Alternatively Activated Macrophages in Intestinal Helminth Infection: Effects on Concurrent Bacterial Colitis

Weng, Meiqian; Huntley, D; Huang, I-Shen; Foye-Jackson, O; Wang, Lijian; Sarkissian, Aliese; Zhou, Qixing; Walker, W. Allan; Cherayil, Bobby J.; Shi, Hai Ning

doi:10.4049/jimmunol.179.7.4721

Cited by 102 publications

(100 citation statements)

References 45 publications

(59 reference statements)

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“…To assess macrophage infiltration of mesenteric fat depots during TNBS-induced colitis, we quantified mRNA expression of the macrophage marker EMR1 (F4/80) (21). We found increased EMR1 (F4/80) mRNA expression in mesenteric fat after TNBS induction, but significantly less EMR1 (F4/80) mRNA expression in mesenteric fat (Ϸ50%) of NT KO mice compared with wild-type controls (Fig.…”

Section: Nt Stimulates Preadipocyte-dependent Macrophage Migration VImentioning

confidence: 90%

Neurotensin induces IL-6 secretion in mouse preadipocytes and adipose tissues during 2,4,6,-trinitrobenzensulphonic acid-induced colitis

Koon

Kim²,

Xu³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Mesenteric fat is known to undergo inflammatory changes after 2,4,6,-trinitrobenzensulphonic acid (TNBS)-induced colitis. Neurotensin (NT) and neurotensin receptor 1 (NTR1) have been shown to play a major role in the pathogenesis of intestinal inflammation. This led us to explore whether NT and NTR1 are expressed in the mesenteric fat depots during TNBS-induced colitis and whether NT participates in the increased interleukin (IL)-6 secretion in this inflammatory response. TNBS-induced inflammation in the colon increases NT and NTR1 expression in mesenteric adipose tissues, including mesenteric preadipocytes. Compared with wild-type mice, NT knockout (KO) mice have reduced TNBS-induced colitis accompanied by diminished inflammatory responses in mesenteric adipose tissue. Specifically, IL-6 and p65 phosphorylation levels in mesenteric fat of NT KO mice are also reduced compared with wild-type mice. Mouse 3T3-L1 preadipocytes express NTR1 and its expression is increased after stimulation of preadipocytes with proinflammatory cytokines. NT stimulation of 3T3-L1 preadipocytes overexpressing NTR1 causes PKC␦ phosphorylation and IL-6 secretion in a time-and dose-dependent fashion. Moreover, NT-mediated IL-6 expression is nuclear factor-B and PKC␦ dependent. We also found that supernatants from NT-exposed 3T3-L1-NTR1 preadipocytes and mesenteric fat obtained from wild-type mice 2 days after TNBS administration stimulate an IL-6 -dependent macrophage migration measured by a macrophage migration assay, whereas this response is reduced when mesenteric fat from NT KO mice is used. These results demonstrate an important role for NT in acute colitis and adipose tissue inflammation associated with experimental colitis that involves direct NT proinflammatory responses in preadipocytes.cytokine ͉ intestinal inflammation ͉ macrophages ͉ neuropeptide

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Section: Nt Stimulates Preadipocyte-dependent Macrophage Migration VImentioning

confidence: 90%

Neurotensin induces IL-6 secretion in mouse preadipocytes and adipose tissues during 2,4,6,-trinitrobenzensulphonic acid-induced colitis

Koon

Kim²,

Xu³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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“…In vivo counterparts of M2 macrophage polarization have been observed in tissue remodelling during ontogenesis [28], chronic inflammation [29][30][31][32][33][34][35][36][37][38][39][40][41][42], cancer [9,12,16,17], bacterial [43][44][45][46][47][48][49] and parasitic [50][51][52][53] infections. Evidence has also accumulated that polarized macrophages are more than mere spectators of immunopathology [35][36][37][38][39][40][41][50][51][52].…”

Section: Activation and Adaptive Responses Of Macrophagesmentioning

confidence: 99%

“…Evidence has also accumulated that polarized macrophages are more than mere spectators of immunopathology [35][36][37][38][39][40][41][50][51][52].…”

Section: Activation and Adaptive Responses Of Macrophagesmentioning

confidence: 99%

“…For instance, do MDSC retain an immature phenotype in tumour tissues or do they differentiate into tumourassociated macrophages [9][10][11] [9,12,16,17], bacterial [43][44][45][46][47][48][49] and parasitic [50][51][52][53] infections. Evidence has also accumulated that polarized macrophages are more than mere spectators of immunopathology [35][36][37][38][39][40][41][50][51][52].The macrophage polarization paradigm, with M1 and M2 cells mirroring the Th1 and Th2 lymphocytes, and classic cytokines IFN-g and IL-4 respectively, as the main source of the inducing signals, has had heuristic value; however, one should not forget that this is an oversimplification, albeit a very useful one, with intrinsic limitations. First, fully polarized macrophages are the end of a continuum (Fig.…”

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confidence: 99%

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From phagocyte diversity and activation to probiotics: Back to Metchnikoff

