during and after chronic H. pylori infection. Control and chronically H. pylori-infected Balb/c mice were studied before and 2 mo after bacterial eradication. Gastric motility and emptying were investigated using videofluoroscopy image analysis. Gastric mechanical viscerosensitivity was assessed by cardioautonomic responses to distension. Feeding patterns were recorded by a computer-assisted system. Plasma leptin, ghrelin, and CCK levels were measured using ELISA. IL-1␤, TNF-␣, proopiomelanocortin (POMC), and neuropeptide Y mRNAs were assessed by in situ hybridizations on frozen brain sections. Gastric inflammation was assessed by histology and immunohistochemistry. As shown previously, H. pylori-infected mice ate more frequently than controls but consumed less food per bout, maintaining normal body weight. Abnormal feeding behavior was accompanied by elevated plasma ghrelin and postprandial CCK, higher TNF-␣ (median eminence), and lower POMC (arcuate nucleus) mRNA. Infected mice displayed delayed gastric emptying and visceral hypersensitivity. Eradication therapy normalized gastric emptying and improved gastric sensitivity but had no effect on eating behavior. This was accompanied by persistently increased TNF-␣ in the brain and gastric CD3 ϩ T-cell counts. In conclusion, chronic H. pylori infection in mice alters gastric emptying and mechanosensitivity, which improve after bacterial eradication. A feeding pattern reminiscent of early satiety persists after H. pylori eradication and is accompanied by increased TNF-␣ in the brain. The results support a role for altered gut-brain pathways in the maintenance of postinfective gut dysfunction.inflammation; gut-brain axis; gastric emptying; visceral sensitivity FUNCTIONAL GI DISORDERS SUCH as irritable bowel disease (IBS) and functional dyspepsia (FD) have traditionally been viewed as psychosomatic. The concept that previous infection can trigger the development of functional GI disease is now accepted. A large cohort study identified bacterial gastroenteritis as the most significant risk factor identified to date for the development of IBS (24). IBS symptoms have been reported to develop in a significant proportion of subjects with documented Campylobacter, Salmonella, E. coli, or Shigella infection (12,32,37). A similar case has been also made for functional dyspepsia (18,33). These studies were restricted to acute enteric infections.Accumulating evidence suggests that changes in the bacterial content in the gut can affect the central nervous system (CNS) (10, 13). Most of these studies have dealt with the effect of acute infection and early CNS changes that occurred before the onset of the inflammatory response to the infection. The effect of chronic GI infection and inflammation on the CNS has not yet been investigated. Previous studies suggested that vagal sensory afferents are responsible for the rapid changes that occur in the brain within hours of a GI infection (13). However, multiple...

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Section: Discussionmentioning

confidence: 99%

Role of gut-brain axis in persistent abnormal feeding behavior in mice following eradication of Helicobacter pylori infection

Berčík

Verdú²,

Foster³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Moreover, local IL-18 production can increase tissue eosinophilia through the production of eotaxin from local epithelial cells and macrophages (76). Also, persistent RANTES production in the mucosa has been associated with infiltrating eosinophils in response to H. pylori infection (77). Therefore, it may be important to determine the consequences of RANTES, eotaxin, or IL-18 deficiency for the development of the local mucosal eosinophilia and its impact on resistance against H. pylori infection.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori-Specific Antibodies Impair the Development of Gastritis, Facilitate Bacterial Colonization, and Counteract Resistance against Infection

