RESUMO
Weeds and their influence on pest and natural enemy populations were studied on a commercial ornamental farm during 2009 in the Atlantic Zone of Costa Rica. A baseline survey of the entire production plot was conducted in February, along a 5 by 5 m grid to characterize and map initial weed communities of plants, cicadellids, katydids, and armored scales. In total, 50 plant species from 21 families were found. Seven weed treatments were established to determine how weed manipulations would affect communities of our targeted pests and natural enemies. These treatments were selected based on reported effects of specific weed cover on herbivorous insects and natural enemies, or by their use by growers as a cover crop. Treatments ranged from weed-free to being completely covered with endemic species of weeds. Although some weed treatments changed pest abundances, responses differed among arthropod pests, with the strongest effects observed for Caldwelliola and Empoasca leafhoppers. Removal of all weeds increased the abundance of Empoasca, whereas leaving mostly cyperacaeous weeds increased the abundance of Caldwelliola. Weed manipulations had no effect on the abundance of katydid and scale populations. No weed treatment reduced the abundance of all three of the target pests. Differential responses of the two leafhopper species to the same weed treatments support hypotheses, suggesting that noncrop plants can alter the abundance of pests through their effects on arthropod host finding and acceptance, as well as their impacts on natural enemies.
Assuntos
Biodiversidade , Dracaena/parasitologia , Ecossistema , Hemípteros/fisiologia , Plantas Daninhas/crescimento & desenvolvimento , Agricultura , Animais , Costa Rica , Dinâmica Populacional , Especificidade da EspécieRESUMO
RATIONALE: Idiopathic pulmonary fibrosis (IPF) is a devastating disease characterized by epithelial phenotypic changes and fibroblast activation. Based on the temporal heterogeneity of IPF, we hypothesized that hyperplastic alveolar epithelial cells regulate the fibrotic response. OBJECTIVES: To identify novel mediators of fibrosis comparing the transcriptional signature of hyperplastic epithelial cells and conserved epithelial cells in the same lung. METHODS: Laser capture microscope and microarrays analysis were used to identify differentially expressed genes in IPF lungs. Bleomycin-induced lung fibrosis was evaluated in Mmp19-deficient and wild-type (WT) mice. The role of matrix metalloproteinase (MMP)-19 was additionally studied by transfecting the human MMP19 in alveolar epithelial cells. MEASUREMENTS AND MAIN RESULTS: Laser capture microscope followed by microarray analysis revealed a novel mediator, MMP-19, in hyperplastic epithelial cells adjacent to fibrotic regions. Mmp19(-/-) mice showed a significantly increased lung fibrotic response to bleomycin compared with WT mice. A549 epithelial cells transfected with human MMP19 stimulated wound healing and cell migration, whereas silencing MMP19 had the opposite effect. Gene expression microarray of transfected A549 cells showed that PTGS2 (prostaglandin-endoperoxide synthase 2) was one of the highly induced genes. PTGS2 was overexpressed in IPF lungs and colocalized with MMP-19 in hyperplastic epithelial cells. In WT mice, PTGS2 was significantly increased in bronchoalveolar lavage and lung tissues after bleomycin-induced fibrosis, but not in Mmp19(-/-) mice. Inhibition of Mmp-19 by siRNA resulted in inhibition of Ptgs2 at mRNA and protein levels. CONCLUSIONS: Up-regulation of MMP19 induced by lung injury may play a protective role in the development of fibrosis through the induction of PTGS2.
Assuntos
Ciclo-Oxigenase 2/metabolismo , Fibrose Pulmonar Idiopática/enzimologia , Metaloproteinases da Matriz Secretadas/metabolismo , Animais , Bleomicina , Células Cultivadas , Células Epiteliais/metabolismo , Regulação Enzimológica da Expressão Gênica , Humanos , Fibrose Pulmonar Idiopática/genética , Fibrose Pulmonar Idiopática/patologia , Microdissecção e Captura a Laser , Metaloproteinases da Matriz Secretadas/genética , Camundongos , Camundongos Knockout , Análise de Sequência com Séries de Oligonucleotídeos , Alvéolos Pulmonares/metabolismo , Regulação para CimaRESUMO
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal disorder characterized by fibroproliferation and excessive accumulation of extracellular matrix in the lung. METHODS AND FINDINGS: Using oligonucleotide arrays, we identified osteopontin as one of the genes that significantly distinguishes IPF from normal lungs. Osteopontin was localized to alveolar epithelial cells in IPF lungs and was also significantly elevated in bronchoalveolar lavage from IPF patients. To study the fibrosis-relevant effects of osteopontin we stimulated primary human lung fibroblasts and alveolar epithelial cells (A549) with recombinant osteopontin. Osteopontin induced a significant increase of migration and proliferation in both fibroblasts and epithelial cells. Epithelial growth was inhibited by the pentapeptide Gly-Arg-Gly-Asp-Ser (GRGDS) and antibody to CD44, while fibroproliferation was inhibited by GRGDS and antibody to alphavbeta3 integrin. Fibroblast and epithelial cell migration were inhibited by GRGDS, anti-CD44, and anti-alphavbeta3. In fibroblasts, osteopontin up-regulated tissue inhibitor of metalloprotease-1 and type I collagen, and down-regulated matrix metalloprotease-1 (MMP-1) expression, while in A549 cells it caused up-regulation of MMP-7. In human IPF lungs, osteopontin colocalized with MMP-7 in alveolar epithelial cells, and application of weakest link statistical models to microarray data suggested a significant interaction between osteopontin and MMP-7. CONCLUSIONS: Our results provide a potential mechanism by which osteopontin secreted from the alveolar epithelium may exert a profibrotic effect in IPF lungs and highlight osteopontin as a potential target for therapeutic intervention in this incurable disease.