Table 6. Hypotheses Tested in Airpouch/ Chamber Models.
| Eicosanoids control TNFα expression in acute inflammation | (Ferrandiz & Foster, 1991) |
| Lipoxins and ATL regulate chemokines and cytokines and damped acute inflammation | (Hachicha, et al., 1999) |
| Lipoxin analogues dampen the neutrophil response to P.g. Neutrophils are a rich source of PGE2 | (Pouliot, et al., 2000) |
| P.g. induces an acquired immune response | (Genco, et al., 1991) |
| Serologic diversity of Neisseria can provide protective immunity | (Wong, et al., 1979) |
| P.g. evades phagocyte clearance by failing to activate or degrading complement | (Schenkein, 1989) |
| Immunization with P.g. protects against disseminating infection | (Dahlen & Slots, 1989) (Genco, et al., 1992) |
| P.g. activates blood kinin pathways to escape the vasculature creating a disseminating infection. | (Hu, et al., 2006) |
| Potential and Future Uses of This Model | |
| Determine the role of pharmacologic agents in acute and chronic inflammation. | |
| Assess the role of putative virulence factors of single bacteria and mixed infection in acute and chronic inflammation | |
| Using transgenic animals, determine the role of specific host pathways, enzymes, receptors and ligands in the acute and chronic inflammatory response |