TY - JOUR
T1 - Observations on the pathogenesis of nasal priming
AU - Wachs, Michael
AU - Proud, David
AU - Lichtenstein, Lawrence M.
AU - Kagey-Sobotka, Anne
AU - Norman, Philip S.
AU - Naclerio, Robert M.
N1 - Funding Information:
From the Departments of Medicine (Division of Clinical Immu-nology) and Otolaryngology, The Johns Hopkins University School of Medicine, Baltimore, Md. Supported in part by National Institutes of Health Grants NS 22488, AI 20136, AI 07290, and HL 32272. Received for publication June 22, 1988. Revised April 25, 1989. Accepted for publication May 17, 1989. Reprint requests: Robert M. Naclerio, MD, The Good Samaritan Hospital, Professional Office Building, Suite 402, 5601 Loch Raven Blvd., Baltimore, MD 21239. Publication No. 754 from the O’Neill Laboratories, The Good Samaritan Hospital, Baltimore, Md. *Dr. Lichtenstein is the recipient of a Pfizer Biomedical Research Award. **Dr. Naclerio is the recipient of Teacher Investigator Award NS 00811 from the National Institute of Neurological and Com-municative Disorders and Stroke.
PY - 1989/10
Y1 - 1989/10
N2 - To understand better the response of patients with allergic rhinitis to nasal challenge with antigen, we studied the mechanism of priming, that is, the increased clinical response to daily sequential nasal challenges. Ten subjects with ragweed hay fever were challenged four times with increasing doses of ragweed pollen. The first 2 challenge days were separated by 2 weeks, whereas the last three challenges occurred on sequential days. Nasal lavages, performed before and after each nasal challenge, were evaluated for levels of inflammatory mediators and cellular content. In contrast to control days, a significant (p < 0.05) increase in the number of sneezes occurred on both priming days. Priming was associated with a significant increase in the level of histamine on both priming days, whereas the second priming day was also associated with an increase in TAME-esterase activity, kinins, and prostaglandin D2 obtained after challenge (p < 0.05 for all). In the lavages before challenge on the priming days, the total number of cells and the number of neutrophils, eosinophils, and alcian blue-positive cells were significantly increased, but in contrast, basal levels of mediators were not. The net increase in the number of alcian blue-positive cells correlated with the net increase in the amount of histamine released on the priming days (r = 0.661; p < 0.05). These studies suggest that priming results, in part, from increased mediator release from influxing inflammatory cells.
AB - To understand better the response of patients with allergic rhinitis to nasal challenge with antigen, we studied the mechanism of priming, that is, the increased clinical response to daily sequential nasal challenges. Ten subjects with ragweed hay fever were challenged four times with increasing doses of ragweed pollen. The first 2 challenge days were separated by 2 weeks, whereas the last three challenges occurred on sequential days. Nasal lavages, performed before and after each nasal challenge, were evaluated for levels of inflammatory mediators and cellular content. In contrast to control days, a significant (p < 0.05) increase in the number of sneezes occurred on both priming days. Priming was associated with a significant increase in the level of histamine on both priming days, whereas the second priming day was also associated with an increase in TAME-esterase activity, kinins, and prostaglandin D2 obtained after challenge (p < 0.05 for all). In the lavages before challenge on the priming days, the total number of cells and the number of neutrophils, eosinophils, and alcian blue-positive cells were significantly increased, but in contrast, basal levels of mediators were not. The net increase in the number of alcian blue-positive cells correlated with the net increase in the amount of histamine released on the priming days (r = 0.661; p < 0.05). These studies suggest that priming results, in part, from increased mediator release from influxing inflammatory cells.
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U2 - 10.1016/0091-6749(89)90362-X
DO - 10.1016/0091-6749(89)90362-X
M3 - Article
C2 - 2477429
AN - SCOPUS:0024421306
SN - 0091-6749
VL - 84
SP - 492
EP - 501
JO - The Journal of allergy and clinical immunology
JF - The Journal of allergy and clinical immunology
IS - 4 PART 1
ER -