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.
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.
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.