IL-1α, IL-6 and IL-8 serum values in patients with chronic suppurative otitis media.

Inflammatory mediators play an important role in the pathogenesis of otitis media by initiating and maintaining an inflammatory response to infection. The presence of inflammatory mediators may be one of the reasons, in some patients, for acute otitis media transforming into chronic otitis media. The present study included 60 patients admitted to the Clinical Rehabilitation Hospital, Iasi, Romania, for surgery. The control group comprised 30 healthy individuals. Serum levels of interleukin 1α (IL-1α), interleukin 6 (IL-6) and interleukin 8 (IL-8) were measured prior to surgery and were compared among patients with chronic suppurative otitis media (CSOM), cholesteatoma and cholesteatoma recidivism and the control group. High serum levels of interleukins were recorded in all the groups compared to the healthy control group. IL-6 and IL-8 had the highest value in patients with CSOM and IL-1α had the highest value in patients with cholesteatoma recidivism. Thus, we can consider that inflammatory mediators play a central role in the pathogenesis of CSOM and cholesteatoma by maintaining a systemic and local inflammatory response.

Modulation of the activity of certain genes involved in tumor cell metabolism in the presence of the cytotoxic peptides defensin and cathelicidin LL37.

It is common knowledge that some natural antimicrobial peptides also have a tumoricidal effect. We have shown that the peptides defensin and cathelicidin LL37 have cytostatic effects on human tumor cell lines HT29 (colorectal carcinoma) and A549 (alveolar carcinoma). In order to determine the modulating mechanism of these peptides we assessed the gene expression of the AKT, HIF-1α, XBP, NRF2, PERK, CHOP, BCL2, IRE1α and PI3K molecular targets involved in the survival, growth, proliferation and apoptosis pathways of tumor cells in the presence or absence of the studied peptides. Thus, this research enabled us to determine molecular markers and methods of assessment and monitoring of tumor cell cytotoxicity by high-performance molecular biology techniques. Defensin and cathelicidin LL37 activated tumor cell apoptosis, especially for the HT29, but also for A549 line, by increasing gene expression of CHOP and by lowering BCL2 gene expression. Oxidative stress determined the increase in gene expression of XBP, which directly influenced CHOP. The decrease in NRF2 gene expression highlighted the inhibition of cell proliferation, while the decrease in HIF1α gene expression evidenced the decrease in cell survival.