scholarly journals Similarity and Diversity in Macrophage Activation by Nematodes, Trematodes, and Cestodes

2010 ◽  
Vol 2010 ◽  
pp. 1-14 ◽  
Author(s):  
Stephen J. Jenkins ◽  
Judith E. Allen

This review summarizes current knowledge of macrophages in helminth infections, with a focus not only on delineating the striking similarities in macrophage phenotype between diverse infections but also on highlighting the differences. Findings from many different labs illustrate that macrophages in helminth infection can act as anti-parasite effectors but can also act as powerful immune suppressors. The specific role for their alternative (Th2-mediated) activation in helminth killing or expulsion versus immune regulation remains to be determined. Meanwhile, the rapid growth in knowledge of alternatively activated macrophages will require an even more expansive view of their potential functions to include repair of host tissue and regulation of host metabolism.

2004 ◽  
Vol 122 (3) ◽  
pp. 359-369 ◽  
Author(s):  
Leonie A. Boven ◽  
Marjan van Meurs ◽  
Rolf G. Boot ◽  
Atul Mehta ◽  
Louis Boon ◽  
...  

2020 ◽  
Vol 21 (8) ◽  
pp. 2821 ◽  
Author(s):  
Alexander M. Götze ◽  
Christian Schubert ◽  
Georg Jung ◽  
Oliver Dörr ◽  
Christoph Liebetrau ◽  
...  

Arteriogenesis is a process by which a pre-existing arterioarterial anastomosis develops into a functional collateral network following an arterial occlusion. Alternatively activated macrophages polarized by IL10 have been described to promote collateral growth. This study investigates the effect of different levels of IL10 on hind-limb reperfusion and the distribution of perivascular macrophage activation types in mice after femoral artery ligation (FAL). IL10 and anti-IL10 were administered before FAL and the arteriogenic response was measured by Laser-Doppler-Imaging perioperatively, after 3, 7, and 14 d. Reperfusion recovery was accelerated when treated with IL10 and impaired with anti-IL10. Furthermore, symptoms of ischemia on ligated hind-limbs had the highest incidence after application of anti-IL10. Perivascular macrophages were immunohistologically phenotyped using CD163 and CD68 in adductor muscle segments. The proportion of alternatively activated macrophages (CD163+/CD68+) in relation to classically activated macrophages (CD163−/CD68+) observed was the highest when treated with IL10 and suppressed with anti-IL10. This study underlines the proarteriogenic response with increased levels of IL10 and demonstrates an in-vivo alteration of macrophage activation types in the perivascular bed of growing collaterals.


2007 ◽  
Vol 19 (4) ◽  
pp. 448-453 ◽  
Author(s):  
Timothy Kreider ◽  
Robert M. Anthony ◽  
Joseph F. Urban ◽  
William C. Gause

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Arlett Espinoza-Jiménez ◽  
Roberto De Haro ◽  
Luis I. Terrazas

Type 1 diabetes (T1D) is an autoimmune disease caused by the selective destruction of the pancreatic β-cells, causing inability to produce insulin. Proinflammatory cytokines such as IL-1β, IL-6, TNF-α, IFN-γ, IL-12, IL-17, and NO can be released by CD4 and CD8+ lymphocytes as well as by classically activated macrophages (CAMϕs), which are important in the development of T1D. Helminth infections have been shown to prevent T1D, mainly through Th2-biased responses and increased recruitment of regulatory cell populations. Previously, we have shown that Taenia crassiceps infection in mice significantly reduces hyperglycemia, insulitis, and the incidence of T1D. In this study, we determined whether T. crassiceps-derived products such as soluble (TcS) or excreted/secreted (TcES) antigens might have a beneficial influence on the development of experimental T1D. Treatment with different doses before or after induction of T1D was analyzed. Mice that were pretreated with TcS were unable to develop T1D, whereas those receiving TcES early after T1D induction displayed significantly reduced insulitis and hyperglycemia along with increased recruitment of alternatively activated macrophages (AAMϕs) and myeloid-derived suppressor cells (MDSCs). Finally, we examined the modulatory role of AAMϕs on T1D by depleting macrophages with clodronate-loaded liposomes, demonstrating that AAMϕs are key cells in T1D regulation.


