Pseudomonas aeruginosa coordinates invasion and destruction of Staphylococcus aureus communities by modulating single-cell and collective motility.

Single-cell RNA-sequencing identifies the precise cellular and molecular events that occur along the sepsis timeline in the kidney, pointing to potential biomarkers and therapeutic targets.

Mucosal-associated invariant T (MAIT) cells, highly activated and dysfunctional in sepsis patients, contribute to tissue-specific cytokine responses that are protective against mortality during experimental sepsis.

Killing their neighbors allows bacteria to steal genes, including antibiotic resistance genes, which we observed under a microscope, quantified, modeled, and predicted potentially guiding strategies to combat it.

Apoptotic cells release molecules to recruit macrophages, but do not cause inflammation because they also secrete AMP that functions as a ‘calm down’ signal.

Conserved transcriptomic profile of uropathogenic E. coli in patients identifies an infection-specific metabolic state.

Sepsis-induced numerical loss of naive autoantigen-specific CD4 T cells reduces host capacity to develop autoimmune immune disease, thereby demonstrating an intriguing relationship between infection and autoimmune disease.

Sialoside-based pattern recognition by Siglecs directly regulates toll-like receptor signaling and a sialidase inhibitor protects against endotoxemia.

Interbacterial interactions can promote mutagenesis, and possibly adaptation, when intoxicated cells survive exposure to type VI secretion-delivered DNA deaminase toxins.

Matrix metalloprotease (MMP)-14 cleaves Tie2 at three distinct sites within the fibronectin type-III (FN3) domain and its pharmacological blockade inhibits Tie2 pathological shedding to exert barrier protective effects.