Abstract
Chronic rhinosinusitis (CRS) is marked by an inflamed mucosa of sinuses and is accompanied by a significantly reduced quality of live. Since no guidelines for the treatment of CRS are available, long lasting clinical histories with health care costs adding up to dozens of billion $ annually are caused by CRS. The progression of CRS is often induced by bacterial infections and/or a shift in microbiome as well as biofilm formation. The exact microbiome alterations are still unclear and the impenetrable biofilm renders the treatment with common antibiotics ineffective. This study focuses on characterizing the microbiome changes in CRS and investigating the inhibition of biofilm growth by 1,8-Cineol, a small, non-polar and hence biofilm penetrating molecule with known antimicrobial potential. We performed MALDI-TOF MS based characterization of the microbiomes of healthy individuals and CRS patients (n = 50). The microbiome in our test group was shifted to pathogens (Staphylococcus aureus, Escherichia coli, and Moraxella catarrhalis). In contrast to published studies, solely based on cell culture techniques, we could not verify the abundance of Pseudomonas aeruginosa in CRS. The inhibition of bacterial proliferation and biofilm growth by 1,8-Cineol was measured for these three pathogens. Interestingly, S. aureus, the most prominent germ in CRS, showed a biofilm inhibition not simply correlated to its inhibition of proliferation. RT-qPCR confirmed that this was due to the downregulations of major key players in biofilm generation (agrA, SarA and σB) by 1,8-Cineol. Furthermore we verified this high biofilm inhibition potential in a model host system consisting out of S. aureus biofilm grown on mature respiratory epithelium. A second host model, comprising organotypic slices, was utilized to investigate the reaction of the innate immune system present in the nasal mucosa upon biofilm formation and treatment with 1,8-Cineol. Interestingly Staphylococcus epidermidis, the cause of very common catheter infections, possesses a biofilm generation pathway very similar to S. aureus and might be treatable in a similar fashion. The two presented in vitro model systems might be transferred to combinations of every biofilm forming bacterial with most kind of epithelium and mucosa.
Highlights
The chronic rhinosinusitis (CRS) is defined as a symptomatic inflammation of the nasal and sinus mucosa with persistent symptoms lasting beyond 12 weeks with a prevalence of around 6% in Europe (Hastan et al, 2011)
Our results show that the microbiome of the test group is shifted from commensal bacteria genuses like Corynebacterium and viridans Streptococci to the potential pathogenic species E. coli and M. catarrhalis
The two pathogenic germs E. coli and M. catarrhalis where found with a frequency of 10 and 4% respectively in CRS patients and only 2 and 0% respectively of the healthy test individuals were colonized by this germs
Summary
The chronic rhinosinusitis (CRS) is defined as a symptomatic inflammation of the nasal and sinus mucosa with persistent symptoms lasting beyond 12 weeks with a prevalence of around 6% in Europe (Hastan et al, 2011). Besides the inflammation most patients suffering from CRS exhibit nasal obstruction and facial pressure further more nasal discharge and hyposmia are very common symptoms. In addition about 25–30% of CRS patients develop nasal polyps (CRSwNP) (Stevens et al, 2016). Up to now there are no existing guidelines to treat CRS and its cause. This often results in a long lasting course of disease with a significant reduced quality of life for patients. CRS related health care expenses in the United States are estimated to add up to a total of 8.6 billion $ annually (Bhattacharyya, 2011)
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