A role for altered phagosome maturation in the long-term persistence ofHelicobacter pyloriinfection

2012 ◽  
Vol 303 (2) ◽  
pp. G169-G179 ◽  
Author(s):  
Glenn N. Borlace ◽  
Stacey J. Keep ◽  
Mark J. R. Prodoehl ◽  
Hilary F. Jones ◽  
Ross N. Butler ◽  
...  
Keyword(s):  
Immune Response ◽  
Host Immune Response ◽  
Human Gastric Mucosa ◽  
Phagosome Maturation ◽  
Duodenal Ulcers ◽  
Immune Effector ◽  
Effector Cells ◽  
Gastric Or Duodenal Ulcers ◽  
H Pylori

The vigorous host immune response that is mounted against Helicobacter pylori is unable to eliminate this pathogenic bacterium from its niche in the human gastric mucosa. This results in chronic inflammation, which can develop into gastric or duodenal ulcers in 10% of infected individuals and gastric cancer in 1% of infections. The determinants for these more severe pathologies include host (e.g., high IL-1β expression polymorphisms), bacterial [e.g., cytotoxicity-associated gene ( cag) pathogenicity island], and environmental (e.g., dietary nitrites) factors. However, it is the failure of host immune effector cells to eliminate H. pylori that underlies its persistence and the subsequent H. pylori-associated disease. Here we discuss the mechanisms used by H. pylori to survive the host immune response and, in particular, the role played by altered phagosome maturation.

Correlation of the H. pylori adhesin BabA with gastritis, bacterial colonisation and host immune response

2001 ◽  
Vol 120 (5) ◽  
pp. A514
Author(s):  
Roland Rad ◽  
Markus Gerhard ◽  
Petra Voland ◽  
Thomas Roesch ◽  
Martin Schoeninger ◽  
...  
Keyword(s):  
Immune Response ◽  
Host Immune Response ◽  
Bacterial Colonisation ◽  
H Pylori

scholarly journals ABO blood group, secretor status and detection ofHelicobacter pyloriamong patients with gastric or duodenal ulcers

1991 ◽  
Vol 106 (2) ◽  
pp. 221-229 ◽  
Author(s):  
A. Mentis ◽  
C. C. Blackwell ◽  
D. M. Weir ◽  
C. Spiliadis ◽  
A. Dailianas ◽  
...  
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Gastric Ulcer ◽  
Blood Group ◽  
Local Population ◽  
Abo Blood Group ◽  
Duodenal Ulcers ◽  
Secretor Status ◽  
Gastric Or Duodenal Ulcers ◽  
H Pylori

SUMMARYPatients (454) referred for gastroscopy to the General Hospital of Athens were examined to determine (1) if non-secretors were over-represented among patients with ulcers and (2) is there was an association with ABO blood group or secretor status and carriage ofHelicobacter pylori.Compared with the local population, among patients with either gastric ulcer (51) or duodenal ulcer (96) there was a significant increase in the proportion of those who were blood group O (P< 0·025); however, there were no significant differences in the proportions of non-secretors.H. pyloriwas identified in 62 % of the 454 patients: 59·5 % of those without evidence of ulcers; 62·5 % of those with gastric ulcer; 88% of those with duodenal ulcer (P< 0·0005). These bacteria were cultured more often and in higher numbers from patients with duodenal ulcer (P< 0·025). There was no association between ABO blood group and prevalence ofH. pylori. The prevalence ofH. pyloriamong non-secretors with gastric ulcer (12·5%) was significantly lower than that for non-secretors with duodenal ulcer (100%) (P< 0·0005). This was not observed for secretors.

Immune Self-tuning in Renal Cell Carcinoma

2010 ◽  
Vol 06 (01) ◽  
pp. 70
Author(s):  
Antonia Busse ◽  
Ulrich Keilholz ◽  
◽  
Keyword(s):  
Renal Cell Carcinoma ◽  
Immune Response ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Disease Stabilisation ◽  
Tumour Regression ◽  
Immune Effector ◽  
Effector Cells ◽  
Immune Effector Cells ◽  
Inhibitory Molecules

Although renal cell carcinoma (RCC) is an immunogenic tumour, and although there is evidence that in a small proportion of cases antitumour immune responses may mediate tumour regression or at least disease stabilisation, patients with progressive disease have no effective antitumour immune response. Besides preventing recognition of the tumour by immune effector cells, RCC escapes the immune system by induction of tolerance through manipulating the function and proliferation of immune effector cells. This tuning of the immune response can occur by active suppression of immune effector cells through inhibitory molecules expressed on the tumour surface and through various tumour-secreted soluble factors, or it can be mediated indirectly by induction of immunosuppressive cells. This review provides an overview of the most common mechanisms that mediate immune tolerance in RCC and discusses the therapeutic perspectives of immunoregulatory strategies in the era of targeted therapies.