Mantovani

2008

Eur J Immunol

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In this issue of the European Journal of Immunology, Siamon Gordon gives a detailed account of Metchnikoff's life and his achievements (Eur. J. Immunol. 2008. 38: 3257-3264). Looking back at the roots of innate immunity stimulates reflections on open issues in the field. Here, I give a personal view of some of these issues, including myeloid-derived suppressor cells, macrophage polarization and adaptive responses of mononuclear phagocytes. Key words: Macrophage activation Á Macrophages Á M1/M2 polarization Á Probiotics See accompanying article by Gordon IntroductionIn his scholarly review [1], Siamon Gordon tracks the roots of innate immunity to Elie Metchnikoff. The essay provides a fascinating insight into Metchnikoff's scientific life and how he tackled fundamental issues in science, some of which remain with us to this day. The perspective offered by a major player in the very same field of phagocytes and innate immunity [2,3] adds flavour and fascination to this article not necessarily present in other accounts [4]. Such a reflection on a central part of modern immunology stimulates consideration of remaining open issues and there follows a personal view of some of these.Phagocyte heterogeneity: From microphage-macrophage dichotomy to myeloid-derived suppressor cellsThe fundamental distinction between polymorphonuclear leukocytes (microphages) and mononuclear phagocytes (macrophages) was a major first step in the dissection of phagocyte heterogeneity and lineage differentiation. The identification of myeloid-derived suppressor cells (MDSC) [5][6][7] raises the questions whether the classic sharp distinction between the myeloid and the monocyte-macrophage differentiation and activation pathways is appropriate. In contrast to long-held views, neutrophils express specific transcriptional programmes in response to environmental signals [8]. MDSC include immature myeloid precursors that can further differentiate, and play a key role in the suppression of adaptive immunity in diverse pathological conditions ranging from cancer to chronic infections [5][6][7]. Are we dealing with a blurring of a classic distinction or with a well-defined third phagocyte population? Using current identification and separation criteria (e.g. Gr1, CD11b, F4/80) MDSC in the blood and lymphoid organs are a mixed population, which includes myeloid cells at different stages of differentiation and mononuclear phagocytes. Thus, the definition of MDSC remains an operational one rather than that of a cell type, a reality that is frequently neglected. The issue of lineage of the actual effectors of MDSC-mediated suppression is even more relevant when their recruitment and activation in non-lymphoid tissues is considered. For instance, do MDSC retain an immature phenotype in tumour tissues or do they differentiate into tumourassociated macrophages [9][10][11] [9,12,16,17], bacterial [43][44][45][46][47][48][49] and parasitic [50][51][52][53] infections. Evidence has also accumulated that polarized macrophages are more than mere spectators of i...

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“…26,28,29 Arginase assay The arginase activity assay was performed as previously described. 30,31 Briefly, the cells were lysed in 0.1% Triton X-100. Tris-HCl was then added to the cell lysates at a final concentration of 12.5 mM, and Table 1 The sequences of the primers used for real-time PCR assays…”

Section: Immunofluorescence Staining and Flow Cytometry (Fcm)mentioning

confidence: 99%

Induction of M2-like macrophages in recipient NOD-scid mice by allogeneic donor CD4+CD25+ regulatory T cells

Liu

Hou

et al. 2012

Cell Mol Immunol

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CD4 1 CD25 1 regulatory T cells (Tregs) play an important role in maintaining host immune tolerance via regulation of the phenotype and function of the innate and adaptive immune cells. Whether allogeneic CD4 1 CD25 1 Tregs can regulate recipient mouse macrophages is unknown. The effect of allogeneic donor CD4 1 CD25 1 Tregs on recipient mouse resident F4/80 1 macrophages was investigated using a mouse model in which allogeneic donor CD4 1 CD25 1 Tregs were adoptively transferred into the peritoneal cavity of host NOD-scid mice. The phenotype and function of the recipient macrophages were then assayed. The peritoneal F4/80 1 macrophages in the recipient mice that received the allogeneic CD4 1 CD25 1 Tregs expressed significantly higher levels of CD23 and programmed cell death-ligand 1(PD-L1) and lower levels of CD80, CD86, CD40 and MHC II molecules compared to the mice that received either allogeneic CD4 1 CD25 2 T cells (Teffs) or no cells. The resident F4/80 1 macrophages of the recipient mice injected with the allogeneic donor CD4 1 CD25 1 Tregs displayed significantly increased phagocytosis of chicken red blood cells (cRBCs) and arginase activity together with increased IL-10 production, whereas these macrophages also showed decreased immunogenicity and nitric oxide (NO) production. Blocking arginase partially but significantly reversed the effects of CD4 1 CD25 1 Tregs with regard to the induction of the M2 macrophages in vivo. Therefore, the allogeneic donor CD4 1 CD25 1 Tregs can induce the M2 macrophages in recipient mice at least in part via an arginase pathway. We have provided in vivo evidence to support the unknown pathways by which allogeneic donor CD4 1 CD25 1 Tregs regulate innate immunity in recipient mice by promoting the differentiation of M2 macrophages.

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Alternatively Activated Macrophages in Intestinal Helminth Infection: Effects on Concurrent Bacterial Colitis

Cited by 102 publications

References 45 publications

Neurotensin induces IL-6 secretion in mouse preadipocytes and adipose tissues during 2,4,6,-trinitrobenzensulphonic acid-induced colitis

Neurotensin induces IL-6 secretion in mouse preadipocytes and adipose tissues during 2,4,6,-trinitrobenzensulphonic acid-induced colitis

From phagocyte diversity and activation to probiotics: Back to Metchnikoff

Induction of M2-like macrophages in recipient NOD-scid mice by allogeneic donor CD4+CD25+ regulatory T cells

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