Extract

(See the major article by Winokur et al on pages 728–38.)

Nontypeable Haemophilus influenzae are small gram-negative bacteria that colonize the upper respiratory tract of humans, beginning at a very early age [1]. Although these organisms are normally commensals, when host defenses are compromised by underlying medical conditions such as malnutrition, immunodeficiency, chronic lung disease, or acute viral infection, H. influenzae–associated disease may ensue [2–4]. The contribution of nontypeable H. influenzae to the disease burden of children with otitis media is substantial. Among children in the developed world, this organism is currently responsible for an estimated 40%–50% of the cases of acute otitis media and an even higher percentage of cases of chronic and recurrent disease [5, 6]. In the adult population, particularly among patients with chronic obstructive pulmonary disease, nontypeable H. influenzae are major contributors to the ongoing disease process, particularly during the acute exacerbations that characterize the disease in many patients [4, 7]. Much has been learned about the molecular pathogenesis of disease caused by nontypeable H. influenzae in the past 2 decades, using a variety of in vitro models and in vivo models [8]. The long-term goal of much of this work has been to gain sufficient knowledge about the disease process, such that vaccines or other novel therapies can be developed to prevent nontypeable H. influenzae–associated disease in the future [9]. However, one criticism of this work has been that the findings may not be truly relevant to understanding human disease because many of these earlier studies have been conducted in nonhuman systems. Thus, the study reported by Winokur et al in this issue of the Journal, in which they describe the development of a new human model of nasopharyngeal colonization with nontypeable H. influenzae, is particularly timely and has the potential to be very important for the field [10].

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