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Table 2 Pro-inflammatory and anti-inflammatory mediators

From: The effect of a multicomponent exercise protocol (VIVIFRAIL©) on inflammatory profile and physical performance of older adults with different frailty status: study protocol for a randomized controlled trial

Mediator

Major Cellular Sources

Major Activities

IFN-gamma

Th1 cells, NK cells

Activation of inflammatory macrophages (M1), inhibition of Th2 responses, induction of leukocyte migration.

IL-1beta

Monocyte/macrophages, PMNs.

Synthesis of acute-phase proteins by hepatocytes, induction of local and systemic inflammatory effects.

IL-1RA

Monocyte/macrophages, dendritic cells.

Specific inhibitor of IL-1alpha and IL-1beta by competition with the cellular receptor.

IL-4

Th2 cells, mast cells, B cells

Induction of Th2 lymphocyte development, inhibition of pro-inflammatory and Th1 cytokine production, activation of anti-inflammatory macrophages (M2).

IL-6

Monocyte/macrophages, T cells, PMNs.

Produced during the inflammatory response, induces the synthesis of acute-phase proteins by hepatocytes, but presents an inhibitory effect on TNF- α and IL-1 production by macrophages.

IL-8 (CXCL8)

Monocytes/macrophages, PMNs.

Major chemotactic cytokine (chemokine) for neutrophils.

IL-10

Monocyte/macrophage, Th2 cells, B cells

Inhibition of pro-inflammatory cytokine production by macrophages and neutrophils, inhibition of Th1 cytokine production.

IL-17

Th17 cells

Activation of neutrophils, induction of extracellular matrix remodeling.

IL-22

Th17 and Th22 cells

Induction of epithelial cell proliferation and production of antimicrobial peptides by epithelial cells and neutrophils.

IL-27

Macrophages, dendritic cells.

Antagonist of Th1, Th2 and Th17 inflammatory responses, induction of Tr1 (regulatory) cells.

TNF- α

Monocyte/macrophages, PMNs, T cells.

Synthesis of acute-phase proteins by hepatocytes, recruitment, and activation of cells into inflammatory sites, induction of insulin resistance.