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Hyun-Jae Woo, MD; Jeong-Ki Min, MD; Chang Hoon Bai, MD; Si-Youn Song, MD; Hee Joon Kang, MD; Heung-Man Lee, MD; Yong-Dae Kim, MD

Arch Otolaryngol Head Neck Surg. 2008;134(11):1182-1186.

Objective  To investigate the expression and localization of neutrophil gelatinase–associated lipocalin (NGAL), an antimicrobial peptide, in the normal nasal mucosa and human nasal polyps. Neutrophil gelatinase–associated lipocalin has been identified as a key element in the innate host defense system. However, scant knowledge exists about the expression of NGAL in the human sinonasal tract.

Design  Prospective study.

Setting  Academic medical center.

Patients  Normal inferior turbinate mucosa was obtained from 10 patients who were undergoing augmentation rhinoplasty. The nasal polyps were obtained from 10 patients who were undergoing endoscopic sinus surgery for chronic rhinosinusitis with polyps.

Interventions  We performed semiquantitative reverse transcription–polymerase chain reaction, immunohistochemical staining, and Western blot analysis.

Main Outcome Measures  We analyzed the expression of the NGAL messenger RNA (mRNA) and localization of the NGAL protein.

Results  The NGAL mRNA and NGAL protein were highly expressed in the nasal polyps. The ratio of NGAL mRNA to glyceraldehyde-3-phosphate dehydrogenase mRNA in the nasal polyps was greater compared with that in the normal turbinate mucosa (P = .002). The NGAL protein was observed in the epithelium, the infiltrating inflammatory cells, and the submucosal gland of the nasal polyps, but it was very rarely detected in the normal nasal mucosa.

Conclusion  Expression of NGAL is upregulated in nasal polyps, and additional work is needed to reveal the possible role of NGAL in the defense systems of the nasal mucosa and the process of polyp formation.

Author Affiliations: Departments of Otorhinolaryngology–Head and Neck Surgery, Colleges of Medicine, Yeungnam University, Daegu, South Korea (Drs Woo, Min, Bai, Song, and Kim), and Korea University, Seoul, South Korea (Drs Kang and Lee).

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