Arginase activity is associated with fibrosis in experimental infection with Taenia crassiceps, but does not play a major role in resistance to infection

Moura, Vânia Beatriz Lopes; Silva, Mayara M.; Batista, Lucas Ferreira; Gomes, Clayson Moura; Leenen, Pieter J. M.; Lino, Ruy S.; Oliveira, Milton Adriano Pelli de

doi:10.1016/j.exppara.2013.09.014

Cited by 8 publications

(6 citation statements)

References 30 publications

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“…A classic side effect of strong Th2-type-biased responses induced by helminths is potential development of fibrosis [ 9 , 27 ]. Here we found that T. crassiceps -infected and DSS-treated mice did not display an excess of collagen in the colon tissue, thus ruling out fibrosis as a side effect of this infection during the modulation of colitis ( Figure 7(b) .…”

Section: Resultsmentioning

confidence: 99%

Extraintestinal Helminth Infection Limits Pathology and Proinflammatory Cytokine Expression during DSS-Induced Ulcerative Colitis: A Role for Alternatively Activated Macrophages and Prostaglandins

Ledesma-Soto

Callejas

Terrazas

et al. 2015

BioMed Research International

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Chronic inflammation of the intestinal mucosa is characteristic of inflammatory bowel diseases such as ulcerative colitis and Crohn's disease. Helminth parasites have developed immunomodulatory strategies that may impact the outcome of several inflammatory diseases. Therefore, we investigated whether Taenia crassiceps infection is able to decrease the inflammatory effects of dextran sulfate sodium- (DSS-) induced ulcerative colitis in BALB/c and C57BL/6 mice. Preinfection significantly reduced the manifestations of DSS-induced colitis, as weight loss and shortened colon length, and decreased the disease activity index independently of the genetic background of the mice. Taenia infection decreased systemic levels of proinflammatory cytokines while increasing levels of IL-4 and IL-10, and the inflammatory infiltrate into the colon was also markedly reduced. RT-PCR assays from colon showed that T. crassiceps-infected mice displayed increased expression of Arginase-1 but decreased expression of iNOS compared to DSS-treated uninfected mice. The percentages of T regulatory cells were not increased. The adoptive transfer of alternatively activated macrophages (AAMФs) from infected mice into mice with DSS-induced colitis reduced the severity of colon inflammation. Administration of indomethacin abrogated the anticolitic effect of Taenia. Thus, T. crassiceps infection limits the pathology of ulcerative colitis by suppressing inflammatory responses mechanistically associated with AAMФs and prostaglandins.

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Section: Resultsmentioning

confidence: 99%

Extraintestinal Helminth Infection Limits Pathology and Proinflammatory Cytokine Expression during DSS-Induced Ulcerative Colitis: A Role for Alternatively Activated Macrophages and Prostaglandins

Ledesma-Soto

Callejas

Terrazas

et al. 2015

BioMed Research International

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“…The doses of nor-NOHA used were 10 and 20 mg/kg, after reference to previous studies. [10][11][12][13] Control PKD mice were treated with normal saline (1.5 ml/g, daily) via i.p. injection.…”

Section: Macrophage Depletion In Pkd Micementioning

confidence: 99%

Interactions between Macrophages and Cyst-Lining Epithelial Cells Promote Kidney Cyst Growth in Pkd1-Deficient Mice

Yang

Chen

Zhou

et al. 2018

JASN

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“…ARG1 is important in wound healing and resolution via the production of L-ornithine, a precursor of prolines and polyamines that are required for collagen deposition and cell proliferation respectively. While over-production of ARG1 would be expected to contribute to fibrosis (McLarren et al, 2011;Moura et al, 2013), a role for AAM-associated ARG1 in fibrosis has been disputed (Pesce et al, 2009), and, furthermore, its absence has been shown to impair cutaneous wound healing (Campbell et al, 2013): AAM ARG1 has been implicated in the anti-colitic effect of these cells (McLarren et al, 2011), and ARG1 levels are reduced in patients with atopic dermatitis (Dimitriades et al, 2014). NO produced by the constitutive NOS has important roles in wound healing (Witte and Barbul, 2002).…”

