Role of Circulating White Blood Cells in the Enhancement of Antigen-Induced Bronchoconstriction after Intravascular Complement Activation with Cobra Venom Factor

1991 ◽  
Vol 629 (1 Advances in t) ◽  
pp. 388-391
Author(s):  
JEAN F. REGAL ◽  
DANIEL G. FRASER
Keyword(s):  
Complement Activation ◽  
Blood Cells ◽  
White Blood Cells ◽  
Cobra Venom ◽  
Cobra Venom Factor

scholarly journals C3b-Independent Complement Activation in Ischemia/Reperfusion Mesenteric Tissue Injury in Autoimmune Prone (B6.MRL/lpr) Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-9
Author(s):  
J. Tofferi ◽  
S. Peng ◽  
C. M. Moratz
Keyword(s):  
Lupus Erythematosus ◽  
Complement Activation ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Cobra Venom ◽  
Cobra Venom Factor ◽  
Inflammatory Tissue

Complement plays a critical role in the development of tissue injury in systemic lupus erythematosus. The B6.MRL/lpr mouse, an autoimmune prone mouse, exhibits accelerated and intensified tissue injury in the ischemia/reperfusion (IR) model. It has been demonstrated in nonautoimmune mice that inhibition of complement attenuates inflammatory tissue injury in IR models. The role of complement is not as clear in the B6.MRL/lpr strain. B6.MRL/lpr-C3 deficient animals are susceptible to injury, but long-term use of C3 inhibitors in B6.MRL/lpr-C3 competent animals restrained the development of nephritis. To clarify the role of complement in the B6.MRL/lpr strain, initial and midpathway inhibitors were evaluated. C1 inhibition attenuated tissue injury, thrombin deposition, and C5a generation in the B6.MRL/lpr strain. Downstream of C1 inhibition of C3 activation by administration of cobra venom factor suppressed IR injury in immune competent mice, but was not as effective in B6.MRL/lpr mice. C3 levels in both strains were decreased after cobra venom factor treatment; however, C5a generation, thrombin deposition, and tissue injury were observed in the B6.MRL/lpr strain. These studies suggest that in the B6.MRL/lpr autoimmune prone strain C1 activation leads to C3-dependent and C3-independent pathways of complement activation.

Possible role of glucocorticoids in a complement-activated state induced by cobra venom factor in rats

1986 ◽  
Vol 112 (1) ◽  
pp. 122-129 ◽  
Author(s):  
Kiwao Nakano ◽  
Seiji Suzuki ◽  
Oh Chanho ◽  
Kazuo Yamashita
Keyword(s):  
Complement Activation ◽  
Serum Levels ◽  
Iron Chelator ◽  
Cobra Venom ◽  
Cyclooxygenase Inhibitors ◽  
Cobra Venom Factor ◽  
Deferoxamine Mesylate ◽  
Thromboxane Synthetase ◽  
Activated State

Abstract. Activation of the complement system of adrenalectomized rats with an injection of cobra venom factor (CVF) caused death of the rats within 2.5 h. Morphologically, this activation provoked distinct congestion of the gastric glandular mucosa and pulmonary leukostasis. Pretreatment of the animals with dexamethasone abolished the undesirable responses completely. Injection of CVF to intact rats produced only slight responses, but caused a marked increase in the serum levels of corticosterone. Dexamethasone was found to be replaced by promethazine (H1-antihistamine) or dimethylsulphoxide (scavenger of hydroxyl radicals) but not by indomethacine, ibuprofen (cyclooxygenase inhibitors), deferoxamine mesylate (iron chelator) or imidazole (thromboxane synthetase inhibitor). These results suggest that glucocorticoids protect the animals from the adverse effects of excessive complement activation and that they act as an inhibitor of the production or action of histamine and toxic oxygen products induced by complement activation.

scholarly journals The Enigma of Eosinophil Degranulation

2021 ◽  
Vol 22 (13) ◽  
pp. 7091
Author(s):  
Timothée Fettrelet ◽  
Lea Gigon ◽  
Alexander Karaulov ◽  
Shida Yousefi ◽  
Hans-Uwe Simon
Keyword(s):  
Blood Cells ◽  
Inflammatory Diseases ◽  
White Blood Cells ◽  
Exact Role ◽  
Effector Cells ◽  
Effector Functions ◽  
Cytotoxic Effector ◽  
Eosinophil Degranulation

Eosinophils are specialized white blood cells, which are involved in the pathology of diverse allergic and nonallergic inflammatory diseases. Eosinophils are traditionally known as cytotoxic effector cells but have been suggested to additionally play a role in immunomodulation and maintenance of homeostasis. The exact role of these granule-containing leukocytes in health and diseases is still a matter of debate. Degranulation is one of the key effector functions of eosinophils in response to diverse stimuli. The different degranulation patterns occurring in eosinophils (piecemeal degranulation, exocytosis and cytolysis) have been extensively studied in the last few years. However, the exact mechanism of the diverse degranulation types remains unknown and is still under investigation. In this review, we focus on recent findings and highlight the diversity of stimulation and methods used to evaluate eosinophil degranulation.

Candida albicans Shunt Infection: Report of Two Cases

Neurosurgery ◽  
1986 ◽  
Vol 19 (1) ◽  
pp. 111-113 ◽  
Author(s):  
David J. Gower ◽  
Kerry Crone ◽  
Eben Alexander ◽  
David L. Kelly
Keyword(s):  
Candida Albicans ◽  
Blood Cells ◽  
White Blood Cells ◽  
Shunt Infection ◽  
Cerebrospinal Fluid Shunts ◽  
Previous Therapy ◽  
Relationship Of ◽  
The Relationship ◽  
Overall Mortality

Abstract Infection of cerebrospinal fluid shunts with Candida albicans is reported in two patients. Scanning electron microscopy in one case demonstrates the relationship of the Candida hyphae to the white blood cells and to silicone plastic. A review of 10 previously reported cases of Candida shunt infection indicates that the infection usually follows a major bacterial infection or direct contamination or occurs spontaneously, Previous therapy has usually involved removal of the shunt, and the role of parenteral antifungal therapy is still unclear. Overall mortality to date is 25%.

Sign in / Sign up

Export Citation Format

Share Document