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- W2099817563 abstract "RATIONALE: We investigate the role of nuclear factor κB (NF-κB) in asthma-like disease in a T cell-deficient adenosine deaminase (ada-/-) knockout mouse model. METHODS: Lungs were collected from ada-/-, ada-/- nfkb-/- mice and their normal littermates and stained with hematoxylin/eosin, PAS, and anti-MBP. RNA and protein were extracted. RNA was analyzed by real-time RT-PCR for gene expression of select cytokines. Proteins were analyzed by cytokine array membranes (RayBiotech). RESULTS: The cardinal manifestations of both mouse strains are failure to thrive, dyspnea, and death at day 15-19. Sections of stained lungs from both strains revealed thickening of alveolar septi and increased cellularity, with accumulation of macrophages in alveoli. Eosinophil infiltration was observed in ada-/- mice, but not in ada-/- nfkb-/- mice. Bronchial epithelial linings were thickened in both mutants. More goblet cells were observed in ada-/- mice when compared to ada-/- nfkb-/- mice. The most striking finding in the double knockout is hyperplasia/hypertrophy of smooth muscle cells surrounding arterioles. Real-time and RT-PCR, as well as cytokine array analysis have shown that the cytokines IL-6, TARC, MCP-1, -2, -5, KC/grO, and eotaxin are upregulated in the lungs of ada-/- mice. All of these cytokines have NF-κB binding sites in their transcriptional regulatory domains. However, analysis of ada-/- nfkb-/- mouse lungs showed no significant change (≤ 2 fold) in these cytokines when compared to ada-/- mouse lungs. CONCLUSIONS: We demonstrate that despite similarity in select cytokine expression profiles, inflammation is drastically reduced in the lungs of ada-/- mice in the absence of NF-κB." @default.
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- W2099817563 date "2005-02-01" @default.
- W2099817563 modified "2023-09-27" @default.
- W2099817563 title "Role of NF-κB in eosinophilic lung inflammation in adenosine deaminase-null mice" @default.
- W2099817563 doi "https://doi.org/10.1016/j.jaci.2004.12.480" @default.
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