In:
Immunology & Cell Biology, Wiley, Vol. 96, No. 3 ( 2018-03), p. 257-272
Abstract:
Arginase‐1 (Arg‐1)‐expressing M2‐like macrophages are associated with Th2‐skewed immune responses, allergic airway pathology, ectopic B16 melanoma cancer growth in murine models, and can be induced by Oncostatin M ( OSM ) transient overexpression in vivo . Here, we compare OSM to the gp130‐cytokine IL ‐6 in mediating macrophage polarization, and find that IL ‐6 overexpression alone (Ad vector, Ad IL ‐6) did not induce Arg‐1 protein in mouse lungs at day 7, nor ectopic melanoma tumor growth at day 14, in contrast to overexpression of OSM (Ad OSM ). Ad OSM elevated levels of IL ‐4, IL ‐5 and IL ‐13 in bronchoalveolar lavage fluid, whereas Ad IL ‐6 did not. Bone marrow‐derived macrophages respond with Arg‐1 enzymatic activity to M2 stimuli ( IL ‐4/ IL ‐13), which was further elevated in combination with IL ‐6 stimulation; however, OSM or LIF had no detectable activity in vitro . Arg‐1 mRNA expression induced by Ad OSM was attenuated in IL ‐6‐/‐ and STAT 6‐/‐ mice, suggesting requirements for both IL ‐6 and IL ‐4/ IL ‐13 signaling in vivo . Ectopic B16 tumor burden was also reduced in IL ‐6‐/‐ mice. Thus, OSM induces Arg‐1+ macrophage accumulation indirectly through elevation of Th2 cytokines and IL ‐6 in vivo , whereas IL ‐6 acts directly on macrophages but requires a Th2 microenvironment, demonstrating distinct roles for OSM and IL ‐6 in M2 macrophage polarization.
Type of Medium:
Online Resource
ISSN:
0818-9641
,
1440-1711
DOI:
10.1111/imcb.2018.96.issue-3
Language:
English
Publisher:
Wiley
Publication Date:
2018
detail.hit.zdb_id:
2011707-3
SSG:
12
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