BCG Vaccination Induces Long-Term Functional Reprogramming of Human Neutrophils.

The tuberculosis vaccine bacillus Calmette-Guérin (BCG) protects against some heterologous infections, probably via induction of non-specific innate immune memory in monocytes and natural killer (NK) cells, a process known as trained immunity. Recent studies have revealed that the induction of trained immunity is associated with a bias toward granulopoiesis in bone marrow hematopoietic progenitor cells, but it is unknown whether BCG vaccination also leads to functional reprogramming of mature neutrophils. Here, we show that BCG vaccination of healthy humans induces long-lasting changes in neutrophil phenotype, characterized by increased expression of activation markers and antimicrobial function.

Autoantibodies to neutrophil extracellular traps represent a potential serological biomarker in rheumatoid arthritis.

Neutrophil extracellular traps (NETs) are networks of extracellular chromatin decorated with antimicrobial proteins, formed by neutrophils to entrap pathogens. NETs have been implicated in the generation of autoimmune reactions. Here, we investigate the reactivity of rheumatoid arthritis (RA) serum antibodies with NETs and explore whether anti-NET antibodies (ANETA) have a potential as biomarker in RA.

Stimulus-dependent chromatin dynamics, citrullination, calcium signalling and ROS production during NET formation.

Neutrophils can release their chromatin to form neutrophil extracellular traps (NETs), a process known as NETosis. Although NET formation can be induced by various stimuli, recent evidence suggests that these stimuli do so via different mechanisms. Here, we have analysed NET formation induced by lipopolysaccharide (LPS), phorbol 12‑myristate 13‑acetate (PMA) and the calcium (Ca) ionophore A23187.

NETosis, complement, and coagulation: a triangular relationship.

NETosis is a regulated form of neutrophil cell death that contributes to the host defense against pathogens and was linked to various diseases soon after its first description in 2004. During NETosis, neutrophils release neutrophil extracellular traps (NETs), which can capture and kill bacteria and other pathogens to prevent them from spreading. Although substantial progress has been made in our understanding of NETosis, the precise mechanism underlying NETosis is still a matter of debate.

Alternative pathway regulation by factor H modulates Streptococcus pneumoniae induced proinflammatory cytokine responses by decreasing C5a receptor crosstalk.

Bacterial pathogens not only stimulate innate immune receptors, but also activate the complement system. Crosstalk between complement C5a receptor (C5aR) and other innate immune receptors is known to enhance the proinflammatory cytokine response. An important determinant of the magnitude of complement activation is the activity of the alternative pathway, which serves as an amplification mechanism for complement activation.