Abstract
As a novel cytokine, cytokine-like 1 (CYTL1) is a classical secretory protein, and its potential biological function remains to be determined. In this study, we found that expression of CYTL1 was upregulated in neutrophils upon inflammatory stimuli. We demonstrated that CYTL1 enhanced phagocytosis of Escherichia coli by activated neutrophils both in vivo and in vitro through phosphorylation of protein kinase B (Akt). CYTL1-induced chemotactic activity in lipopolysaccharide (LPS) stimulated neutrophils, and the mechanism may be related to CC chemokine receptor 2 (CCR2) mediated action. CYTL1 also increased the release of reactive oxygen species (ROS) in LPS-stimulated neutrophils. These data indicate that upon inflammatory stimulation, neutrophil-derived CYTL1 may play a crucial role in the activation of neutrophils during pathogenic infections.
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