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Published ahead of print on December 2, 2004, doi:10.1165/rcmb.2003-0435OC

Am. J. Respir. Cell Mol. Biol., Volume 32, Number 3, March 2005, 218-224

A more recent version of this article appeared on March 1, 2005
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Submitted on December 4, 2003
Revised on December 2, 2004

Toll-like Receptor 4 or 2 Agonists Decrease Allergic Inflammation

German Velasco1, Monica Campo1, Oscar J Manrique1, Abdelouahab Bellou1, Hongzhen He1, Ruth S.S. Arestides1, Bianca Schaub1, David L Perkins2, and Patricia W Finn1*

1 Respiratory and Critical Care Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA, 2 Immunogenetics and Transplantation, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: pwfinn{at}rics.bwh.harvard.edu.

Toll-like receptors (TLRs) recognize highly conserved microbial molecular patterns, such as found in endotoxin. This study tested whether TLR4 and TLR2 stimulation in vivo would modulate subsequent adaptive (allergic) immune responses. We analyzed the effects of pulmonary administration of a TLR4 agonist, lipid A (LpA), and two TLR2 agonists, peptidoglycan (Ppg) and PamCys, in a murine model of allergic inflammation. The TLR agonists were administered during allergen sensitization or challenge. Both TLR agonists decreased the allergen-induced pulmonary recruitment of eosinophils when administered at sensitization or challenge. When given prior to sensitization, the TLR4 and TLR2 agonists decreased additional allergen-induced parameters of inflammation (pulmonary eosinophilia, bronchoalveolar lavage IL-13, total serum IgE, and airway hyperresponsiveness). Interestingly, TLR4 and 2 agonists decreased the number of CD4+ cells in the lung. Also, at the site of local allergen-stimulation, the draining thoracic lymph nodes, allergen-induced lymphocyte proliferation, and IL-13 secretion were decreased by administration of LpA and Ppg. These data provide a distinct example of the modulation of adaptive (allergic) responses by non-antigen-dependent stimuli. Our findings also demonstrate that both TLR4 and TLR2 agonists decrease allergic responses, supporting the concept that exposure to bacterial components under defined conditions may protect against allergic disease.




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