Biodegradation is a cost-effective process commonly used to eliminate many xenobiotic hydrocarbons such as diesel oils. However, their hydrophobic character reduces the biodegradation efficiency. In order to overcome this hurdle, kurstakins isolated from Bacillus thuringiensis strain 7SA were used as emulsifying agents. The influence of kurstakin molecules on diesel oil degradation by Acinetobacter haemolyticus strain 2SA was evaluated in the presence and absence of the aforementioned lipopeptide. The degradation rates and gene expressions of alkane hydroxylases were evaluated at days 4, 10, 14 and 21. Results showed that kurstakin molecules increased the hydrophobicity of 2SA. Moreover, diesel oil degradation activities were higher in the presence of kurstakin with 29%, 35%, 29% and 23% improvement at 4th, 10th, 14th and 21st day respectively. Statistical analysis indicated that the difference between the degradation rates in the presence and absence of kurstakin was significant with p = 0.03. The detection of three different hydroxylase genes namely alkB, almA and cyp153 in 2SA genome, might have allowed more efficient degradability of alkanes. According to the real-time PCR results, cyp153 was the most induced gene during diesel oil degradation in the presence and absence of kurstakin. Yet, the three genes demonstrated higher levels of expression in the presence of kurstakin when compared to its absence. This study showed that kurstakins enhance the diesel oil biodegradation rate by increasing the hydrophobicity of 2SA. In addition to their anti-fungal activities, kurstakins can be used as biosurfactant to increase biodegradation of diesel oil.

The implementation of nanotechnology in pulmonary delivery systems might result in better and more specific therapy. Therefore, a nano-sized drug carrier should be toxicologically inert and not induce adverse effects. We aimed to investigate the responses of a polymer nano drug carrier, a lysine poly-hydroxyethyl methacrylate nanoparticle (NP) [Lys-p(HEMA)], loaded with formoterol, both in vitro and in vivo in an ovalbumin (OVA) asthma model. The successfully synthesized nanodrug formulation showed an expectedly steady in vitro release profile. There was no sign of in vitro toxicity, and the 16HBE and THP-1 cell lines remained vital after exposure to the nanocarrier, both loaded and unloaded. In an experimental asthma model (Balb/c mice) of ovalbumin sensitization and challenge, the nanocarrier loaded and unloaded with formoterol was tested in a preventive strategy and compared to treatment with the drug in a normal formulation. The airway hyperresponsiveness (AHR) and pulmonary inflammation in the bronchoalveolar lavage (BAL), both cellular and biochemical, were assessed. The application of formoterol as a regular drug and the unloaded and formoterol-loaded NP in OVA-sensitized mice followed by a saline challenge was not different from the control group. Yet, both the NP formulation and the normal drug application led to a more deteriorated lung function and increased lung inflammation in the OVA-sensitized and -challenged mice, showing that the use of the p(HEMA) nanocarrier loaded with formoterol needs more extensive testing before it can be applied in clinical settings.