Background: Endometriosis is a disease that shows auto-immune and chronic characteristics, suggesting a role for proteins mediating immune interactions in its pathophysiology. The aim was to evaluate C3a and C5a for their role in inflammatory responses and C6 as the down-stream interactor following our previous findings on C5 mRNA expression changes in endometriosis [1].
Methods: Sera from 71 endometriosis patients and 77 women without endometriosis were taken. While the samples were taken only once from the controls, the patient samples were taken before, in 1st and in 7th days after laparoscopy. Levels of complement proteins C3a, C5a and C6 were measured with ELISA assays. MPV (Mean Platelet Volume), CRP (C-Reactive Protein) and NLR (Neutrophil-to-Leukocyte Ratio) were also analyzed from the retrospective data.
Results: C6 levels of early-stage patients at postoperative 1st day were significantly higher than controls. Patients with high MPV measurements had significantly higher C3a (p < 0.0001) and C6 (p < 0.05) levels than controls at all times of measurement.
Conclusions: C6, an integral component of the membrane attack complex (MAC), could play a role at early disease-stage. The changes in levels of complement proteins and their relation to high MPV levels suggest a broader area of interplay for immune interactors in endometriosis. Although a bigger and longitudinal study design is needed to obtain more accurate results to evaluate these proteins as potential biomarkers, an important role of complement system within the pathophysiology of endometriosis is apparent.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.clinbiochem.2020.04.005 | DOI Listing |
Nan Fang Yi Ke Da Xue Xue Bao
November 2024
Xi'an TANK Medicinal Biology Institute, Xi'an 710032, China.
Objective: To explore the therapeutic mechanism of maggot for psoriasis-like lesions in mice from the perspective of immune stress and complement activation regulation.
Methods: Thirty-six male C57BL/6 mice were randomly divided into control group, model group, maggot (1.25%, 2.
Front Immunol
November 2024
Immunochemistry Laboratory, Butantan Institute, São Paulo, Brazil.
Introduction: Complement activation split products are signatures of many immunopathological disorders. Among the laboratory findings observed in these diseases, a reduction in the level of circulating intact complement components can be mentioned, and this change has also been detected in envenomation by multiple Africanized honeybee (Apis mellifera) stings. Although envenomation by these animals elicits diverse life-threatening reactions, the capacity of bee venom (AmV) to activate the human complement system remains elusive.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Division of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Fabry disease is a rare X-linked lysosomal storage disorder caused by mutations in the galactosidase alpha () gene, resulting in the accumulation of globotriaosylceramide (Gb3) and its deacetylated form, globotriaosylsphingosine (Lyso-Gb3) in various tissues and fluids throughout the body. This pathological accumulation triggers a cascade of processes involving immune dysregulation and complement system activation. Elevated levels of complement 3a (C3a), C5a, and their precursor C3 are observed in the plasma, serum, and tissues of patients with Fabry disease, correlating with significant endothelial cell abnormalities and vascular dysfunction.
View Article and Find Full Text PDFFront Nephrol
October 2024
Department of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology, Hans Knöll Institute, Jena, Germany.
C3 glomerulopathy (C3G) is an ultra-rare complement-mediated kidney disease caused by to the deregulation of the alternative pathway (AP) of proximal complement. Consequently, all effector loops of the complement are active and can lead to pathologies, such as C3a- and C5a-mediated inflammation, C3b opsonization, surface C3b-mediated AP C3 convertase assembly, C3 cleavage product deposition in the glomerulus, and lytic C5b-9/MAC cell damage. The most common pathologic mechanisms are defective chronic alternative pathway deregulation, mostly occurring in the plasma, often causing C3 consumption, and chronic complement-mediated glomerular damage.
View Article and Find Full Text PDFCell Immunol
November 2024
Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil. Electronic address:
The Complement System is composed of more than 40 proteins that act in innate and adaptive immunity. C3 is the most abundant one and C3-deficient patients are more susceptible to recurrent and severe infections. Several studies have demonstrated the importance of C3 in controlling infections.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!