title: Interleukin-1 beta, interleukin-5, interleukin-6, interleukin-8, and tumor necrosis factor-alpha in chronic sinusitis: response to systemic corticosteroids.
abstract: Recently, the role of various cytokines in the pathogenesis of chronic rhinosinusitis has come under investigation. Various studies have reported increased levels of interleukin-3, interleukin-4, interleukin-5, interleukin-13, and granulocyte macrophage-colony stimulating factor in the sinonasal mucosa of patients with chronic rhinosinusitis. The present study investigated the levels of pro-inflammatory cytokines, including interleukin-1 beta (IL-1 beta), interleukin-5 (IL-5), interleukin-6 (IL-6) interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-alpha), in the sinonasal mucosa of patients with chronic rhinosinusitis, and evaluated the response of these cytokines to oral corticosteroids. Chronic rhinosinusitis subjects (n = 15) and control subjects (n = 9) underwent nasal endoscopy and biopsy of the sinonasal mucosa. Chronic rhinosinusitis subjects were subsequently treated with a 10-day tapering dose of prednisone followed by a second sinonasal endoscopic exam and biopsy. Mucosal biopsy specimens were immunostained for IL-1 beta, IL-5, IL-6, IL-8, and TNF-a. In chronic rhinosinusitis subjects, mucosal levels of IL-1 beta, IL-6, IL-8, and TNF-alpha were significantly elevated when compared with control subjects, and levels of IL-5 demonstrated a strong trend toward elevation. In posttreatment chronic rhinosinusitis subjects, levels of IL-6 were significantly decreased when compared with pretreatment levels, and TNF-alpha levels demonstrated a significant trend toward reduction. These findings support the hypothesis that the inflammatory response in chronic rhinosinusitis is associated with elevated levels of pro-inflammatory cytokines, and suggest that oral corticosteroids may exert a beneficial effect by significantly reducing the levels of IL-6 and TNF-alpha.
authors.affiliation: Division of Otolaryngology, Walter Reed Army Medical Center, Washington, DC, USA.
authors.forename: C M
authors.initials: CM
authors.lastname: Lennard
authors.forename: E A
authors.initials: EA
authors.lastname: Mann
authors.forename: L L
authors.initials: LL
authors.lastname: Sun
authors.forename: A S
authors.initials: AS
authors.lastname: Chang
authors.forename: W E
authors.initials: WE
authors.lastname: Bolger
mesh_terms: D000284:Administration, Oral; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D002908:Chronic Disease; D016207:Cytokines / Q000502:physiology*; D004724:Endoscopy; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007375:Interleukin-1 / Q000502:physiology; D015848:Interleukin-5 / Q000502:physiology; D016209:Interleukin-8 / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps / Q000188:drug therapy; D011241:Prednisone / Q000008:administration & dosage / Q000627:therapeutic use*; D012220:Rhinitis / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D012852:Sinusitis / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D007375:Interleukin-1; D015848:Interleukin-5; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D011241:Prednisone