The construction of a spatiotemporal map of canonical BMP signalling during lung development and adult lung tissue injury repair (summarised in Figure 10 and table S2) will facilitate interpretation of earlier genetic studies and guide rational targeting of BMP signaling components in future experiments. Moreover, the ease isolation of living eGFP pos i.e. BMP responding, subpopulations of lung cells by cell sorting will greatly facilitate definitive clarification of the mechanisms of action of this signaling system during early lung development and repair of lung tissue injury in the adult. Figure S3 FGF10, BMP4 and a Sonic Hedgehog agonist affect expression of the BRE-eGFP reporter. A) Whole E12 lung-explants were cultured on Nuclepore membranes for eight hours in the presence of vehicle, FGF10 (250 ng/ml), BMP4 (100 ng/ml) or Sonic Hedgehog agonist Purmorphamin (500 nM). Upper panel shows bright field images of representative explants. Lower panel shows eGFP expression in the same explants. B) Confocal images of tissue sections prepared from the explants described above stained for eGFP (green stain). Nuclei were counterstained with DAPI. Note the strong upregulation of eGFP expression in the FGF10 and BMP4 treated explants, and the Figure S4 Correlation between pSmad1/5/8 and BRE-eGFP immune-staining in P1 lung tissue sections. Adjacent tissue section of lungs from BRE-eGFP reporter animals were stained with anti-GFP or anti-pSmad1/5/8 antibodies as described in materials and methods. A) Staining of adjacent sections of a large airway with anti-GFP and anti pSmad1/5/ 8antibodies or normal rabbit IgG fraction as isotype control. B) Representative images from the indicated tissue regions demonstrating that tissue areas with intense BRE-eGFP expression coincide with regions exhibiting pSma1/5/8 immuno-staining. The scale bar corresponds to 25 mm. (TIF) Figure S5 The zone of eGFP pos CC10 pos cells coincides with the NEB-rich portion of the airway tree. A) Confocal image of a lung tissue section derived from a P1 BRE-eGFP animal stained for eGFP (green staining), CC10 (red staining) and CGRP (white staining). The images illustrate the zone in the airway-tree where co-expression of eGFP and CC10 occurs. The lower images, showing the CGRP and DAPI channels of the upper images, illustrate the coincidence of eGFP pos -CC10 pos zone with the NEB-rich regions of the airway tree. B) Confocal images of the transitional zone between the eGFP pos -CC10 neg and eGFP neg -CC10pos domains of the airways demonstrating the preferential association of eGFP pos -CC10 low cells with NEBs. The image depicting NEBs is obtained from a section sequential to the ones depicting CC10 and eGFP expression. Nuclei were counterstained with DAPI (blue staining). (TIF) Figure S6 Minimal eGFP expression in the Foxj-1 pos airway ciliated cells. Representative confocal images demonstrating minimal activation of the BRE-eGFP transgene in FoxJ1 pos ciliated airway epithelial cells. Tissue section collected from E17.5, E19.5, P1, P15 and adult BRE-eGFP transgenic lungs were stained for eGFP (green staining), FoxJ1 (red staining) and CGRP (white staining). Nuclei were counterstained with DAPI (blue staining). The images demonstrate the presence of remark-ably low number of eGFP pos -FoxJ1 pos epithelial cell (depicted with yellow arrows). (TIF) Figure S7 A small, however, detectable number of BRE-eGFP developing type-I pneumocytes (T1a pos ) express eGFP. Representative confocal images of lung sections of E14.5, E17.5, E19.5, P1, P15 and adult BRE-eGFP transgenic lungs stained for eGFP (green staining), CD31 (red staining) and T1a (white staining). Nuclei were counterstained with DAPI (blue staining). The Scale bars are 20 mm. The images demonstrate that whereas the majority of the developing endothelial cells express eGFP, only a small number of type-I pneumocytes, shown in the inserts of the P1 and P15 image, are eGFP pos . (TIF)  Pulmonary sequelae in a patient recovered from swine flu The pandemic of swine flu (H1N1) influenza spread to involve the whole world rapidly. Many patients manifested a mild clinical illness but some developed pneumonia and respiratory failure. High mortality was observed in patients with severe disease. Among survivors, studies are limited. Ground-glass opacities on a high-resolution computerized tomography scan and reduced diffusion capacity were noted after 3 months in a study. But long-term complications in patients with swine flu pneumonia have not been studied well. We are presenting an unusual case of swine flu pneumonia who developed interstitial lung disease after recovery.  Dengue Virus Serotype 2 Blocks Extracellular Signal-Regulated Kinase and Nuclear Factor-κB Activation to Downregulate Cytokine Production BACKGROUND: Dengue virus (DENV) infection is the most common mosquito-borne viral disease threatening human health around the world. Type I interferon (IFN) and cytokine production are crucial in the innate immune system. We previously reported that DENV serotype 2 (DENV-2) induced low levels of interferon regulatory factor 3 and NF-κB activation, thus leading to reduced production of IFN-β in the early phase of infection. Here, we determined whether DENV infection not only hampers type I IFN activation but also cytokine production triggered by Toll-like receptor (TLR) signaling. METHODOLOGY/PRINCIPAL FINDINGS: We used quantitative RT-PCR and found that only low levels of IFN-β and inflammatory cytokines such as interleukin 10 (IL-10), IL-12 and tumor necrosis factor α (TNFα) mRNA were detected in DENV-2–infected bone-marrow–derived dendritic cells. Furthermore, DENV-2 infection repressed cytokine production triggered by TLR signaling. To elucidate the molecular mechanisms underlying this suppression event, we measured NF-κB activation by p65 nuclear translocation and luciferase reporter assay and found that NF-κB activation triggered by TLR ligands was blocked by DENV-2 infection. As well, extracellular signal-regulated kinase (ERK) activity was suppressed by DENV-2 infection. CONCLUSIONS/SIGNIFICANCE: To downregulate the host innate immunity, DENV-2 by itself is a weak inducer of type I IFN and cytokines, furthermore DENV-2 can also block the TLR-triggered ERK–NF-κB activation and cytokine production. Dengue virus (serotypes DENV-1, -2, -3 and -4) is a positivestrand RNA virus belonging to the family Flaviviridae, genus Flavivirus. Mosquitoes transmitting DENV in humans has been a major cause of dengue diseases in tropical and subtropical counties; approximately one-third of the world's population is at risk of the infection. People infected with DENV typically show self-limited febrile dengue fever and dengue hemorrhagic fever (DHF). Life-threatening dengue shock syndrome (DSS) is more likely to occur after a second DENV infection [1, 2] . Other than supportive treatments, no specific therapy is available for denguerelated diseases. Several tetravalent DENV vaccine candidates are under development, but an effective, safe and affordable dengue vaccine remains elusive [3] .