Several miRNAs such as miR-155, miR-26a, let-7, miR-29, miR-15/miR-16, miR-223, miR-146a/b and the miR-17-92 cluster have been shown to be involved in homeostasis and in the lung development ( Table 4 ). The pulmonary role of miR-155 was studied in murine lung, where it has been shown that miR-155 is crucially involved in the differentiation of naive T-cells into Th1 and Th2 cells [70, 71] . Mice deficient in bic/miR-155 became immunodeficient and displayed increased lung remodelling, higher bronchoalveolar leukocytes and impaired T-and B-cell responses to inflammatory stimuli [70] . Another member of miRNA family, miR-26a, has been shown to be selectively expressed in the bronchial and alveolar epithelial cells in murine lung [72] . Target mRNA of miR-26a is the transcription factor SMAD1, which is involved in the regulation of bone morphogenic protein signalling during lung development and pulmonary vascular remodelling [73, 74] . Thus, miR-26a might be important in controlling essential developmental and physiological events in the lung [75] . Also the miR-17-92 cluster is believed to regulate the lung development because its expression is high in embryonic development and steadily declines through development into adulthood [76] . Mice deficient in the miR-17-92 cluster died shortly after birth and lung hypoplasia/ventricular septal defects were demonstrated; moreover the absence of the miR-17-92 cluster let to upregulation of the pro-apoptotic protein Bim and inhibition of B-cell development [77] . On the other side, the overexpression of the miR-17-92 cluster in murine models resulted in an abnormal phenotype manifested by absence of terminal air sacs, which were replaced by highly proliferative, undifferentiated pulmonary epithelium [76] . Other miRNAs found to be involved in the pulmonary homeostasis are members of let-7 family [78] , miR-29 [79] , miR-15 and miR-16 [80, 81] , which Northern blot analysis [54] Quantitative real-time PCR [55] Ribonuclease protection assay [56] in situ hybridization [57] , [58] miRNA mimics [59] Western blot [60] Immunocytochemistry [61] Bead-based flow cytometry method [62] Suppression of miRNA expression in cells by antisense locked-nucleic acid oligonucleotides [63] Antagomir assays [64] , [65] Immunoprecipitation of Ago-bound mRNAs [66] , [67] function as tumor suppressors in lung cells. In addition, another miRNA, miR-223, has been shown to be crucial for normal granulocyte development and function in the lung [82] . MiR-223 mutant mice spontaneously developed neutrophilic lung inflammation with tissue destruction after endotoxin challenge [82] .