Response in Experimental Models

As discussed above, studies performed in autopsy tissues from patients afflicted with parkinsonian syndromes have led to the conclusion that inflammation is part of the neuropathological picture of these neurodegenerative disorders. While the descriptive data provided by these studies are invaluable, the 

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It is generally accepted that two types of immune response are involved in the host defence against salmonellosis - cellular and humoral (41). In attempts to control salmonellosis by active immunization of humans, or of animals in experimental model systems, living vaccines have been superior to killed vaccines consequently, cellular immunity has been considered to be of greater importance for the host resistance (42, 43). 

Antigen delivery through liposomes, hollow membrane-bound spheres, can be achieved by entrapping the molecule in the lipid membrane or inside the hollow cavity. Modified liposomes have been able to induce mucosal IgA responses compared to free antigen (Ann Clark et al. 2001 Aziz et al. 2007). Liposomes containing pertussis toxin (Guzman et al. 1993), Streptococcus mutans (Childers et al. 2002), or bovine serum albumin (Therien et al. 1990) as vaccine antigens have been tested in experimental models and induced effective antibody- and cell-mediated immune responses. 

Apoptosis is programed cell death and differs from necrosis in that it results in minimal inflammation and release of genetic material. Although necrosis is the predominant process that follows acute ischemia, apoptosis is important after more minor injury, particularly within the ischemic penumbra. Apoptosis is executed by the production, activation and action of caspases, which are protein-cleaving enzymes that dismantle cytoskeleton proteins and enzymes responsible for cellular repair (Zhang et al. 2004). Neurons are particularly susceptible to caspase-mediated cell death after cerebral ischemia, as demonstrated by the reduction in infarct size by caspase inhibitors in experimental models. 

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