Exposure to Endotoxins during Sensitization Prevents Further Endotoxin-Induced Exacerbation of Airway Inflammation in a Mouse Model of Allergic Asthma

Vol. 138, No. 4, 2005

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Original Paper

Exposure to Endotoxins during Sensitization Prevents Further Endotoxin-Induced Exacerbation of Airway Inflammation in a Mouse Model of Allergic Asthma
Carine Delayre-Orthez^a, Julien Becker^a, Frédéric de Blay^{a, b}, Nelly Frossard^a, Françoise Pons^a

^aEA 3771, Inflammation et environnement dans l'asthme, Faculté de Pharmacie, Université Louis Pasteur-Strasbourg I, Illkirch,
^bService de Pneumologie, Hôpital Lyautey, Hôpitaux Universitaires de Strasbourg, Strasbourg, France

Address of Corresponding Author

Int Arch Allergy Immunol 2005;138:298-304 (DOI: 10.1159/000088867)

Key Words

Asthma
Allergy
Endotoxin
Inflammation
Immunoglobulin E
Th2/Th1 cytokines
Mouse

Abstract

Background: We have shown previously that lipopolysaccharides (LPS) inhibited airway inflammation in allergen-sensitized and challenged mice when administered during sensitization, while exacerbating the inflammation when given upon challenge. We have here investigated the effect of LPS administered during both sensitization and challenge on airway inflammation, as well as on the profile of the T-helper (Th) response to allergen. Methods: Mice were sensitized and challenged with ovalbumin (OVA), in the presence or absence of effective doses of LPS, namely 1 µg during sensitization and 1 ng during challenge. Inflammation was assessed by measuring cell counts and cytokine levels in bronchoalveolar lavage fluid (BALF). The profile of the Th response was determined by quantifying OVA-specific IgE and IgG2a in serum and Th1/Th2 cytokines in the culture medium of splenocytes and in BALF. Results: Allergen-induced airway eosinophilia was increased in mice exposed to LPS during challenge only when compared with controls, whereas it was similarly reduced in animals exposed during sensitization only and during both sensitization and challenge. Mice exposed to LPS during sensitization only or during both sensitization and challenge also displayed a decrease in IgE and an increase in IgG2a, suggesting a switch in the immune response toward the Th1 profile. This was confirmed by quantification of Th1/Th2 cytokines in culture medium of splenocytes and in BALF. Conclusions: Our data demonstrate that exposure to endotoxins during sensitization prevents allergen-induced airway inflammation, as well as its exacerbation triggered by further exposure to endotoxins during challenge, while switching the immune response to allergen from a Th2 to a Th1 profile.

Author Contacts

Correspondence to: Dr. Françoise Pons
EA 3771, Inflammation et environnement dans l'asthme
Faculté de Pharmacie, 74 route du Rhin, BP 60024
FR-67401 Illkirch cedex (France)
Tel. +33 3 90 24 42 03, Fax +33 3 90 24 43 09, E-Mail pons@pharma.u-strasbg.fr

Article Information

Received: February 7, 2005
Accepted after revision: August 4, 2005
Published online: October 10, 2005
Number of Print Pages : 7
Number of Figures : 4, Number of Tables : 0, Number of References : 30

Medline Abstract (ID 16220006)

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