The contribution of Arpc5 for gene expression in intestinal macrophages

Patients with loss-of-function mutations in the ARPC5 subunit of the Arp2/3 complex develop inflammation and immunodeficiency after birth, leading to early mortality. However, the mechanistic basis for these phenotypes remains obscure. Our work demonstrate that loss of Arpc5 in the murine hematopoietic system causes early-onset intestinal inflammation. This condition is initiated by microbiota breaching the ileal mucosa, leading to local and systemic inflammation. Macrophage infiltrate into the ileum, but in the absence of Arpc5 fail to restrict microbial invasion. So, we wanted to investigate the Arpc5 contribution for intestinal macrophages expression. Overall design: intestinal content from control and mutant mice was extracted, FACS sorted and sequenced for analysis. The intestines were divided in small intestine and colon. Small intestines were subdivided in intraepithelial and lamina propria phases.