Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells

TLDR

Infections by helminths or bacteria cause tissue damage that requires macrophage cleanup. The authors used mouse models of helminth infection and fibrosis to investigate macrophage function. They showed that surfactant protein A and C1q enhance IL‑4/IL‑13–mediated macrophage activation, accelerating helminth clearance, reducing lung injury, aiding liver repair, and that IL‑4/IL‑13 promote tissue repair only in the presence of apoptotic cells. See Minutti et al.

Abstract

Local macrophage clean-up Infection, especially by helminths or bacteria, can cause tissue damage (see the Perspective by Bouchery and Harris). Minutti et al. studied mouse models of helminth infection and fibrosis. They expressed surfactant protein A (a member of the complement component C1q family) in the lung, which enhanced interleukin-4 (IL-4)-mediated proliferation and activation of alveolar macrophages. This activation accelerated helminth clearance and reduced lung injury. In the peritoneum, C1q boosted macrophage activation for liver repair after bacterial infection. By a different approach, Bosurgi et al. discovered that after wounding caused by migrating helminths in the lung or during inflammation in the gut of mice, IL-4 and IL-13 act only in the presence of apoptotic cells to promote tissue repair by local macrophages. Science , this issue p. 1076 , p. 1072 ; see also p. 1014