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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]