Cellular side of acquired immunity (T cells)

2013 ◽  
Author(s):  
Assia Eljaafari ◽  
Pierre Miossec
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Immune System ◽  
Disease Process ◽  
T Cell Response ◽  
Th2 Cells ◽  
Cell Mediated Immunity ◽  
Immune Effector ◽  
Effector Cells ◽  
Th22 Cells

The adaptive T-cell response represents the most sophisticated component of the immune response. Foreign invaders are recognized first by cells of the innate immune system. This leads to a rapid and non-specific inflammatory response, followed by induction of the adaptive and specific immune response. Different adaptive responses can be promoted, depending on the predominant effector cells that are involved, which themselves depend on the microbial/antigen stimuli. As examples, Th1 cells contribute to cell-mediated immunity against intracellular pathogens, Th2 cells protect against parasites, and Th17 cells act against extracellular bacteria and fungi that are not cleared by Th1 and Th2 cells. Among the new subsets, Th22 cells protect against disruption of epithelial layers secondary to invading pathogens. Finally these effector subsets are regulated by regulatory T cells. These T helper subsets counteract each other to maintain the homeostasis of the immune system, but this balance can be easily disrupted, leading to chronic inflammation or autoimmune diseases. The challenge is to detect early changes in this balance, prior to its clinical expression. New molecular tools such as microarrays could be used to determine the predominant profile of the immune effector cells involved in a disease process. Such understanding should provide better therapeutic tools to counteract deregulated effector cells.

scholarly journals Listeriolysin O is a target of the immune response to Listeria monocytogenes.

1992 ◽  
Vol 175 (6) ◽  
pp. 1467-1471 ◽  
Author(s):  
H G Bouwer ◽  
C S Nelson ◽  
B L Gibbins ◽  
D A Portnoy ◽  
D J Hinrichs
Keyword(s):  
Immune Response ◽  
Listeria Monocytogenes ◽  
Gene Product ◽  
Cell Subset ◽  
Target Antigen ◽  
Target Cells ◽  
Listeriolysin O ◽  
Immune Effector ◽  
Effector Cells ◽  
Cytotoxic Cells

The immunologic mechanism of protective immunity to the intracellular parasite Listeria monocytogenes (Lm) is not well understood, however, antilisterial immunity can be adoptively transferred with T lymphocytes from Lm-immune donors. The Lm-immune cells are believed to produce macrophage-activating lymphokines, which leads to the eventual macrophage-dependent eradication of the bacterium. Increasing evidence suggests that immunity to Lm resides exclusively within the CD8+ T cell subset. It is possible that the Lm-immune CD8+ T cells function to release sequestered Lm from nonprofessional phagocytes to awaiting activated macrophage populations. This study was conducted to determine if listeriolysin O (LLO), which is an essential determinant of Lm pathogenicity, is also a target of the antilisterial immune response. We have found that target cells infected with a LLO+ Lm strain are lysed by Lm-immune cytotoxic cells, whereas target cells infected with a LLO- Lm mutant, or pulsed with a heat-killed Lm preparation, are not lysed by the Lm-immune effector cells. We have used a Bacillus subtilis (Bs) construct that expresses the LLO gene product and found that target cells infected with the LLO+ Bs construct are lysed by antilisterial cytotoxic cells. The antilisterial cytotoxic response is targeted against LLO, in that we have also used a Bs construct that expresses the perfringolysin (PLO) gene product and found that target cells infected with the PLO+ Bs are not lysed by antilisterial cytotoxic effector cells. These data strongly suggest that LLO is a target antigen of antilisterial immunity and may represent the dominant target during the expression of the immune response to Lm.

Unravelling some mysteries of porcine respiratory and reproductive syndrome virus (PRRSV) infections: new insights from modelling studies

2009 ◽  
Vol 2009 ◽  
pp. 30-30
Author(s):  
A Doeschl-Wilson ◽  
I Kyriazakis ◽  
L Galina-Pantoja
Keyword(s):  
Immune Response ◽  
Host Immune Response ◽  
Growing Pigs ◽  
Modelling Studies ◽  
Porcine Respiratory ◽  
Insight Into

Porcine reproductive and respiratory syndrome (PRRS) is an endemic pig disease in most European countries, causing respiratory distress, fever and growth reductions in growing pigs and increased litter mortality in sows. The disease is characterised by exceptionally long-term viral persistence within the host, a weak innate host immune response and delayed adaptive host immune response, and large between animal variation in the immune response (Murtaugh et al., 2004). Although numerous in-vitro and in-vivo studies produced valid insight into the fine details of the virus dynamics and its interaction with the host’s immune response, several fundamental questions concerning the role of diverse immune components and host genetics remain unanswered. In this study mathematical models were developed to investigate the role of diverse processes caused by the virus or the immune response on the infection characteristics.

Do CD8 effector cells need IL-7R expression to become resting memory cells?

