Increased expression of acidic mammalian chitinase in chronic rhinosinusitis with nasal polyps

Research output: Contribution to journalArticle

Abstract

Background: Chitin is an abundant polysaccharide found in fungi, insects, and parasitic nematodes. Innate immune host defense against chitin-containing pathogens include production of chitinases. In human lower airways, acidic mammalian chitinase (AMCase) is produced in epithelial cells via a Th2-specific, IL-13-dependent pathway, and may act as an inflammatory mediator in asthma. The role of AMCase in chronic rhinosinusitis (CRS) has not been studied previously. Methods: Eleven controls and 22 subjects with medically recalcitrant CRS were prospectively enrolled before undergoing endoscopic sinus surgery. RNA was extracted from surgically obtained ethmoid mucosa, and real-time PCR was used to determine expression of AMCase, eotaxin, and IL-13. Subjects were followed for at least 6 months postoperatively to assess for polyp recurrence. Based on the presence or absence of polyps, the subjects were classified as either recalcitrant or responsive to therapy. Results: AMCase mRNA was detected in the sinus mucosa of 72% of control subjects and in 72% of patients with eosinophilic CRS with nasal polyps (CRSwNP). The expression of AMCase was significantly greater in recalcitrant CRSwNP than it was in treatment-responsive CRSwNP. There was no significant difference in IL-13 expression between these two groups. Conclusion: AMCase may be an important mediator in the pathogen esis of Th2 inflammatory diseases of the respiratory tract. Failure of medical and surgical therapy in CRSwNP is associated with significantly increased expression of AMCase, but not the Th2 cytokines IL-13 and eotaxin. Additional studies are needed to determine the potential of AMCase as a therapeutic target in CRSwNP.

Original languageEnglish (US)
Pages (from-to)330-335
Number of pages6
JournalAmerican Journal of Rhinology
Volume20
Issue number3
DOIs
StatePublished - May 2006

Fingerprint

Nasal Polyps
Chitinases
Interleukin-13
Chitin
Polyps
Mucous Membrane
Respiratory Tract Diseases
Therapeutics
Polysaccharides
Insects
Real-Time Polymerase Chain Reaction
Fungi
Asthma
Epithelial Cells
RNA
Cytokines
Recurrence
Messenger RNA

ASJC Scopus subject areas

  • Otorhinolaryngology

Cite this

Increased expression of acidic mammalian chitinase in chronic rhinosinusitis with nasal polyps. / Ramanathan, Murugappan; Lee, Won Kyung; Lane, Andrew P.

In: American Journal of Rhinology, Vol. 20, No. 3, 05.2006, p. 330-335.

Research output: Contribution to journalArticle

@article{cebd680c481d4bc7892b8dec89e5daf0,
title = "Increased expression of acidic mammalian chitinase in chronic rhinosinusitis with nasal polyps",
abstract = "Background: Chitin is an abundant polysaccharide found in fungi, insects, and parasitic nematodes. Innate immune host defense against chitin-containing pathogens include production of chitinases. In human lower airways, acidic mammalian chitinase (AMCase) is produced in epithelial cells via a Th2-specific, IL-13-dependent pathway, and may act as an inflammatory mediator in asthma. The role of AMCase in chronic rhinosinusitis (CRS) has not been studied previously. Methods: Eleven controls and 22 subjects with medically recalcitrant CRS were prospectively enrolled before undergoing endoscopic sinus surgery. RNA was extracted from surgically obtained ethmoid mucosa, and real-time PCR was used to determine expression of AMCase, eotaxin, and IL-13. Subjects were followed for at least 6 months postoperatively to assess for polyp recurrence. Based on the presence or absence of polyps, the subjects were classified as either recalcitrant or responsive to therapy. Results: AMCase mRNA was detected in the sinus mucosa of 72{\%} of control subjects and in 72{\%} of patients with eosinophilic CRS with nasal polyps (CRSwNP). The expression of AMCase was significantly greater in recalcitrant CRSwNP than it was in treatment-responsive CRSwNP. There was no significant difference in IL-13 expression between these two groups. Conclusion: AMCase may be an important mediator in the pathogen esis of Th2 inflammatory diseases of the respiratory tract. Failure of medical and surgical therapy in CRSwNP is associated with significantly increased expression of AMCase, but not the Th2 cytokines IL-13 and eotaxin. Additional studies are needed to determine the potential of AMCase as a therapeutic target in CRSwNP.",
author = "Murugappan Ramanathan and Lee, {Won Kyung} and Lane, {Andrew P}",
year = "2006",
month = "5",
doi = "10.2500/ajr.2006.20.2869",
language = "English (US)",
volume = "20",
pages = "330--335",
journal = "American Journal of Rhinology and Allergy",
issn = "1945-8924",
publisher = "OceanSide Publications Inc.",
number = "3",

