Macrophage Infiltrate Is Elevated in CRSwNP Sinonasal Tissue Regardless of Atopic Status.

Objective: Macrophages are major producers of inflammatory cytokines; however, their role in chronic rhinosinusitis (CRS) has not been clearly defined. The aim of this study was to quantify macrophages in sinus tissue of patients with various subtypes of CRS and determine the impact of atopic status on macrophage infiltrate.

Study Design: Prospective immunohistochemical study of human sinonasal tissue.

Reactive oxygen species in chronic rhinosinusitis and secondhand smoke exposure.

Objective: Reactive oxygen species (ROS) can potentiate cellular injury and inflammation. This study aimed to (1) assess the presence of reactive oxygen species in the sinus tissue of patients with chronic rhinosinusitis (CRS) and (2) assess the impact of secondhand smoke (SHS) exposure on reactive oxygen species (ROS) production.

Study Design: Retrospective cohort study.

Vitamin D3 deficiency increases sinus mucosa dendritic cells in pediatric chronic rhinosinusitis with nasal polyps.

Objective: Dendritic cells are professional antigen presenting cells, capable of initiating Th1 or Th2 responses, and have been implicated in the pathogenesis of a number of diseases, including sinusitis. Vitamin D(3) is a steroid hormone that acts on dendritic cells in a manner similar to corticosteroids. Investigators examined whether children with allergic fungal rhinosinusitis (AFRS) or chronic rhinosinusitis with nasal polyposis (CRSwNP) were vitamin D(3) deficient and the relationship of vitamin D(3) deficiency to dendritic cell infiltrate in the sinus mucosa.

Increased presence of dendritic cells and dendritic cell chemokines in the sinus mucosa of chronic rhinosinusitis with nasal polyps and allergic fungal rhinosinusitis.

Background: The aim of this study was to determine if there is a link between local dendritic cells (DCs) and various subtypes of chronic rhinosinusitis (CRS): CRS with nasal polyposis (CRSwNP), CRS without nasal polyposis (CRSsNP), and allergic fungal rhinosinusitis (AFRS). Once DC presence was established we considered possible mechanisms for DC recruitment to the sinuses.

Methods: Biopsy specimens were taken from the osteomeatal complex during endoscopic sinus surgery in patients with AFRS (n ≥ 5), CRSsNP (n ≥ 6), and CRSwNP (n ≥ 6).

Murine complement deficiency ameliorates acute cigarette smoke-induced nasal damage.

Objective: Exposure to cigarette smoke is a risk factor for chronic rhinosinusitis. Current literature confirms complement fragments are activated in human nasal mucosa. The mechanism(s) responsible for this activation is unclear.

Alterations in gene expression of complement components in chronic rhinosinusitis.

Background: The complement cascade forms part of the initial innate response to pathogens in the airway. Complement activation is important in the maintenance of host homeostasis, but excessive and uncontrolled activation may lead to inflammation and disease. The role of the complement pathway in the innate response in chronic rhinosinusitis (CRS) is poorly characterized Methods: Sinus mucosa biopsy specimens from the anterior ethmoid or uncinate process of patients with allergic fungal rhinosinusitis (AFRS), CRS without NPs (CRS-NPs), and controls were harvested and gene and protein expression of C3, factor B (fB), C5, and C7 complement proteins were analyzed using quantitative polymerase chain reaction and immunohistochemical techniques.