Phospholipase A₂ (PLA₂) is a superfamily of enzymes that promote inflammation by releasing arachidonic acid for the synthesis of eicosanoids and lysophospholipid for the synthesis of platelet-activating factor (PAF). On the other hand, several members of the PLA₂ family (VIIA, VIIB, VIIIA and VIIIB) are able to degrade PAF and are therefore potentially important anti-inflammatory enzymes. The precise roles of the different PLA₂ enzymes in airways inflammation are not known and the gene expression of the different PLA₂s in the human nasal mucosa has not previously been examined. Using reversed transcription-polymerase chain reaction (RT-PCR) techniques, this thesis investigated (i) the occurrence of mRNAs for different PLA₂ types in the nasal mucosa of healthy subjects; (ii) the effects of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) on the gene expression of different PLA₂s in human nasal epithelial cells (RPMI 2650); (iii) the effects of IFN-γ and lipopolysaccharide (LPS) on the gene expression of different PLA₂ types in human monocyte-derived macrophages; (iv) the effects of exudates from LPS- or ß-glucan exposed macrophages on the gene expression of different PLA₂ types in RPMI 2650 cells, and (v) the levels of different PLA₂ mRNAs in the nasal mucosa of patients with seasonal allergic rhinitis (SAR) and healthy controls. The relative abundances of the different PLA₂ transcripts in normal human nasal mucosa were found to be X ≈ IVA > IIA ≈ IIE ≈ IVB ≈ VI > IB ≈ IID ≈ III ≈ IVC ≈ VII ≈ VIB. In RPMI 2650 cells, TNF-α increased the expression of PLA₂ IVA and IVC, while IFN-γ increased the expression of PLA₂ IIA and IID. In macrophages, IFN-γ increased the expression of both PLA₂ IID and IVA while LPS increased the expression of PLA₂ IVA but decreased that of IID. Medium from macrophages exposed to LPS or ß-glucan increased the expression of PLA₂ IVC in RPMI 2650 cells; this upregulation was abrogated by antibodies to TNF-α and by the nuclear factor (NF)-κB inhibitor, pyrrolidine dithiocarbamate. Notably, the mRNA levels of PLA₂ VIIA (PAF acetylhydrolase I) were lower in SAR patients than controls during both the pollen season and the off-season for pollen. These findings demonstrate that a large number of PLA₂ types are constitutively expressed in the normal human nasal mucosa, including the newly discovered PLA₂ types IID, IIE, IIF, III, IVB, IVC, VIB, X, XIIA, and XIIB. They also demonstrate that TNF-α and IFN-γ cause increased gene expression of two novel cytosolic and secretory PLA₂ types (IVC and IID, respectively) in human nasal epithelial cells, suggesting that these PLA₂ types may be involved in cytokine-mediated inflammation in the nasal mucosa. Moreover, the findings indicate that both LPS- and ß-glucan-activated macrophages can induce the gene expression of PLA₂ IVC in nasal epithelial cells, and that this upregulation is mediated through TNF-α and under NF-κB control. The observation that PAF acetylhydrolase mRNA expression in the nasal mucosa is lower in SAR patients than in healthy subjects points to the possibility that impaired ability to inactivate PAF might be of importance in SAR.