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Correspondence to: Dr. Ph. Godard, Clinique des maladies respiratoires, Avenue Major Flandre, F-34059 Montpellier (France) Bronchial asthma has been defined as a bronchial disease inducing a reversible airway obstruction. Reed [1] proposed to name it: eosinophilic desquama-tive chronic bronchitis. This term is very interesting because it outlines the importance of inflammation in the pathogenesis of the disease. It has been assumed for a long time that the narrowed airways were preferentially located centrally, that is to say in the large bronchi. However, increasing evidence indicates that the deep lung is also involved in bronchial asthma: (1) it is now well known that many aeroallergens are able to reach the alveoli [2, 3]; (2) the airway obstruction is often located in the peripheral airways, especially in the chronic stages of the disease, as assessed by flow volume curves and additional methods such as the evaluation of ventilation/perfusion abnormalities [4], and (3) extensive studies of the bronchoalveolar lav-age (BAL) fluid in asthmatics have demonstrated a lot of inflammatory cells and mediators in this fluid [5, 6]. Alveolar macrophages (AM) are the principal resident phagocytes in the bronchoalveolar lumen and could be observed in the central airways, as assessed by segmental bronchial wash [7]. Therefore, it can be proposed to name them airway macrophages. In a very elegant and important study, Patterson et al. [8] demonstrated that bronchoalveolar cells obtained by BAL in sensitized monkeys and injected into the trachea of nonsensitized syngenic monkeys were able to promote bronchial asthma after specific inhalation challenge. Since AM accounted for about 90–95% of the cells recovered by BAL, a potential role for AM can be suggested. We would like to review the lines of evidence indicating that macrophages play an important role in the pathophysiology of human bronchial asthma. (1) AM are able to synthesize and release chemical mediators involved in the pathophysiology of bronchial asthma [9]. They can be activated in vitro by an IgE-dependent mechanism [10], phagocytosed particles (zymosan and opsonized zymosan) or soluble stimuli such as a chemoattractant peptide (formyl-methionyl-leucyl-phenylalanine) or a potent activator of protein kinase C (phorbol myristate acetate; PMA), mechanisms which appear to be relevant to bronchial asthma. (2) AM are activated in vivo in asthmatic patients as demonstrated by their enhanced capacity to be stimulated in vitro. This activation correlated with the severity of the disease (as assessed by either the Aas clinical score [11], or airway obstruction, or nonspecific airway