Clinical utility of peri-operative C-reactive protein testing in general surgery.

Introduction: C-reactive protein (CRP) is an acute-phase protein used clinically to diagnose infectious and inflammatory disease and monitor response to treatment. CRP measurement in the peri-operative period was audited and patterns of change analysed for elective general surgical patients.

Patients And Methods: General surgical patients (201) admitted for elective general surgery over a 3-month period were considered for the study.

CD59a deficient mice display reduced B cell activity and antibody production in response to T-dependent antigens.

CD59a is the primary regulator of membrane attack complex in mice. Recently, we have shown that CD59a-deficient (Cd59a-/-) mice exhibit enhanced CD4+ T cell responses. Here, we explored the effects of CD59a on B cell function and antibody production.

p53 regulates cellular resistance to complement lysis through enhanced expression of CD59.

It has been recently hypothesized that the CD59 gene has two putative p53-responsive elements that may be involved in defense of host cells from damage by the complement system in inflammation. Here we have examined the roles of these putative p53-binding sequences within the CD59 gene in regulation of CD59 expression. We have shown that both of these potential responsive elements bind p53 in vitro.

Complement regulator loss on apoptotic neuronal cells causes increased complement activation and promotes both phagocytosis and cell lysis.

In neuroinflammatory disease complement (C) activation and neuronal apoptosis occur in areas of active pathology. C has a role in clearing apoptotic debris, but is also known to cause necrotic cell death by insertion of the membrane attack complex (MAC). It is therefore unclear whether C is protective or injurious in this context.

Novel C5a regulators in inflammatory disease.

Complement is part of the innate immune system, acting to protect the host from microorganisms such as bacteria, and other foreign and abnormal cells. Although primarily protective, complement activation can also cause damage to the host. In a number of inflammatory diseases, including rheumatoid arthritis and dermatitis, there is excessive and inappropriate complement activation.

Beyond lysis: how complement influences cell fate.

Complement is a central component of the innate immune system involved in protection against pathogens. For many years, complement has been known to cause death of targets, either indirectly by attracting and activating phagocytes or directly by formation of a membrane pore, the membrane attack complex. More recently, it has been recognized that complement may cause other 'non-classical' effects that may not directly be aimed at killing of pathogens.