نتایج جستجو برای: complement component c5a

تعداد نتایج: 681062  

Journal: :The Journal of Experimental Medicine 2006
Heather L. Van Epps

The complement activation product C5a prevents heart cells from contracting , according to Niederbichler and colleagues on page 53. This finding may help explain the cardiac dysfunction commonly seen in patients with septic shock—a disease caused by bacterial infections that is characterized in part by the robust activation of the complement system. A central component of septic shock is decrea...

2014
Janus Asbjørn Schatz-Jakobsen Laure Yatime Casper Larsen Steen Vang Petersen Andreas Klos Gregers Rom Andersen

Complement is an ancient part of the innate immune system that plays a pivotal role in protection against invading pathogens and helps to clear apoptotic and necrotic cells. Upon complement activation, a cascade of proteolytic events generates the complement effectors, including the anaphylatoxins C3a and C5a. Signalling through their cognate G-protein coupled receptors, C3aR and C5aR, leads to...

2017
Hanif J. Khameneh Adrian W. S. Ho Federica Laudisi Heidi Derks Matheswaran Kandasamy Baalasubramanian Sivasankar Gim Gee Teng Alessandra Mortellaro

Gouty arthritis results from the generation of monosodium urate (MSU) crystals within joints. These MSU crystals elicit acute inflammation characterized by massive infiltration of neutrophils and monocytes that are mobilized by the pro-inflammatory cytokine IL-1β. MSU crystals also activate the complement system, which regulates the inflammatory response; however, it is unclear whether or how M...

Journal: :The Journal of Experimental Medicine 2006
Heather L. Van Epps

The complement activation product C5a prevents heart cells from contracting , according to Niederbichler and colleagues on page 53. This finding may help explain the cardiac dysfunction commonly seen in patients with septic shock—a disease caused by bacterial infections that is characterized in part by the robust activation of the complement system. A central component of septic shock is decrea...

2015
Rachel Vaivoda Christine Vaine Cassandra Boerstler Kristy Galloway Peter Christmas

CYP4Fs were first identified as enzymes that catalyze hydroxylation of leukotriene B4 (LTB4). CYP4F18 has an unusual expression in neutrophils and was predicted to play a role in regulating LTB4-dependent inflammation. We compared chemotaxis of wild-type and Cyp4f18 knockout neutrophils using an in vitro assay. There was no significant difference in the chemotactic response to LTB4, but the res...

Journal: :The Journal of surgical research 2008
Sherry D Fleming Lauren M Phillips John D Lambris George C Tsokos

BACKGROUND Complement has been implicated in the pathogenesis of intestinal damage and inflammation in multiple animal models. Although the exact mechanism is unknown, inhibition of complement prevents hemodynamic alterations in hemorrhage. MATERIALS AND METHODS C57Bl/6, complement 5 deficient (C5-/-) and sufficient (C5+/+) mice were subjected to 25% blood loss. In some cases, C57Bl/6 mice we...

2010
Motomu Hashimoto Keiji Hirota Hiroyuki Yoshitomi Shinji Maeda Shin Teradaira Shuji Akizuki Paz Prieto-Martin Takashi Nomura Noriko Sakaguchi Jörg Köhl Birgitta Heyman Minoru Takahashi Teizo Fujita Tsuneyo Mimori Shimon Sakaguchi

Activation of serum complement triggers Th17 cell-dependent spontaneous autoimmune disease in an animal model. In genetically autoimmune-prone SKG mice, administration of mannan or beta-glucan, both of which activate serum complement, evoked Th17 cell-mediated chronic autoimmune arthritis. C5a, a chief component of complement activation produced via all three complement pathways (i.e., lectin, ...

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