ement from serum was inhibited with EDTA or EGTA+Mg2+ where only 
the AP can proceed. The MAC level on the Al3 precipitate was barely affected by the addition of EGTA+Mg2+, whereas no MAC was formed in the presence of EDTA, indicating a major involvement of the alternative pathway. This was confirmed by conducting the experiment with factor Bdepleted serum, showing that no or very little MAC is deposited on Al3. The C4 level was measured in serum samples after Al3 treatment and removal of the precipitate and MedChemExpress STA 4783 showed no distinct decrease in C4 concentration, suggesting little activation of the CP and LP. This was confirmed when the anaphylatoxin-levels were analysed and only small C4a increases could be detected. No or little increases in C4a concentration could be detected at increasing Al3 concentration or incubation-time. Collectively these data suggest a major involvement of the alternative pathway. Despite the wide use of aluminum oxide-based adjuvants, their modes 2854067 of action remain relatively poorly understood. When suspended in water, Al2O3 reacts with water to form aluminum hydroxide, Al3, which has the form of an amorphous precipitate. Aluminum hydroxide is thus the name for the chemical compound Al3, i.e. the hydrated form of aluminum oxide. Aluminum hydroxide cannot be isolated as a solid compound, it only exists as an amorphous precipitate, which appears to activate the complement system in a way similar to foreign surfaces. Complement activation by Al3 has been invoked by several groups and in agreement with this, Chen et al. showed, that complement receptor-deficient mice had an impaired response to immunisation with antigen adsorbed to alum. This is in agreement with reports showing that C3 and products of C3 play an important role in TH2 sensitization and antibody production. CP and LP activation by Al3 treatment has previously been suggested by Arvidsson and Ramanathan. Tengvall et al. did not observe properdin deposition on hydrated aluminum oxide but found, that C3 deposition was C1q-dependent. These results are not necessarily in contradiction to our results, as all three pathways seem to be involved to some degree. However, they illustrate the difficulties in differentiating between the three pathways. In conclusion, we have confirmed that Al3 is able to exhaust serum complement and demonstrate a major importance of the AP. We propose that Al3 efficiently activates the AP and thus provide an explanation of how Al3 adjuvant can stimulate an immune response without being antigenic itself by providing a “surface”for complement activation, antigen opsonisation and stimulating antigen removal through complement receptors. Blood-brain barrier disruption results in vasogenic edema posing a risk of hemorrhage in damaged vessels and contributing to a net increase in brain volume and pressure. Loss of BBB integrity can result from an abrupt increase in intraluminal pressure and is influenced by the properties of cerebral tissues. Status epilepticus, defined as continuous seizure activity, is a medical emergency with significant mortality. SE results in neuronal damages, astroglial death, and BBB breakdown. Leakage of serum-derived components into the extracellular space is 9762140 associated with hyperexcitability and seizure onset. Thus, dysfunction of the BBB leads to epileptogenesis and contributes to the progression of epilepsy. Despite the frequent occurrence of vasogenic edema and its undesirable consequences, the molecular mech
