Rapid dendritic cell recruitment is a hallmark of the acute inflammatory response at mucosal surfaces.

TLDR

Acute bacterial inflammation is dominated by neutrophils peaking 24–48 h before mononuclear cells, yet the authors propose that mucosal dendritic‑cell influx may serve as viral surveillance at selected sites. The study questions whether the neutrophil‑dominant paradigm applies to all acute inflammatory responses. After inhalation of Moraxella catarrhalis, dendritic‑cell precursors are recruited into the airway epithelium before neutrophils, differentiate there, acquire dendriform morphology, and then migrate to regional lymph nodes within 48 h. DC recruitment was absent in epidermal or intraperitoneal challenges, suggesting mucosal surfaces uniquely require rapid DC responses during acute inflammation.

Abstract

Immunohistochemical analysis of challenge sites such as skin and the peritoneal cavity has identified neutrophils as virtually the sole cellular participants in acute bacterial inflammation, peak influx occurring 24-48 h in advance of mononuclear cell populations associated with adaptive immunity. This study challenges the general applicability of this paradigm. We demonstrate here that the earliest detectable cellular response after inhalation of Moraxella catarrhalis organisms is the recruitment of putative class II major histocompatibility complex-bearing dendritic cell (DC) precursors into the airway epithelium, the initial wave arriving in advance of the neutrophil influx. Unlike the neutrophils which rapidly transit into the airway lumen, the DC precursors remain within the epithelium during the acute inflammatory response where they differentiate, and develop the dendriform morphology typical of resident DC found in the normal epithelium. During the ensuing 48-h period, these cells then migrate to the regional lymph nodes. No comparable DC response was observed after epidermal or intraperitoneal challenge, and it may be that mucosal surfaces are unique in their requirement for rapid DC responses during acute inflammation. We hypothesize that the role of the DC influx during acute inflammation may be surveillance for opportunistic viruses, and that this covert protective mechanism is operative at a restricted number of mucosal tissue sites.