Blood ◽  
2006 ◽  
Vol 108 (6) ◽  
pp. 1949-1956 ◽  
Author(s):  
Eva Buentke ◽  
Anne Mathiot ◽  
Mauro Tolaini ◽  
James Di Santo ◽  
Rose Zamoyska ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
T Cell ◽  
Half Life ◽  
Effector T Cells ◽  
Memory Cells ◽  
Effector Cells ◽  
Physiological Conditions ◽  
Transgenic Model

Abstract The role for IL-7R expression in the differentiation of effector T cells into resting memory remains controversial. Here, using a conditional IL-7R transgenic model, we were able to test directly whether CD8 effector T cells require IL-7R expression for their differentiation into resting memory cells. In the absence of IL-7R expression, effector cells transferred into “full” hosts underwent a protracted and unremitting contraction compared with IL-7R–expressing control cells and were unable to develop into long-term resting memory cells. Surprisingly, when the same effector cells were transferred into empty T-cell–deficient hosts, they could generate long-lived fully functional resting memory cells independently of IL-7R expression. Formation of these latter cells was found to be dependent on IL-15, because the same IL-7R–deficient effector cells were rapidly lost from IL-15–deficient hosts, having a half-life of less than 40 hours. Therefore, our data suggest that, under physiological conditions, both IL-7 and IL-15 synergize to promote the formation of memory cells directly by limiting the contraction of effectors that occurs following an immune response and that reexpression of IL-7R is a key checkpoint in the regulation of this process.

scholarly journals Long-term Host Immune Response Trajectories Among Hospitalized Patients With Sepsis

2019 ◽  
Vol 2 (8) ◽  
pp. e198686 ◽  
Author(s):  
Sachin Yende ◽  
John A. Kellum ◽  
Victor B. Talisa ◽  
Octavia M. Peck Palmer ◽  
Chung-Chou H. Chang ◽  
...  
Keyword(s):  
Immune Response ◽  
Host Immune Response ◽  
Hospitalized Patients

Studies on the mechanism of long term survival of Taenia taeniaeformis in rats

1978 ◽  
Vol 52 (1) ◽  
pp. 1-6 ◽  
Author(s):  
B. H. Kwa ◽  
F. Y. Liew
Keyword(s):  
Immune Response ◽  
Host Immune Response ◽  
The Other ◽  
Cell Adherence ◽  
Term Survival ◽  
Blocking Antibody ◽  
Long Term Survival ◽  
Other Hand ◽  
Taenia Taeniaeformis

ABSTRACTAn attempt was made to determine if blocking antibody is involved in protecting cysticerci of Taenia taeniaeformis against a host immune response. Immunoflourescence microscopy confirmed that host antibody is present on the parasite surface within the capsule. To test if the larvae can still survive after such a coat of blocking antibody is removed, the larvae were trypsinised and then implanted into recipients. The results indicate that blocking antibody could be involved in the survival of 1 year old established larvae. Untrypsinised larvae were normal 14 days after implantation into control or immunised rats. Trypsinised larvae implanted in control rats were alive but showed on intense cell adherence on their surface. On the other hand, trypsinised larvae implanted into immunised rats were dead and completely encapsulated. However, experiments with 1 month old larvae were inconclusive.

scholarly journals Motion – Helicobacter pylori Causes or Worsens GERD: Arguments for the Motion

2002 ◽  
Vol 16 (9) ◽  
pp. 611-614 ◽  
Author(s):  
Colm A O’Morain ◽  
Asghar Qasim
Keyword(s):  
Helicobacter Pylori ◽  
Epidemiological Data ◽  
Acid Suppression ◽  
Duodenal Ulcers ◽  
Ulcer Disease ◽  
Acid Suppression Therapy ◽  
Premalignant Condition ◽  
H Pylori ◽  
Gerd Symptoms

There are several reasons for eradicating Helicobacter pylori in patients with chronic gastroesophageal reflux disease (GERD). Perhaps the most compelling is the evidence that chronic acid suppression therapy can lead to the development of atrophic gastritis, a premalignant condition, in patients with H pylori infection. Epidemiological data that suggest that H pylori is less prevalent in GERD patients than in control subjects may be susceptible to publication bias, and confounding social and environmental factors may also be involved. Although it has been thought that eradication of the organism might lead to increased esophageal acid exposure, this has not been demonstrated in practice. Studies that appeared to show that GERD could be provoked by antimicrobial therapy of duodenal ulcers also have methodological weaknesses. Underlying GERD symptoms might be unmasked after withdrawal of acid-suppression therapy, for reasons that are unrelated to H pylori. In fact, eradication of the organism has been shown to decrease heartburn in patients with peptic ulcer disease. When H pylori is successfully eradicated in patients with GERD, relapse rates are not increased, and the disease- free interval seems to be prolonged. Eradication of the organism is a wise policy in patients who face long term acid-suppression therapy for GERD.

Sign in / Sign up

Export Citation Format

Share Document