Any disruption of the blood-brain barrier allows protein to leak into the CSF resulting in an increased plasma protein "fibrinogen" level, a substance that causes blood clots. Binding of fibrinogen to the bacterial surface will mask the bacteria so that complementor antibodies cannot opsonize them = impaired phagocytosis. The bacteria may use these proteins to attach to fibrin clots in wounds etc. Hence, bacteria may also contribute to increased production of Fibrinogen.
Increased blood-brain barrier permeability in type II diabetes following loss of blood-brain barrier (BBB) integrity is reported in the literature. S. aureus has on its surface several proteins that bind fibrinogen and fibrin.
Most commonly, fibrinogen is decreased in DIC; however, increased fibrinogen levels do not rule out DIC since fibrinogen is an acute phase protein synthesized in the liver and is often elevated in inflammatory conditions.
Following wounding or invasion of tissues by bacteria, fibrinogen-rich exudates lead to the formation of fibrin gels (fibrin is involved in many aspects of bacterial infection) to which bacteria bind. Fibrinogen or fibrin itself do not afford any protection of bacteria against the action of antibiotics which fail to prevent abscess formation secondary to bacteria trapped in fibrin clots.
Trauma. Some experts believe that injury (trauma) may trigger new or recurrent symptoms by disrupting the blood-brain barrier and allowing immunological attacks on the brain.
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