2007 ◽  
Vol 179 (7) ◽  
pp. 4721-4731 ◽  
Author(s):  
Meiqian Weng ◽  
Deke Huntley ◽  
I-Fei Huang ◽  
Ondulla Foye-Jackson ◽  
Lijian Wang ◽  
...  

2002 ◽  
Vol 70 (7) ◽  
pp. 3656-3664 ◽  
Author(s):  
Miriam Rodríguez-Sosa ◽  
Abhay R. Satoskar ◽  
Rodrigo Calderón ◽  
Lorena Gomez-Garcia ◽  
Rafael Saavedra ◽  
...  

ABSTRACT Helminth infections induce Th2-type biased immune responses. Although the mechanisms involved in this phenomenon are not yet clearly defined, antigen-presenting cells (APC) could play an important role in this process. Here, we have used peritoneal macrophages (F4/80+) recruited at different times after challenge with Taenia crassiceps as APC and tested their ability to regulate Th1/Th2 differentiation. Macrophages from acute infections produced high levels of interleukin-12 (IL-12) and nitric oxide (NO), paralleled with low levels of IL-6 and prostaglandin E2 (PGE2) and with the ability to induce strong antigen-specific CD4+ T-cell proliferation in response to nonrelated antigens. In contrast, macrophages from chronic infections produced higher levels of IL-6 and PGE2 and had suppressed production of IL-12 and NO, associated with a poor ability to induce antigen-specific proliferation in CD4+ T cells. Failure to induce proliferation was not due to a deficient expression of accessory molecules, since major histocompatibility complex class II, CD40, and B7-2 were up-regulated, together with CD23 and CCR5 as infection progressed. These macrophages from chronic infections were able to bias CD4+ T cells to produce IL-4 but not gamma interferon (IFN-γ), contrary to macrophages from acute infections. Blockade of B7-2 and IL-6 and inhibition of PGE2 failed to restore the proliferative response in CD4+ T cells. Furthermore, studies using STAT6−/− mice revealed that STAT6-mediated signaling was essential for the expansion of these alternatively activated macrophages. These data demonstrate that helminth infections can induce different macrophage populations that have Th2-biasing properties.


2007 ◽  
Vol 13 (supplement) ◽  
pp. 644
Author(s):  
M Weng ◽  
D Huntley ◽  
O Foye-Jackson ◽  
J Wang ◽  
W Walker ◽  
...  

2009 ◽  
Vol 182 (5) ◽  
pp. 3084-3094 ◽  
Author(s):  
Katie J. Mylonas ◽  
Meera G. Nair ◽  
Lidia Prieto-Lafuente ◽  
Daniel Paape ◽  
Judith E. Allen

2021 ◽  
Vol 17 (7) ◽  
pp. e1009768
Author(s):  
Ruth Forman ◽  
Larisa Logunova ◽  
Hannah Smith ◽  
Kelly Wemyss ◽  
Iris Mair ◽  
...  

The intestinal nematode parasite Trichuris muris dwells in the caecum and proximal colon driving an acute resolving intestinal inflammation dominated by the presence of macrophages. Notably, these macrophages are characterised by their expression of RELMα during the resolution phase of the infection. The RELMα+ macrophage phenotype associates with the presence of alternatively activated macrophages and work in other model systems has demonstrated that the balance of classically and alternatively activated macrophages is critically important in enabling the resolution of inflammation. Moreover, in the context of type 2 immunity, RELMα+ alternatively activated macrophages are associated with the activation of macrophages via the IL4Rα. Despite a breadth of inflammatory pathologies associated with the large intestine, including those that accompany parasitic infection, it is not known how colonic macrophages are activated towards an alternatively activated phenotype. Here, we address this important knowledge gap by using Trichuris muris infection, in combination with transgenic mice (IL4Rαfl/fl.CX3CR1Cre) and IL4Rα-deficient/wild-type mixed bone marrow chimaeras. We make the unexpected finding that education of colonic macrophages towards a RELMα+, alternatively activated macrophage phenotype during T. muris infection does not require IL4Rα expression on macrophages. Further, this independence is maintained even when the mice are treated with an anti-IFNγ antibody during infection to create a strongly polarised Th2 environment. In contrast to RELMα, PD-L2 expression on macrophages post infection was dependent on IL4Rα signalling in the macrophages. These novel data sets are important, revealing a surprising cell-intrinsic IL4R alpha independence of the colonic RELMα+ alternatively activated macrophage during Trichuris muris infection.


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