To explore the effect of loratadine on YKL-40 production in Mite extract stimulated A549 and THP-1 cells

The chitinase-like protein, YKL-40, plays an important role in allergic diseases pathogenesis. Allergens induce its production from macrophages and epithelial cells. Some investigations indicated that loratadine has anti-inflammatory effects apart from its H1 receptors antagonist activity. We sought to know whether human epithelial cells and macrophages stimulated for YKL-40 synthesis by house dust mite (HDM) extract, might be influenced by loratadine. We used the human pulmonary type II epithelial cell line A549 and the human monocytic cell line (THP-1) for our in vitro study. This research is an experimental study. After dose-finding studies using neutral red cytotoxicity assay, the cells were pre-incubated with loratadine (0.5 μg/ml) and then stimulated by HDM extract (GREER Lab). Also, in post-treatment condition; A549 and THP-1 cells were stimulated with HDM extract followed by incubation with loratadine. Finally, the amount of YKL-40 released into the cell supernatants was determined by a specific ELISA. Data were analyzed using SPSS software v.16.

A549 cells cannot produce and secret YKL-40 at baseline level or in HDM stimulated condition. In spite of A549, THP-1 cells stimulated with HDM extract showed a significantly increased release of YKL-40. In comparison with control cells, Pre-incubation with loratadine diminished the YKL-40 release from the HDM stimulated THP-1 cells in a significant manner. The YKL-40 level in loratadine group was 4470 pg/ml while it was 8700 pg/ml in the control group (P≤0.05). Although in HDM pretreated cells followed by incubation with loratadine YKL-40 decrease was not found. The Neutral Red Assay results represented nontoxicity of treatments. A549 cells that are used widely in in-vitro models of allergic reactions cannot produce YKL-40 as a mediator of allergic reactions. Therefore, this cell line should not use alone in these studies. Loratadine may have anti-inflammatory effects by suppressing YKL-40 secretion from myeloid cells. As regard to the ability of loratadine to attenuate YKL-40, therefore, we suggest that further studies are warranted to examine its therapeutic potential in diseases that YKL-40 plays a critical role in the pathogenesis.