Akhiani

Schön

Franzén

et al. 2004

The Journal of Immunology

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In recent years, Abs have been considered a correlate rather than an effector of resistance against Helicobacter pylori infection. However, it is still poorly understood to what extent Ab production correlates with gastric immunopathology. Here we report that Abs not only are dispensable for protection, but they are detrimental to elimination of the bacteria and appear to impair gastric inflammatory responses. We found that the initial colonization with H. pylori bacteria was normal in the B cell-deficient (μMT) mice, whereas at later times (>8 wk) most of the bacteria were cleared, concomitant with the development of severe gastritis. In contrast, wild-type (WT) mice exhibited extensive bacterial colonization and only mild gastric inflammation, even at 16 wk after inoculation. Oral immunizations with H. pylori lysate and cholera toxin adjuvant stimulated comparable levels of protection in μMT and WT mice. The level of protection in both strains correlated well with the severity of the postimmunization gastritis. Thus, T cells were responsible for the gastritis, whereas Abs, including potentially host cell cross-reactive Abs, were not involved in causing the gastritis. The T cells in μMT and WT mice produced high and comparable levels of IFN-γ to recall Ag at 2 and after 8 wk, whereas IL-4 was detected after 8 wk only, indicating that Th1 activity dominated the early phase of protection, whereas later a mixed Th1 and Th2 activity was seen.

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“…Notwithstanding the fact that IFN-␥ is particularly important for the development of gastric inflammation, eosinophilic cells may be involved in driving the postimmunization gastritis observed in H. pylori-infected and protected WT animals (6). Whether postimmunization gastritis is a prerequisite for protection is currently being debated (6,12,18,19,67). In any case, eosinophilic cells may contribute to protection (67,68).…”

Section: Discussionmentioning

confidence: 99%

“…Whether postimmunization gastritis is a prerequisite for protection is currently being debated (6,12,18,19,67). In any case, eosinophilic cells may contribute to protection (67,68). However, it should be remembered that another cytokine, IL-5, is better known to play a key regulatory role for eosinophilic cells (31)(32)(33)69).…”

Section: Discussionmentioning

confidence: 99%

Vaccine-Induced Immunity againstHelicobacter pyloriInfection Is Impaired in IL-18-Deficient Mice

Akhiani

Schön

Lycke

2004

The Journal of Immunology

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Protective immunity against Helicobacter pylori infection in mice has been associated with a strong Th1 response, involving IL-12 as well as IFN-γ, but recent studies have also demonstrated prominent eosinophilic infiltration, possibly linked to local Th2 activity in the gastric mucosa. In this study we investigated the role of IL-18, because this cytokine has been found to be a coregulator of Th1 development as well as involved in Th2-type responses with local eotaxin production that could influence gastric eosinophilia and resistance to infection. We found that IL-18−/− mice failed to develop protection after oral immunization with H. pylori lysate and cholera toxin adjuvant, indicating an important role of IL-18 in protection. Well-protected C57BL/6 wild-type (WT) mice demonstrated substantial influx of CD4+ T cells and eosinophilic cells in the gastric mucosa, whereas IL-18−/− mice had less gastritis, few CD4+ T cells, and significantly reduced numbers of eosinophilic cells. T cells in well-protected WT mice produced increased levels of IFN-γ and IL-18 to recall Ag. By contrast, unprotected IL-18−/− mice exhibited significantly reduced gastric IFN-γ and specific IgG2a Ab levels. Despite differences in gastric eosinophilic cell infiltration, protected WT and unprotected IL-18−/− mice had comparable levels of local eotaxin, suggesting that IL-18 influences protection via Th1 development and IFN-γ production rather than through promoting local production of eotaxin and eosinophilic cell infiltration.

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The relationship between persistent secretion of RANTES and residual infiltration of eosinophils and memory T lymphocytes afterHelicobacter pylori eradication

Cited by 38 publications

References 34 publications

Role of gut-brain axis in persistent abnormal feeding behavior in mice following eradication of Helicobacter pylori infection

Role of gut-brain axis in persistent abnormal feeding behavior in mice following eradication of Helicobacter pylori infection

Helicobacter pylori-Specific Antibodies Impair the Development of Gastritis, Facilitate Bacterial Colonization, and Counteract Resistance against Infection

Vaccine-Induced Immunity againstHelicobacter pyloriInfection Is Impaired in IL-18-Deficient Mice

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