Results 21 to 30 of about 17,322 (203)

7α-Hydroxycholesterol induces monocyte/macrophage cell expression of interleukin-8 via C5a receptor.

open access: yesPLoS ONE, 2017
We investigated effects of 7-oxygenated cholesterol derivatives present in atherosclerotic lesions, 7α-hydroxycholesterol (7αOHChol), 7β-hydroxycholesterol (7βOHChol), and 7-ketocholesterol (7K), on IL-8 expression.
Hyok-Rae Cho   +6 more
doaj   +1 more source

Activated complement protein C5a does not affect brain-derived endothelial cell viability and zonula occludens-1 levels following oxygen-glucose deprivation

open access: yesBrain Circulation, 2017
BACKGROUND AND PURPOSE: Ischemic brain injury induces both functional and structural disarray affecting the blood–brain barrier (BBB) which in return aggravates stroke outcomes.
Aren Khoyetsyan   +5 more
doaj   +1 more source

The relationship of anti-phospholipase A2 receptor antibody and C5a complement with disease activity and short-term outcome in idiopathic membranous nephropathy

open access: yesJournal of the Formosan Medical Association, 2019
Background: The binding of anti-phospholipase A2 receptor (anti-PLA2R) antibody to podocyte and complement activation is the mechanisms of idiopathic membranous nephropathy (IMN).
Jyun Ni Chi   +9 more
doaj   +1 more source

Association of C5a/C5aR pathway to activate ERK1/2 and p38 MAPK in acute kidney injury – a mouse model

open access: yesRomanian Journal of Laboratory Medicine, 2022
Acute inflammation is accompanied by complement system activation and inflammatory cell accumulation. Acute kidney injury (AKI) is one of the common clinical symptoms, it is not clear whether complement system-mediated signaling pathway is involved. This
Zhang Zeying
doaj   +1 more source

Netrin-1 Reduces Monocyte and Macrophage Chemotaxis towards the Complement Component C5a.

open access: yesPLoS ONE, 2016
Netrin-1, acting at its cognate receptor UNC5b, has been previously demonstrated to inhibit CC chemokine-induced immune cell migration. In line with this, we found that netrin-1 was able to inhibit CCL2-induced migration of bone marrow derived ...
Lewis Taylor   +4 more
doaj   +1 more source

NOD2-mediated suppression of CD55 on neutrophils enhances C5a generation during polymicrobial sepsis. [PDF]

open access: yesPLoS Pathogens, 2013
Nucleotide-binding oligomerization domain (NOD) 2 is a cytosolic protein that plays a defensive role in bacterial infection by sensing peptidoglycans. C5a, which has harmful effects in sepsis, interacts with innate proteins.
Sae Jin Oh, Ji Hyung Kim, Doo Hyun Chung
doaj   +1 more source

C5a receptor and thymocyte apoptosis in sepsis [PDF]

open access: yesThe FASEB Journal, 2002
ABSTRACT In sepsis, apoptosis occurs in many different organs. The mediators responsible for induction of apoptosis are not clearly known, although there are some suggestions that C5a and the C5a receptor (C5aR) might be directly linked to apoptosis.
Riedemann, Niels C.   +7 more
openaire   +3 more sources

Pro-inflammatory regulatory mechanism of C5a/C5aR pathway in GCRV-infected grass carp (Ctenopharyngodon idella)

open access: yesAquaculture Reports, 2023
Death of grass carp (Ctenopharyngodon idella) caused by grass carp reovirus (GCRV) infection severely restricts the development of the grass carp industry.
Baohong Xu   +8 more
doaj   +1 more source

The role of the host—Neutrophil biology

open access: yesPeriodontology 2000, EarlyView., 2023
Abstract Neutrophilic polymorphonuclear leukocytes (neutrophils) are myeloid cells packed with lysosomal granules (hence also called granulocytes) that contain a formidable antimicrobial arsenal. They are terminally differentiated cells that play a critical role in acute and chronic inflammation, as well as in the resolution of inflammation and wound ...
Iain L. C. Chapple   +4 more
wiley   +1 more source

Systemic inhibition of the membrane attack complex impedes neuroinflammation in chronic relapsing experimental autoimmune encephalomyelitis

open access: yesActa Neuropathologica Communications, 2018
The complement system is a key driver of neuroinflammation. Activation of complement by all pathways, results in the formation of the anaphylatoxin C5a and the membrane attack complex (MAC).
Iliana Michailidou   +17 more
doaj   +1 more source

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