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Table 2 Different cell-type in inflammation resolution action

From: Role of specialized pro-resolving lipid mediators in pulmonary inflammation diseases: mechanisms and development

Cell type General function Actions in inflammation resolution Ref.
Neutrophils Phagocytosis
Pro-inflammation
NETosis
Accelerate cytokines and chemokines secretion
Apoptosis
NETosis
Egress to Lymph node
[7, 51, 55]
Macrophages PRR
Phagocytosis
Efferocytosis
M2 formation
Effercytosis
Secrete pro-inflammation cytokines, such as IL-10, TGF-β
Egress to Lymph nodes
Promote SPMs, including resolvins, maresins, protectins formation
[80, 81, 191]
Eosinophils Phagocytosis
Cytotoxic substances
IL-4, IL-13 secretion
Lipoxin A4 production
[46]
Mast cells Secretion of vasoactive substances Mediators secretion [51]
DCs Sensing DAMPs
PRR
TGF-b, IL-10 secretion
Inhibits migration
Maintain the homeostasis after inflammation resolute
[20, 21]
ILC2 Produce type 2 cytokines
Express surface markers and receptors for chemokine
Inhibits IL-13 secretion,
Express the chemokine receptors CXCR6 and CCR9
IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) to induce inflammation formation and eosinophilic infiltration
[115, 117, 192]
Epithelial cells Physical barrier
Mucociliary clearance
Maintain mucosal integrity and to modulate local immune responses
Decrease and limit pro-inflammatory mediators and proteins
Increases proliferation after acid injury and promote tissue repair
Immune regulator
[24, 193]
Endothelial cells Regulation transduction and exudation Inhibits TNF-a, IL-1b and IL-18 secretion
Blocks the generation of reactive oxygen species
[51]
Fibroblasts Tissue support
Cytokine secretion
Growth factors inducement
Inhibits CTGF-induced proliferation
[46, 194]