Gut complement induced by the microbiota combats pathogens and spares commensals.

Canonically, the complement system is known for its rapid response to remove microbes in the bloodstream. However, relatively little is known about a functioning complement system on intestinal mucosal surfaces. Herein, we report the local synthesis of complement component 3 (C3) in the gut, primarily by stromal cells.

Microbiome induced complement synthesized in the gut protects against enteric infections.

Unlabelled: Canonically, complement is a serum-based host defense system that protects against systemic microbial invasion. Little is known about the production and function of complement components on mucosal surfaces. Here we show gut complement component 3 (C3), central to complement function, is regulated by the composition of the microbiota in healthy humans and mice, leading to host-specific gut C3 levels.

Development of a blocker of the universal phosphatidylserine- and phosphatidylethanolamine-dependent viral entry pathways.

Envelope phosphatidylserine (PtdSer) and phosphatidylethanolamine (PtdEtr) have been shown to mediate binding of enveloped viruses. However, commonly used PtdSer binding molecules such as Annexin V cannot block PtdSer-mediated viral infection. Lack of reagents that can conceal envelope PtdSer and PtdEtr and subsequently inhibit infection hinders elucidation of the roles of the envelope phospholipids in viral infection.

Beyond Homeostasis: Potassium and Pathogenesis during Bacterial Infections.

Potassium is an essential mineral nutrient required by all living cells for normal physiological function. Therefore, maintaining intracellular potassium homeostasis during bacterial infection is a requirement for the survival of both host and pathogen. However, pathogenic bacteria require potassium transport to fulfill nutritional and chemiosmotic requirements, and potassium has been shown to directly modulate virulence gene expression, antimicrobial resistance, and biofilm formation.