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Int Immunopharmacol. 2018 Mar;56:217-221. doi: 10.1016/j.intimp.2018.01.036. Epub 2018 Feb 3.

Interleukin-8 favors pro-inflammatory activity of human monocytes/macrophages.

Author information

1
Immanuel Kant Baltic Federal University, 14 A.Nevskogo St., Kaliningrad 236016, Russia.
2
Immanuel Kant Baltic Federal University, 14 A.Nevskogo St., Kaliningrad 236016, Russia. Electronic address: omelashchenko@kantiana.ru.
3
Scientific Research Institute of Fundamental and Clinical Immunology, Siberian Branch, Russian Academy of Sciences, 14 Yadrintsevskaya St., Novosibirsk 630099, Russia.
4
Immanuel Kant Baltic Federal University, 14 A.Nevskogo St., Kaliningrad 236016, Russia. Electronic address: seledtsov@rambler.ru.

Abstract

Interleukin-8 (IL-8, CXCL8) belongs to major chemokines to stimulate migration of neutrophils and monocytes/macrophages (Mc/Mphs) into the inflammation sites. We studied the direct effects of IL-8 on the functionality of human Mc/Mphs in vitro. CD14-positive cells were isolated from human peripheral blood mononuclear cells (PBMCs) by positive magnetic separation and were further cultured with or without lipopolysaccharide (LPS, 1.0 μg/ml) for 24 h. We showed that upon LPS activation of Mc/Mphs, IL-8 reduced markedly both the percentages and median fluorescence intensity (MFI) of CD16 (FcγRIII)-positive cells among CD14high cells, as well as in cells that reduced the expression of СD14 during their culturing. IL-8 was also found to be capable of reducing the expression of СD124 (IL-4 receptor subunit alpha, IL-4RA), with concomitant enhancement of the expression of both CD119 (interferon-gamma receptor 1) and CD197 (CCR7) in Mph cells. In addition, IL-8 up-regulated production of IL-6 and IL-1β [but not tumor necrosis factor-α (TNF-α) and IL-10] by activated Mc/Mphs. Our results suggest the ability for IL-8 to directly favor pro-inflammatory M1-type Mph activity.

KEYWORDS:

Inflammation; Interleukin-8; Lipopolysaccharide; Macrophage activation; Monocyte/macrophage

PMID:
29414654
DOI:
10.1016/j.intimp.2018.01.036
[Indexed for MEDLINE]

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