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1.
Figure 8

Figure 8. Allergic peritoneal responses are unaltered inaP2–/– mice. . From: The adipocyte fatty acid-binding protein aP2 is required in allergic airway inflammation.

(A) Mice were sensitized and challenged with OVA or PBS as a control. Peritoneal cells were obtained and total cells enumerated. Data represent mean ± SEM; n = 5 mice per group. (B) Differential assessment of cells from peritoneal lavages of allergic or control mice. Data represent mean values ± SEM.

Bennett O.V. Shum, et al. J Clin Invest. 2006 August 1;116(8):2183-2192.
2.
Figure 1

Figure 1. Identification of IL-4–responsive genes in HBE.. From: The adipocyte fatty acid-binding protein aP2 is required in allergic airway inflammation.

Transcriptional profiling of HBEs following stimulation with IL-4 was performed using microarray. Signal intensity and fold change of the 20 most highly upregulated genes common to 3 experiments (A, B, and C) are shown. Genes are listed in decreasing order of maximal fold change.

Bennett O.V. Shum, et al. J Clin Invest. 2006 August 1;116(8):2183-2192.
3.
Figure 4

Figure 4. Evidence for the role of aP2 in Th2-mediated airway inflammation (A) HBEs were treated with a panel of cytokines and stimuli and aP2 expression assessed with real-time PCR. . From: The adipocyte fatty acid-binding protein aP2 is required in allergic airway inflammation.

Data represent mean ± SEM of 3 experiments for IL-4, IL-13, and IFN-γ; 1 experiment for IL-9 and MCP-1; and 2 experiments for the other treatments. (B) BALB/c mice in which allergic lung inflammation was induced or control mice were immunostained for aP2: brown, positive aP2 staining; blue, nuclei. Images are representative of 3 mice per condition. Original magnification, ×400.

Bennett O.V. Shum, et al. J Clin Invest. 2006 August 1;116(8):2183-2192.
4.
Figure 5

Figure 5. aP2 deficiency ameliorates allergic lung inflammation and airway eosinophilia.. From: The adipocyte fatty acid-binding protein aP2 is required in allergic airway inflammation.

WT or aP2–/– mice were sensitized and challenged with OVA for airway inflammation (Allergic) or with PBS as a control (Nonallergic). Total (A) and differential (B) cell counts from BAL. E, eosinophil; M, monocyte/macrophage; L, lymphocyte; N, neutrophil. Data represent mean values ± SEM for n = 10 nonallergic and n = 12–15 allergic WT or aP2–/– mice from 2 experiments. *P < 0.05, #P < 0.0005 compared with WT. (C) Histological examination of lungs stained with H&E (upper panel; original magnification, ×100) or Alcian blue–PAS (lower panel; original magnification, ×400) for mucus. Magenta staining is indicative of mucus.

Bennett O.V. Shum, et al. J Clin Invest. 2006 August 1;116(8):2183-2192.
5.
Figure 6

Figure 6. Allergic cytokine production is decreased in allergic aP2-deficient mice.. From: The adipocyte fatty acid-binding protein aP2 is required in allergic airway inflammation.

(A) Detection of IL-5, IL-13, and eotaxin in BAL fluid from nonallergic (n = 10) and allergic (n = 12–15) aP2+/+ or aP2–/– mice. Data represent mean values ± SEM. *P < 0.05; **P < 0.005. (B) IL-5 was measured in culture supernatants from lung-draining lymph node cells restimulated in vitro with OVA or PBS only (Ctrl). Data represent mean ± SEM of 3–4 cultures in triplicate wells with cells pooled from 3–4 mice per culture. #P < 0.0005. (C) Unimpaired T cell proliferation in aP2–/– mice. Splenocytes from OVA/alum-immunized or PBS/alum control mice were stimulated with OVA antigen in vitro and cellular proliferation assayed. Data represent mean ± SEM of triplicate wells with 5 and 2 mice per genotype for OVA/alum and PBS/alum groups, respectively.

