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news.bitop, which specializes in the development and marketing of Ectoin containing medical devices, said that Ectoin has reduced nanoparticle-induced inflammatory reaction in rat lungs, one of the animal models for chronic obstructive pulmonary disease (COPD).
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Ectoin is a cyclic amino acid that is produced mainly by halophilic bacteria to protect the cells from the extreme osmotic stress associated with saline conditions.
bitop claimed that it is the first time that Ectoin has been shown to have such an effect on nanoparticle-induced lung inflammation. Current therapy for COPD is treatment with glucocorticoids that, however, have only limited effect on nanoparticle-induced lung inflammation even when inhaled.
In the study, Ectoin, given locally with or before the application of nanoparticles, reduced neutophil influx by about 30%. Furthermore, Ectoin has prevented CNP-induced increase in cinc-1 release. Cinc-1 is the rat homologue of human IL-8, a cytokine that mediates CNP induced influx of neutrophil granulocytes.
bitop said that pretreatment with Ectoin also reduces CNP-induced release of other major proinflammatory cytokines that play a critical role in the induction of lung fibrosis or in the pathogenic cascade leading to asthma.
Dirk Probst, CEO of bitop, said: “Our findings suggest that Ectoin can be used for the development of medical devices to protect individuals against unavoidable environmental nanoparticle-induced inflammatory reaction in the lung.”