TY - JOUR
T1 - Nitric oxide is a mediator of the late-phase response in an animal model of nasal allergy
AU - Durland, William F.
AU - Lane, Andrew P.
AU - Durland, Kimberly W.
AU - Smith, Timothy L.
AU - Johnson, Kenneth L.
AU - Prazma, Jiri
AU - Pillsbury, Harold C.
N1 - Funding Information:
Supported by an AAOA/AAO-HNSF research grant and a UNC School of Medicine 1-year research fellowship.
PY - 2000/5
Y1 - 2000/5
N2 - The presence of nitric oxide (NO) in the nose is well documented; however, the role of this molecule in nasal physiology is still poorly understood. Our laboratory has previously demonstrated that NO is a mediator of the immediate secretory response to an intranasal histamine challenge in a rat model of nasal allergy. Histamine challenge, however, does not elicit a late-phase response (LPR). To study the role of NO in the LPR, we developed a model of nasal allergy in which brown Norway rats are actively sensitized to the allergen ovalbumin and later challenged intranasally with either phosphatebuffered saline solution (vehicle), ovalbumin in vehicle, or ovalbumin and the NO synthase inhibitor N-nitro-L-arginine methyl ester. In each experiment, nasal lavage samples were collected 30, 120, 240, and 360 minutes after challenge. Lavage samples were analyzed for albumin content by ELISA, inflammatory cell concentration with a hemocytometer, and evidence of inflammation by light microscopy. Blocking NO synthesis with N-nitro-L-arginine methyl ester significantly inhibited both albumin exudation and inflammatory cell influx into the nasal cavity during the LPR. These data suggest that NO plays a role in the LPR of nasal allergy.
AB - The presence of nitric oxide (NO) in the nose is well documented; however, the role of this molecule in nasal physiology is still poorly understood. Our laboratory has previously demonstrated that NO is a mediator of the immediate secretory response to an intranasal histamine challenge in a rat model of nasal allergy. Histamine challenge, however, does not elicit a late-phase response (LPR). To study the role of NO in the LPR, we developed a model of nasal allergy in which brown Norway rats are actively sensitized to the allergen ovalbumin and later challenged intranasally with either phosphatebuffered saline solution (vehicle), ovalbumin in vehicle, or ovalbumin and the NO synthase inhibitor N-nitro-L-arginine methyl ester. In each experiment, nasal lavage samples were collected 30, 120, 240, and 360 minutes after challenge. Lavage samples were analyzed for albumin content by ELISA, inflammatory cell concentration with a hemocytometer, and evidence of inflammation by light microscopy. Blocking NO synthesis with N-nitro-L-arginine methyl ester significantly inhibited both albumin exudation and inflammatory cell influx into the nasal cavity during the LPR. These data suggest that NO plays a role in the LPR of nasal allergy.
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U2 - 10.1067/mhn.2000.104015
DO - 10.1067/mhn.2000.104015
M3 - Article
C2 - 10793351
AN - SCOPUS:0034088695
SN - 0194-5998
VL - 122
SP - 706
EP - 711
JO - Otolaryngology - Head and Neck Surgery (United States)
JF - Otolaryngology - Head and Neck Surgery (United States)
IS - 5
ER -