In order to study the factors related to complement activation, the complement activation products C3bc and TCC were measured in plasma at admittance and during the stay in the intensive care unit in 108 consecutive patients with multiple injuries. These patients were admitted to the surgical department during a 4-month period. Complement activation occurred immediately after the trauma and correlated strongly with the Injury Severity Score and was inversely correlated to the Base Excess. Complement activation also correlated with the number of transfusions. Sepsis caused complement activation later during the stay in hospital. All seven patients developing the adult respiratory distress syndrome (ARDS) had increased complement activation, either on admission or later during the stay in the intensive care unit. Complement activation is known to contribute to organ damage following ischemia and reperfusion. Clinical studies have demonstrated the importance of early restoration of adequate circulation and the present demonstration of a strong negative correlation between complement activation and Base Excess indicates that early restoration of aerobic metabolism may reduce complement activation and the risk for organ dysfunction.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/s0020-1383(98)00113-2 | DOI Listing |
Alzheimers Dement
December 2024
Indiana University School of Medicine, Indianapolis, IN, USA.
Background: SHIP1 is a phosphatidyl inositol phosphatase encoded by INPP5D, which has been identified as a risk gene for Alzheimer's disease (AD). SHIP1 is expressed in microglia, the resident macrophage in brain. It is a complex, multidomain protein that acts as a negative regulator downstream from TREM2.
View Article and Find Full Text PDFBackground: Neuroinflammation is a critical factor of Alzheimer's Disease (AD). Dysregulation of complement leads to excessive inflammation, direct damage to self-cells and propagation of injury. This is likely of particular relevance in the brain where inflammation is poorly tolerated and brain cells are vulnerable to direct damage by complement.
View Article and Find Full Text PDFBackground: In the brain as in other organs, complement contributes to immune defence and housekeeping to maintain homeostasis. Sources of complement may include local production by brain cells and influx from the periphery, the latter severely restricted by the blood brain barrier (BBB) in healthy brain. Dysregulation of complement leads to excessive inflammation, direct damage to self-cells and propagation of injury.
View Article and Find Full Text PDFCurr Mol Med
January 2025
Department of Obstetrics and Gynecology, Beijing Shijitan Hospital, Capital Medical University, Beijing, 100038, China.
Aim: The activation of the complement system is accompanied by the occurrence and development of preeclampsia, as well as kidney diseases. Here, the role of complement C3 [C3] in renal injury in preeclampsia was explored, and its potential application as an early diagnostic biomarker or drug target to ameliorate kidney injury induced by preeclampsia was preliminarily evaluated.
Method: A total of 48 subjects were included in the present study, and the complement C3 levels and renal function were analyzed.
FASEB J
January 2025
Jiangsu Institute of Hematology, National Clinical Research Center for Hematologic Diseases, NHC Key Laboratory of Thrombosis and Hemostasis, The First Affiliated Hospital of Soochow University, Suzhou, China.
Acute liver failure (ALF) is a life-threatening condition that occurs when the liver sustains severe damage and rapidly loses its function. The primary cause of ALF is the overdose of acetaminophen (APAP), and its treatment is relatively limited. The involvement of the complement system in the development of ALF has been implicated.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!