Table 2.

Cytokines secreted during sepsis that may be responsible for neutrophils’ phagocytosis.

Cytokine	Organism	Setting	Target	Effect	Ref.
CYTL1	in vitro Human, in vivo Mice	Escherichia coli infection	phosphorylation of protein kinase B (Akt)	enhanced phagocytosis	[113]
IL-6	Mice	Staphylococcus aureus infection	phosphorylation of STAT3	augmented the uptake of bacteria and phagosome acidification	[114]
IL-6	Human	Staphylococcus aureus infection	n.i.	enhanced phagocytosis and stimulated ROS generation	[115]
IL-10	Mice	Escherichia coli induced meningitis	increased expression of CR3	enhanced phagocytosis	[116]
IL-12	Mice	polymicrobial sepsis induced by cecal ligation and puncture (CLP)	induction of IFNγ	enhanced phagocytosis	[117]
IL-17	Mice	Candida albicans induced sepsis, and zymosan-induced multiple organ failure	n.i.	enhanced phagocytosis	[118]
IL-18	Mice	polymicrobial sepsis induced by cecal ligation and puncture (CLP)	n.i.	did not affect phagocytosis	[117]
IL-34	in vitro Human, in vivo Mice	sepsis	n.i.	enhanced phagocytosis	[119]

n.i.—not identified.