Macrophage origin limits functional plasticity in helminth-bacterial co-infection

• DOI: 10.1371/journal.ppat.1006233
• Publication Date: 2017-03-24T02:26:27Z
• Authors: Dominik Rückerl; Sharon M. Campbell; Sheelagh Duncan; Tara E. Sutherland; Stephen J. Jenkins; James P. Hewitson; Tom A. Barr; Lucy H. Jackson-J...; Rick M. Maizels; Judith E. Allen
• Keywords: Heligmosomoides polygyrus; Salmonella enterica; Monocyte; Nematode infection

Rapid reprogramming of the macrophage activation phenotype is considered important in defense against consecutive infection with diverse infectious agents. However, setting persistent, chronic functional importance macrophage-intrinsic adaptation to changing environments vs. recruitment new macrophages remains unclear. Here we show that resident peritoneal expanded by nematode Heligmosomoides polygyrus bakeri altered their response Salmonella enterica ser. Typhimurium vitro and vivo. The nematode-expanded F4/80high efficiently upregulated bacterial induced effector molecules (e.g. MHC-II, NOS2) similarly newly recruited monocyte-derived macrophages. Nonetheless, blood occurred equal magnitude co-infected animals caused displacement nematode-expanded, tissue resident-derived from cavity. Global gene expression analysis revealed although made an anti-bacterial response, this was muted as compared F4/80low adopted unique characteristics included enhanced neutrophil-stimulating chemokine production. Thus, our data provide evidence plastic MΦ does occur vivo, but cellular plasticity outweighed capabilities specific origin cell.