Am. J. Respir. Crit. Care Med., Volume 163, Number 5, April 2001, 1101-1107

The Relationship between Atopic Status and IL-10 Nasal Lavage Levels in the Acute and Persistent Inflammatory Response to Upper Respiratory Tract Infection

JONATHAN M. CORNE, LAURIE LAU, STEPHEN J. SCOTT, RHYS DAVIES, SEBASTIAN L. JOHNSTON, and PETER H. HOWARTH

University Medicine, Southampton General Hospital, Southampton; and Department of Respiratory Medicine, NHLI at St. Mary's, Imperial College School of Medicine, London, United Kingdom

We examined the influence of atopy on virus-induced airway inflammation by comparing the nasal response to naturally acquired upper respiratory tract infection in atopic and nonatopic subjects by measurement of cytokine, chemokine, and mediator levels in nasal lavage from 44 adults (23 atopic) taken during the acute and the convalescent phases of the common cold. Nasal aspirates were examined for the presence of upper respiratory viruses by RT-PCR. In atopic and nonatopic subjects there were increased levels of IL-1, IL-6, IL-8, TNF-, RANTES, sICAM-1, MPO, ECP, IL-10, and IFN- in nasal lavage during the acute compared with the convalescent phase (p < 0.001). During the acute phase histamine levels were significantly higher in the atopic than in the nonatopic subjects (p < 0.05), whereas IL-10 levels were significantly greater in the nonatopic than in the atopic subjects (p < 0.05). At convalescence levels of IL-1, IL-6, sICAM-1, ECP, RANTES and albumin were significantly higher in the atopic group (p < 0.05). An upper respiratory tract virus was found in 27 volunteers (61%) during the acute stage and in two volunteers (4%) at convalescence. We conclude that virus-induced inflammatory changes within the nose are more prolonged in atopic than in nonatopic subjects and that this is associated with reduced IL-10 levels in atopic compared with nonatopic subjects during the acute phase of upper respiratory tract infection.

This article has been cited by other articles:

				A M Singh and W W Busse Asthma exacerbations {middle dot} 2: Aetiology. Thorax, September 1, 2006; 61(9): 809 - 816. [Abstract] [Full Text] [PDF]

				T. V. Grissell, H. Powell, D. R. Shafren, M. J. Boyle, M. J. Hensley, P. D. Jones, B. F. Whitehead, and P. G. Gibson Interleukin-10 Gene Expression in Acute Virus-induced Asthma Am. J. Respir. Crit. Care Med., August 15, 2005; 172(4): 433 - 439. [Abstract] [Full Text] [PDF]

				R. F. Lemanske Jr. Is Asthma an Infectious Disease?: Thomas A. Neff Lecture Chest, March 1, 2003; 123(2007): 385S - 390S. [Abstract] [Full Text] [PDF]

				C. G. Lee, R. J. Homer, L. Cohn, H. Link, S. Jung, J. E. Craft, B. S. Graham, T. R. Johnson, and J. A. Elias Transgenic Overexpression of Interleukin (IL)-10 in the Lung Causes Mucus Metaplasia, Tissue Inflammation, and Airway Remodeling via IL-13-dependent and -independent Pathways J. Biol. Chem., September 13, 2002; 277(38): 35466 - 35474. [Abstract] [Full Text] [PDF]

				N. G. Papadopoulos, M. Moustaki, M. Tsolia, A. Bossios, E. Astra, A. Prezerakou, D. Gourgiotis, and D. Kafetzis Association of Rhinovirus Infection with Increased Disease Severity in Acute Bronchiolitis Am. J. Respir. Crit. Care Med., May 1, 2002; 165(9): 1285 - 1289. [Abstract] [Full Text] [PDF]

				M. J. TOBIN Asthma, Airway Biology, and Nasal Disorders in AJRCCM 2001 Am. J. Respir. Crit. Care Med., March 1, 2002; 165(5): 598 - 618. [Full Text] [PDF]