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Summary: Background. Chronic rhinosinusitis (CRS) is an inflammatory disease that affects the nasal mucosa and the paranasal sinuses. CRS can be associated by nasal polyposis (CRSwNP phenotype) in up to 30% of patients and it is frequently associated with bronchial asthma. CRSwNP shows predominantly an underlying activation of type 2 inflammatory pathways with the involvement of eosinophils, IgE, interleukin (IL)-4, IL-5 and IL-13. Biological drugs that target these inflammatory cytokines are currently a therapeutic option recognized by guidelines for the treatment of uncontrolled form of the disease. Methods. As part of the activity of the "ARIA-Italy" working group, a panel of 255 Italian Ear, Nose and Throat (ENT) specialists, pneumologists and immuno-allergologists actively participated in this national survey and answered a series of questions geared toward understanding the main criteria for patient characterization and therapeutic decision, highlighting multidisciplinarity, and the implementation of the management of CRSwNP patients, as a part of the precision medicine concept and the appropriate use of the biologicals. Results. Two hundred and fifty-five experts and specialists participated in the survey. Conclusions. The results of this survey obtained from an extensive number of active specialists throughout Italy allow some important concluding remarks to be drawn. The main points of agreement were that multidisciplinary care teams provide many benefits but that, once the team is established, meetings and communication between members must be coordinated. Finally, the dissemination of national disease registries and the continuous updating of guidelines and position papers related to CRSwNP and comorbidities should be encouraged.
RESUMEN
Unstimulated peritoneal cells (PC) from mice sensitized with nonviable Mycobacterium tuberculosis in an oil-droplet emulsion inhibit encephalomyocarditis virus (EMCV) replication in mouse embryo fibroblast monolayers. Concentrations of mycobacteria ranging from 50 to 500 microgram elicit PC that inhibit EMCV replication greater than 99%. PC collected 2 to 6 weeks post-inoculation of mycobacteria are most effective (greater than 99% inhibition), although cells harvested from mice 7 through 10 weeks inhibit viral replication greater than 90%. Inhibition of replication is not detected unless PC are in contact with infected monolayers for a minimum of 8 to 10 hr; nonviable PC are not effective. Optimal inhibition occurs in cultures infected with a low multiplicity of EMCV that are incubated at 37 degrees C. Inhibition of replication is not due to pH changes or depletion of nutrients in cultures, adsorption and/or inactivation of EMCV by macrophages, or killing of monolayers by the PC. Inhibition of viral replication by the unstimulated PC appears to be due to an interferon that is similar but not identical to classical mouse Type II interferon.