Host-microbial interactions in patients with chronic rhinosinusitis

Abstract

There has been considerable investigation of host-microbial interactions in patients with chronic rhinosinusitis (CRS) in hopes of elucidating mechanisms of disease and better treatment. Most attention has been paid to bacterial infection and potential underlying defects in innate immunity. Bacterial biofilm is present in most patients with CRS undergoing surgical intervention, and its presence is associated with more severe disease and worse surgical outcomes. A role for viral or fungal infection in patients with CRS is less clear. There is no evidence for a primary defect in mucociliary clearance in most patients with CRS. Decreased levels of certain antimicrobial proteins, most notably lactoferrin, have been found in sinus secretions, whereas levels of other antimicrobial proteins have been found to be normal. No primary defects in Toll-like receptors have been found in patients with CRS, although a 50% reduced expression of Toll-like receptor 9 was reported in patients with recalcitrant nasal polyps. A polymorphism in a bitter taste receptor was recently associated with refractory CRS and persistent Pseudomonas aeruginosa infection. A downregulation of innate immunity by maladaptive TH2 tissue inflammation has also been described in patients with recalcitrant nasal polyps, suggesting a link to persistent infection. To date, an effective means of restoring host-microbial balance and mitigating disease in patients with CRS remains elusive.

Role of the bitter taste receptor T2R38 in upper respiratory infection and chronic rhinosinusitis

“…The sinonasal cavity is the front line of respiratory defense; host–pathogen interactions occur with every breath [13]. Nevertheless, in most individuals, immune mechanisms ensure that the sinonasal cavity remains free of infection [14–16].…”

“…However, upper respiratory defenses do sometimes fail, often resulting in the onset of CRS, a complex syndrome involving ineffective sinonasal mucociliary clearance (MCC), stasis of sinonasal secretions, and subsequent chronic infection and/or persistent inflammation [15,17,18]. Chronic infection and biofilm formation contribute to medically recalcitrant CRS, necessitating surgical intervention [13,15,17–19]. This results in a tremendous impact on quality of life.…”

Taste receptors in innate immunity

“…In addition to warming and humidifying inspired air, the sinonasal cavity is also the front line of defense of the respiratory tract [92–98]. Host-pathogen interactions occur with every breath containing aerosolized fungal spores, bacteria, and virus particles [95]. However, in most individuals, the upper and lower airways remain free of pathological bacterial.…”

The use of intranasal glucocorticosteroids in the treatment of rhinosinusitis: Focus on mometasone furoate

“…цилиарного клиренса и др., приводящие к cложному вза-имодействию между реакциями врожденного и адаптив-ного иммунитета [20][21][22][23]. Инфильтрация слизистой обо-лочки ОНП нейтрофилами, макрофагами, лимфоцитами и эозинофилами вызывает развитие воспалительного процесса, который впоследствии вызывает фиброз, утол-щение слизистой оболочки и обструкцию остиомеаталь-ного комплекса (рис.…”