Ignite Creation Date:
2024-05-06 @ 6:49 PM
Last Modification Date:
2024-10-26 @ 2:55 PM
Study NCT ID:
NCT05793983
Status:
RECRUITING
Last Update Posted:
2023-03-31
First Post:
2021-10-08
Brief Title:
S100A8A9 and Innate Immunity in Liver Disease
Sponsor:
St Georges University of London
Organization:
St Georges University of London
Study Overview
Official Title:
The Interaction of the S100A8A9 Protein With the Innate Immune System in the Immunopathology of Acute and Chronic Liver Disease
Status:
RECRUITING
Status Verified Date:
2023-03
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
This observational study evaluates the concentration of immune protein S100A8A9 in different liver failure syndromes its interaction with the immune system and validity as an immunotherapeutic target to improve survival in patients with advanced cirrhosis andor acute on chronic liver failure
Detailed Description:
A paradox exists in chronic liver disease whereby there is a general recognition that chronic inflammation is part of the pathophysiology heightened when there is an acute deterioration and organ failure acute-on-chronic liver failure yet there is an increased susceptibility to infection due to a dysfunctional immune system which is often the trigger for organ failure and the reason for death in these patients
A danger signal reported in other inflammatory conditions called S100A8A9 calprotectin is known to activate the immune system by production of pro-inflammatory cytokines but has also been observed to promote the development immunosuppressive signals eg IL-10 and MDSCs
In an attempt to explain this paradox in liver disease this study proposes to identify at the cellular and molecular level the triggers for S100A8A9 production how it varies with time in stable patients and those that have acute deteriorations including the development of organ failure and its interaction with innate immune cells in the circulation and at tissue level
By studying this the Investigators hope to be able to identify immunotherapeutic targets and understand whether potential immunotherapy could be applied locally or systemically The Investigators observations in this study could provide the basis for the future development of clinical immunomodulating agents which may ameliorate immunopathology reduce susceptibility to infection and could reduce mortality in critically ill patients with liver disease Findings in this study may also have more generalizable impact especially with the recent recognition in the COVID-19 pandemic that immunomodulatory therapies may improve the clinical outcomes of inflammatory phenotypes in virus-induced severe sepsis
A danger signal reported in other inflammatory conditions called S100A8A9 calprotectin is known to activate the immune system by production of pro-inflammatory cytokines but has also been observed to promote the development immunosuppressive signals eg IL-10 and MDSCs
In an attempt to explain this paradox in liver disease this study proposes to identify at the cellular and molecular level the triggers for S100A8A9 production how it varies with time in stable patients and those that have acute deteriorations including the development of organ failure and its interaction with innate immune cells in the circulation and at tissue level
By studying this the Investigators hope to be able to identify immunotherapeutic targets and understand whether potential immunotherapy could be applied locally or systemically The Investigators observations in this study could provide the basis for the future development of clinical immunomodulating agents which may ameliorate immunopathology reduce susceptibility to infection and could reduce mortality in critically ill patients with liver disease Findings in this study may also have more generalizable impact especially with the recent recognition in the COVID-19 pandemic that immunomodulatory therapies may improve the clinical outcomes of inflammatory phenotypes in virus-induced severe sepsis
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| 285573 | OTHER | Integrated Research Application System | None |