Bennett O.V. Shum, et al. J Clin Invest. 2006 August 1;116(8):2183-2192.
6.
Figure 2

Figure 2. Regulation of aP2 expression in HBEs is enhanced by IL-4 and IL-13.. From: The adipocyte fatty acid-binding protein aP2 is required in allergic airway inflammation.

(A) Time course of aP2 induction in HBEs after 1, 3, 6, 12, 18, 24, 48, and 72 hours or of mal1 induction after 3, 6, 18, 24, and 48 hours, using real-time PCR activation after treatment with IL-4 or IL-13. Data represent mean ± SEM of 3 experiments. The data for the one-hour time point represent the mean of duplicate experiments. (B) BEAS-2B and A549 cells were treated with IL-4 or IL-13 for 18 hours and aP2 expression assayed by real-time PCR. (C) HBEs were stimulated with BSA (Ctrl), IL-4, or IL-13 for 24 hours and stained with anti-aP2 or isotype control antibodies with immunofluorescence. Images are representative of 3 experiments. Original magnification, ×400.

Bennett O.V. Shum, et al. J Clin Invest. 2006 August 1;116(8):2183-2192.
7.
Figure 7

Figure 7. Non-hematopoietic cells are responsible for reduced allergic airway inflammation inaP2–/– mice. . From: The adipocyte fatty acid-binding protein aP2 is required in allergic airway inflammation.

WT or aP2–/– (KO) bone marrow was transferred into irradiated mice to generate KO→WT, WT→KO, or WT→WT (donor→recipient) chimeras, and their responses to allergic airway inflammation assessed. Total (A) and differential (B) cell counts from BAL of bone marrow chimeric mice. Data represent mean values ± SEM for n = 13 KO→WT mice, n = 11 WT→KO mice, and n = 6 WT→WT mice. *P < 0.05 compared with KO→WT mice. (C) Detection of IL-5 and eotaxin in BAL fluid from allergic chimeric mice. Data represent mean ± SEM for n = 13 KO→WT mice and n = 11 WT→KO mice. *P < 0.05; **P < 0.005. (D and E) Detection of IL-5 and IL-13 from culture supernatants of allergic chimeric mouse lung-draining lymph node cells restimulated in vitro with OVA. Data represent mean ± SEM of 3 cultures from cells pooled from 4–5 mice per condition. ND, not detected.

Bennett O.V. Shum, et al. J Clin Invest. 2006 August 1;116(8):2183-2192.
8.
Figure 3

Figure 3. Differential expression and regulation ofaP2 expression by PPARγ activation in HBEs and adipocytes. . From: The adipocyte fatty acid-binding protein aP2 is required in allergic airway inflammation.

(A) HBEs and 3T3-L1 preadipocytes were treated with rosiglitazone (Ros.) or vehicle control and aP2 mRNA expression assessed. Data represent mean of 3 HBE and two 3T3-L1 experiments. (B) CD36 message levels were determined in HBEs after rosiglitazone treatment. Data represent mean of 2 experiments. (C) Relative abundance of aP2 message from 100 ng RNA was compared among human adipose tissue, HBEs, HBEs plus IL-4, THP-1 monocytes, and THP-1 monocytes plus PMA. (D) Transient transfection of BEAS-2B cells with WT STAT6, constitutively active STAT6 mutant (STAT6VT), or empty vector plasmids for 72 hours. aP2 expression was monitored by real-time PCR. Data represent mean ± SEM of 3 experiments. *P < 0.05 compared with vector control. (E) Transient transfection of BEAS-2B cells with STAT6 dominant negative (STAT6DN) or empty vector plasmids. Twenty-four hours after transfection, cells were treated with IL-4 for 18 hours, and aP2 transcript was quantified. Data represent mean ± SEM of 4 experiments. (F) Time course of aP2 expression in WT AECs after 3 or 18 hours treatment with IL-4 and TNF-α. Data represent the mean results from 2 independent cultures. (G) STAT6-deficient AECs were cultured in vitro and treated with IL-4 for 18 hours, and aP2 mRNA expression was assessed. Data represent the mean results of 2 independent cultures.

Bennett O.V. Shum, et al. J Clin Invest. 2006 August 1;116(8):2183-2192.

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