Lill JK, Thiebes S, Pohl JM, et al. - Researchers focused on the phenotypical as well as functional capacities of tissue-resident macrophages during STEC [shiga toxin (Stx)-producing E.coli]-hemolytic uremic syndrome. As per preclinical study, using state of the art microscopy and mass spectrometry imaging, there occurred a phenotypic as well as functional switch of tissue-resident macrophages post-disease induction in mice. It was also noted that kidney cortex was infiltrated by neutrophils and macrophage depletion resulted in significant reduction in the recruitment of neutrophils and expression of the neutrophil-attracting chemokines C-X-C motif ligand type 1 (CXCL1) and CXCL2. It was demonstrated by intravital microscopy that a significant reduction in the infiltration of neutrophils as well as decrease in kidney injury was brought about by CXCR2 inhibition, the receptor for CXCL1 and CXCL2. Therefore, findings revealed that tissue-resident macrophages got activated during shiga toxin-producing E. coli-hemolytic uremic syndrome, and this caused disease-promoting tumor necrosis factor α generation as well as CXCR2-dependent recruitment of neutrophils.