PM2.5 is one of the most harmful components of airborne pollution and includes particles with diameters of less than 2.5 μm. Almost 90% of the world’s population lives in areas with poor air quality exceeding the norms established by the WHO. PM2.5 exposure affects various organs and systems of the human body including the upper respiratory tract which is one of the most prone to its adverse effects. PM2.5 can disrupt nasal epithelial cell metabolism, decrease the integrity of the epithelial barrier, affect mucociliary clearance, and alter the inflammatory process in the nasal mucosa. Those effects may increase the chance of developing upper respiratory tract diseases in areas with high PM2.5 pollution. PM2.5’s contribution to allergic rhinitis (AR) and rhinosinusitis was recently thoroughly investigated. Numerous studies demonstrated various mechanisms that occur when subjects with AR or rhinosinusitis are exposed to PM2.5. Various immunological changes and alterations in the nasal and sinonasal epithelia were reported. These changes may contribute to the observations that exposure to higher PM2.5 concentrations may increase AR and rhinosinusitis symptoms in patients and the number of clinical visits. Thus, studying novel strategies against PM2.5 has recently become the focus of researchers’ attention. In this review, we summarize the current knowledge on the effects of PM2.5 on healthy upper respiratory tract mucosa and PM2.5’s contribution to AR and rhinosinusitis. Finally, we summarize the current advances in developing strategies against PM2.5 particles’ effects on the upper respiratory tract.

Chronic rhinosinusitis (CRS) is related to persistent inflammation with a dysfunctional relationship between environmental agents and the host immune system. Disturbances in the functioning of the sinus mucosa lead to common clinical symptoms. The major processes involved in the pathogenesis of CRS include airway epithelial dysfunctions that are influenced by external and host-derived factors which activate multiple immunological mechanisms. The molecular bases for CRS remain unclear, although some factors commonly correspond to the disease: bacterial, fungal and viral infections, comorbidity diseases, genetic dysfunctions, and immunodeficiency. Additionally, air pollution leads increased severity of symptoms. CRS is a heterogeneous group of sinus diseases with different clinical courses and response to treatment. Immunological pathways vary depending on the endotype or genotype of the patient. The recent knowledge expansion into mechanisms underlying the pathogenesis of CRS is leading to a steadily increasing significance of precision medicine in the treatment of CRS. The purpose of this review is to summarize the current state of knowledge regarding the immunological aspects of CRS, which are essential for ensuring more effective treatment strategies.

Bee venom (BV) is valued therapeutically mainly for its peptides, melittin and apamin. This study determined the dose-dependent biological activity of bee venom standardized to its melittin and apamin content by UHPLC-ESI-MS, as well as that of its principal peptides, melittin and apamin, tested at matched concentrations. Antibacterial activity was assessed as showing the minimum inhibitory and minimum bactericidal concentrations (MIC, MBC) against Staphylococcus aureus (MSSA and MRSA) and Staphylococcus epidermidis (MRSE). Cytotoxicity toward primary human keratinocytes (HEKa) was determined by MTT and LDH assays and the mode of cell death by Annexin V-FITC/propidium iodide staining. The standardized bee venom contained 608.21 µg/mg of melittin and 22.17 µg/mg of apamin. Melittin was the only active constituent (MIC 2.5 to 5 µg/mL, MBC/MIC ≤ 2), whereas apamin was inactive (>10 µg/mL). Bee venom was active only against Staphylococcus epidermidis (MRSE), with both MIC and MBC values equal to 10 µg/mL. At concentrations of 5 and 10 µg/mL, both bee venom and melittin were markedly cytotoxic to keratinocytes. The selectivity index (CC50/MIC) did not exceed 1.6 for melittin and reached 0.2 for bee venom. On a melittin-equivalent basis, whole venom was more cytotoxic than pure melittin (CC50 1.33 versus 3.91 µg/mL), indicating that constituents other than melittin contribute to keratinocyte damage. Melittin is therefore the principal antibacterial constituent, but its narrow selectivity does not support direct topical use. Combination experiments evaluating bee venom or its isolated peptides in combination with antibiotics were not performed here and remain a defined direction for future work. Standardization to melittin content predicts potency but not safety, which has to be assessed on the whole standardized venom.