Two miRNAs, miR-146a and miR-146b, have been shown to play central role in the negative feedback regulation of IL-1β-induced inflammation; the mechanism is down-regulation of two proteins IRAK1 and TRAF6 involved in Toll/interleukin-1 receptor (TIR) signalling [83, 84] . Also other miRNAs have been shown to regulate the inflammation in mouse lung exposed to aerosolized lipopolysaccharide (LPS): miR-21, -25, -27b, -100, -140, -142-3p, -181c, -187, -194, -214, -223 and -224 [72] . Increase in these miRNAs correlated with the downregulation of pro-inflammatory cytokine production such as TNFα [72] . The deregulation of miR-155, the miR-17-92 cluster and miR-223, miRNAs involved in lung development and homeostasis, resulted in the uncontrolled lung inflammation in murine models [70, 77, 82] . Based on the studies in murine models, there is evidence that miRNA expression may influence also the course of pulmonary viral infections [85, 86] . MiR-200a and miR-223 were detected in lethal influenza virus infection presumably contributing to the extreme miR-155 important for normal lung airway remodelling (A) [70] alteration of T-cell differentiation (A) [71] miR-26a highly expressed within bronchial and alveolar epithelial cells, important for lung development (H) [75] let-7 highly expressed in normal lung tissue, functions as a tumor suppressor in lung cells (H) [78] miR-29 functions as tumor suppressor in lung cells (H) [79] miR-15, miR-16 function as tumor suppressor genes (H) [80] , [81] miR-223 control of granulocyte development and function (A) [82] miR-146a/b central to the negative feedback regulation of IL-1β-induced inflammation (H) [83] , [84] miR-200a, miR-223 contribution to the extreme virulence of the r1918 influenza virus (A) [85] miR-17 family, miR-574-5p, miR-214 upregulated at the onset of SARS infection (A, H) [86] virulence of the r1918 influenza virus [85] . MiR-17 family, miR-574-5p and miR-214 were upregulated at the onset of SARS infection: these miRNAs may help the virus to evade the host immune system and are responsible for effective transmission at the initial stage of viral infection [86] .