C5a anaphylatoxin and its role in critical illness-induced organ dysfunction

Autor: Alexander J.T. Wood, Charlotte Summers, Edwin R. Chilvers, Andrew Conway-Morris, Arlette Vassallo
Přispěvatelé: Wood, Alexander JT [0000-0001-7819-0447], Summers, Charlotte [0000-0002-7269-2873], Chilvers, Edwin R [0000-0002-4230-9677], Conway-Morris, Andrew [0000-0002-3211-3216], Apollo - University of Cambridge Repository
Jazyk: angličtina
Rok vydání: 2018
Předmět:
0301 basic medicine
Anaphylatoxins
medicine.medical_treatment
PLATELET ACTIVATION
Clinical Biochemistry
Complement C5a
Cell Communication
Research & Experimental Medicine
Cardiovascular System
Biochemistry
COMPLEMENT-INDUCED ACTIVATION
0302 clinical medicine
complement
General Clinical Medicine
immunosuppression
MOLECULAR-MECHANISMS
NEUTROPHIL DYSFUNCTION
neutrophil
Immunosuppression
General Medicine
3. Good health
Immune System Diseases
Medicine
Research & Experimental
medicine.symptom
Life Sciences & Biomedicine
Blood Platelets
C5a
Multiple Organ Failure
chemical and pharmacologic phenomena
EXPERIMENTAL SEPSIS
03 medical and health sciences
Immune system
Medicine
General & Internal
General & Internal Medicine
medicine
Humans
critical illness
Anaphylatoxin
Platelet activation
SUPEROXIDE-PRODUCTION
Blood Coagulation
Receptor
Anaphylatoxin C5a
Innate immune system
Science & Technology
business.industry
Organ dysfunction
1103 Clinical Sciences
ENDOTHELIAL-CELLS
Immunity
Innate
infection
Complement system
030104 developmental biology
TISSUE FACTOR ACTIVITY
DELAYS APOPTOSIS
Immunology
INNATE IMMUNITY
Endothelium
Vascular
business
030215 immunology
Popis: Critical illness is an aetiologically and clinically heterogeneous syndrome that is characterised by organ failure and immune dysfunction. Mortality in critically ill patients is driven by inflammation-associated organ damage and a profound vulnerability to nosocomial infection. Both factors are influenced by the activated complement protein C5a, released by unbridled activation of the complement system during critical illness. C5a exerts deleterious effects on organ systems directly and suppresses antimicrobial functions of key immune cells. Whilst several recent reports have added key knowledge of the cellular signalling pathways triggered by C5a, there remain a number of areas that are incompletely understood and therapeutic opportunities are still being evaluated. In this review, we summarise the cellular basis for C5a-induced vulnerability to nosocomial infection and organ dysfunction. We focus on cells of the innate immune system, highlighting the major areas in need of further research and potential avenues for targeted therapies.
Databáze: OpenAIRE
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