}

TY - JOUR

T1 - Increased expression of acidic mammalian chitinase in chronic rhinosinusitis with nasal polyps

AU - Ramanathan, Murugappan

AU - Lee, Won Kyung

AU - Lane, Andrew P

PY - 2006/5

Y1 - 2006/5

N2 - Background: Chitin is an abundant polysaccharide found in fungi, insects, and parasitic nematodes. Innate immune host defense against chitin-containing pathogens include production of chitinases. In human lower airways, acidic mammalian chitinase (AMCase) is produced in epithelial cells via a Th2-specific, IL-13-dependent pathway, and may act as an inflammatory mediator in asthma. The role of AMCase in chronic rhinosinusitis (CRS) has not been studied previously. Methods: Eleven controls and 22 subjects with medically recalcitrant CRS were prospectively enrolled before undergoing endoscopic sinus surgery. RNA was extracted from surgically obtained ethmoid mucosa, and real-time PCR was used to determine expression of AMCase, eotaxin, and IL-13. Subjects were followed for at least 6 months postoperatively to assess for polyp recurrence. Based on the presence or absence of polyps, the subjects were classified as either recalcitrant or responsive to therapy. Results: AMCase mRNA was detected in the sinus mucosa of 72% of control subjects and in 72% of patients with eosinophilic CRS with nasal polyps (CRSwNP). The expression of AMCase was significantly greater in recalcitrant CRSwNP than it was in treatment-responsive CRSwNP. There was no significant difference in IL-13 expression between these two groups. Conclusion: AMCase may be an important mediator in the pathogen esis of Th2 inflammatory diseases of the respiratory tract. Failure of medical and surgical therapy in CRSwNP is associated with significantly increased expression of AMCase, but not the Th2 cytokines IL-13 and eotaxin. Additional studies are needed to determine the potential of AMCase as a therapeutic target in CRSwNP.

AB - Background: Chitin is an abundant polysaccharide found in fungi, insects, and parasitic nematodes. Innate immune host defense against chitin-containing pathogens include production of chitinases. In human lower airways, acidic mammalian chitinase (AMCase) is produced in epithelial cells via a Th2-specific, IL-13-dependent pathway, and may act as an inflammatory mediator in asthma. The role of AMCase in chronic rhinosinusitis (CRS) has not been studied previously. Methods: Eleven controls and 22 subjects with medically recalcitrant CRS were prospectively enrolled before undergoing endoscopic sinus surgery. RNA was extracted from surgically obtained ethmoid mucosa, and real-time PCR was used to determine expression of AMCase, eotaxin, and IL-13. Subjects were followed for at least 6 months postoperatively to assess for polyp recurrence. Based on the presence or absence of polyps, the subjects were classified as either recalcitrant or responsive to therapy. Results: AMCase mRNA was detected in the sinus mucosa of 72% of control subjects and in 72% of patients with eosinophilic CRS with nasal polyps (CRSwNP). The expression of AMCase was significantly greater in recalcitrant CRSwNP than it was in treatment-responsive CRSwNP. There was no significant difference in IL-13 expression between these two groups. Conclusion: AMCase may be an important mediator in the pathogen esis of Th2 inflammatory diseases of the respiratory tract. Failure of medical and surgical therapy in CRSwNP is associated with significantly increased expression of AMCase, but not the Th2 cytokines IL-13 and eotaxin. Additional studies are needed to determine the potential of AMCase as a therapeutic target in CRSwNP.

UR - http://www.scopus.com/inward/record.url?scp=33746177512&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33746177512&partnerID=8YFLogxK

U2 - 10.2500/ajr.2006.20.2869

DO - 10.2500/ajr.2006.20.2869

M3 - Article

C2 - 16871939

AN - SCOPUS:33746177512

VL - 20

SP - 330

EP - 335

JO - American Journal of Rhinology and Allergy

JF - American Journal of Rhinology and Allergy

SN - 1945-8924

IS - 3

ER -