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Published ahead of print on February 12, 2004, doi:10.1165/rcmb.2003-0229OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 1, July 2004, 22-27

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Submitted on June 18, 2003
Revised on February 12, 2004

Adoptive Transfer of Alveolar Macrophages Abrogates Bronchial Hyperresponsiveness

Eric Careau1* and Elyse Y Bissonnette1

1 Hopital Laval, Institut universitaire de cardiologie et de pneumologie de l'Universite Laval, Centre de recherche, Sainte-Foy, Quebec, Canada

* To whom correspondence should be addressed. E-mail: eric.careau{at}crhl.ulaval.ca.

Increasing evidence suggests that alveolar macrophages (AM) are involved in asthma pathogenesis. To better understand the role that these cells play, we investigated the capacity of AM from allergy-resistant rat, Sprague Dawley (SD), to modulate airway hyperresponsiveness of allergy-susceptible rat, Brown Norway (BN). AM of ovalbumin (OVA)-sensitized BN rats were eliminated by intratracheal instillation of liposomes containing clodronate. AM from OVA-sensitized SD rats were transferred into AM-depleted BN rats 24 h before allergen challenge. Airway responsiveness to methacholine was measured the following day. Instillation of liposomes containing clodronate in BN rats eliminated 85% AM after 3 days compared with saline liposomes. Methacholine concentration needed to increase lung resistance by 200% (EC200RL) was significantly lower in OVA-challenged BN rats (27.9 ± 2.8 mg/ml) compared with SD rats (63.9 ± 8.6 mg/ml). However, when AM from SD rats were transferred into AM-depleted BN rats, airway responsiveness (64.0 ± 11.3 mg/ml) was reduced to the level of naive rats (54.4 ± 3.7 mg/ml) in a dose-dependent manner. Interestingly, transfer of AM from BN rats into SD rats did not modulate airway responsiveness. To our knowledge, this is the first direct evidence showing that AM may protect against the development of airway hyperresponsiveness.




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