Accumulating evidence shows that periostin, a matricellular protein, is involved in many fundamental biological processes such as cell proliferation, cell invasion, and angiogenesis. Changes in periostin expression are commonly detected in various cancers and pre-cancerous conditions, and periostin may be involved in regulating a diverse set of cancer cell activities that contribute to tumorigenesis, cancer progression, and metastasis. Periostin has also been shown to be involved in many aspects of allergic inflammation, such as eosinophil recruitment, airway remodeling, development of a Th2 phenotype, and increased expression of inflammatory mediators. In an in vivo model, bronchoalveolar lavage (BAL) fluid obtained from ovalbumin-challenged mice was found to contain significantly higher levels of periostin compared to BAL samples from control mice. To date, the molecular mechanisms involving periostin in relation to asthma in humans have not been fully elucidated. This review will focus on what is known about periostin and its role in the pathophysiological mechanisms that mediate asthma in order to evaluate the potential for periostin to serve as a biomarker and therapeutic target for the detection and treatment of asthma, respectively.

MicroRNAs (miRNAs), a class of small non-coding RNAs of 18–24 nucleotides in length, function to posttranscriptionally regulate protein expression. miR-155 was one of the first identified and, to date, the most studied miRNA, and has been linked to various cellular processes such as modulation of immune responses and oncogenesis. Previous studies have identified miR-155 as a crucial positive regulator of Th1 immune response in autoimmune diseases, but as a suppressor of Th2 immunity in allergic disorders. However, recent studies have found new evidence that miR-155 plays an indispensible role in allergic asthma. This review summarizes the recent findings with respect to miR-155 in immune responses and the underlying mechanisms responsible for miR-155-related allergic diseases, as well as the similarities between miR-155 and glucocorticoids in immunity.

Galectins constitute an evolutionary conserved family that bind to β-galactosides. Increasing evidence shows that galectins are involved in many fundamental biological processes such as cellular communication, inflammation, differentiation and apoptosis. Changes in galectin-3 (Gal-3) expression are commonly seen in cancer and pre-cancerous conditions, and Gal-3 may be involved in the regulation of diverse cancer cell activities that contribute to tumourigenesis, cancer progression and metastasis. In addition, Gal-3 is a pro-inflammatory regulator in rheumatoid arthritis. Gal-3 has been shown to be involved in many aspects in allergic inflammation, such as eosinophil recruitment, airway remodeling, development of a Th2 phenotype as well as increased expression of inflammatory mediators. In an in vivo model it was shown that bronchoalveolar lavage (BAL) fluid from ovalbumin-challenged mice contained significantly higher levels of Gal-3 compared to control mice. The molecular mechanisms of Gal-3 in human asthma have not been fully elucidated. This review will focus on what is known about the Gal-3 and its role in the pathophysiological mechanisms of asthma to evaluate the potential of Gal-3 as a biomarker and therapeutic target of asthma.