CXCL12 ameliorates neutrophilia and disease severity in SARS-CoV-2 infection.

Neutrophils, particularly low-density neutrophils (LDNs), are believed to contribute to acute COVID-19 severity. Here, we showed that neutrophilia can be detected acutely and even months after SARS-CoV-2 infection in patients and mice, while neutrophil depletion reduced disease severity in mice. A key factor in neutrophilia and severe disease in infected mice was traced to the chemokine CXCL12 secreted by bone marrow cells and unexpectedly, endothelial cells.

Genome sequence of phage CandC.

We report the discovery and genome sequence of CandC, a lytic bacteriophage with siphovirus morphology. CandC was isolated from a soil sample from Plattsburgh, NY, USA (Fall 2021). It has a genome size of 62,344 bp with 106 predicted protein-encoding genes, 30 of which are assigned putative functions.

Syntaxin-4 and SNAP23 are involved in neutrophil degranulation, but not in the release of mitochondrial DNA during NET formation.

Neutrophils are a specialized subset of white blood cells, which have the ability to store pre-formed mediators in their cytoplasmic granules. Neutrophils are well-known effector cells involved in host protection against pathogens through diverse mechanisms such as phagocytosis, degranulation, extracellular traps, and oxidative burst. In this study, we provide evidence highlighting the significance of the SNARE proteins syntaxin-4 and synaptosomal-associated protein (SNAP) 23 in the release of azurophilic granules, specific granules, and the production of reactive oxygen species in human neutrophils.

Understanding inhibitory receptor function in neutrophils through the lens of CLEC12A.

Neutrophils are the first leukocytes recruited from the circulation in response to invading pathogens or injured cells. To eradicate pathogens and contribute to tissue repair, recruited neutrophils generate and release a host of toxic chemicals that can also damage normal cells. To avoid collateral damage leading to tissue injury and organ dysfunction, molecular mechanisms evolved that tightly control neutrophil response threshold to activating signals, the strength and location of the response, and the timing of response termination.