Section: Figurementioning

confidence: 99%

Bidirectional crosstalk via IL‐6, PGE₂and PGD₂between murine myofibroblasts and alternatively activated macrophages enhances anti‐inflammatory phenotype in both cells

Fernando

Giembycz

McKay

2016

British J Pharmacology

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BACKGROUND AND PURPOSEAlternatively activated macrophages (AAMs) are important cells in the resolution of inflammation and tissue repair. We examined the impact of myofibroblasts, a vital cell in wound healing and tissue repair, on the development and function of AAMs. EXPERIMENTAL APPROACHThe interaction between AAMs and myofibroblasts was tested using conditioned medium from murine dermal myofibroblasts and bone marrow-derived macrophages. AAMs were differentiated with IL-4 and IL-13. KEY RESULTSConditioned medium from myofibroblasts enhanced the expression of AAM markers, arginase 1 and Ym1 (chitinase-3-like 3) and the spontaneous production of IL-10, while suppressing LPS-induced nitric oxide production. IL-6 from the myofibroblasts contributed to the amplification of the AAM phenotype; the selective COX-2 inhibitor, NS-398, significantly reduced the ability of myofibroblasts to promote an AAM phenotype. Pharmacological analyses indicated that myofibroblast-derived IL-6 enhanced arginase activity and spontaneous IL-10 output, while PGE 2 , via the EP 4 receptor, enhanced arginase expression and LPS-evoked IL-10 production. PGD 2 suppressed LPS-evoked nitric oxide via the DP 1 receptor. Reciprocally, conditioned medium from macrophages treated with IL-4 + IL-13 and myofibroblast conditioned medium components, but not macrophages given IL-4 + IL-13 only, reduced myofibroblast migration, the expression of COX-2, and the production of PGE 2 and PGD 2 . CONCLUSIONS AND IMPLICATIONSThese findings define mechanisms by which myofibroblasts enhance an AAM phenotype, which can promote wound healing directly, and/or via feedback communication to the myofibroblast, subsequently down-regulating its capacity to promote AAM function. This is an important homeostatic regulatory pathway in wound healing that can also limit unwanted fibrosis.Abbreviations AAM, alternatively activated macrophage; ECM, extracellular matrix; MCM, macrophage conditioned medium; MFbCM, myofibroblast conditioned medium; M-CSF, macrophage-colony stimulating factor; SMA, smooth muscle actin BJP British Journal of Pharmacology

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Arginase activity is associated with fibrosis in experimental infection with Taenia crassiceps, but does not play a major role in resistance to infection

Cited by 8 publications

References 30 publications

Extraintestinal Helminth Infection Limits Pathology and Proinflammatory Cytokine Expression during DSS-Induced Ulcerative Colitis: A Role for Alternatively Activated Macrophages and Prostaglandins

Extraintestinal Helminth Infection Limits Pathology and Proinflammatory Cytokine Expression during DSS-Induced Ulcerative Colitis: A Role for Alternatively Activated Macrophages and Prostaglandins

Interactions between Macrophages and Cyst-Lining Epithelial Cells Promote Kidney Cyst Growth in Pkd1-Deficient Mice

Bidirectional crosstalk via IL‐6, PGE₂and PGD₂between murine myofibroblasts and alternatively activated macrophages enhances anti‐inflammatory phenotype in both cells

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Arginase activity is associated with fibrosis in experimental infection with Taenia crassiceps, but does not play a major role in resistance to infection

Cited by 8 publications

References 30 publications

Extraintestinal Helminth Infection Limits Pathology and Proinflammatory Cytokine Expression during DSS-Induced Ulcerative Colitis: A Role for Alternatively Activated Macrophages and Prostaglandins

Extraintestinal Helminth Infection Limits Pathology and Proinflammatory Cytokine Expression during DSS-Induced Ulcerative Colitis: A Role for Alternatively Activated Macrophages and Prostaglandins

Interactions between Macrophages and Cyst-Lining Epithelial Cells Promote Kidney Cyst Growth in Pkd1-Deficient Mice

Bidirectional crosstalk via IL‐6, PGE2and PGD2between murine myofibroblasts and alternatively activated macrophages enhances anti‐inflammatory phenotype in both cells

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Bidirectional crosstalk via IL‐6, PGE₂and PGD₂between murine myofibroblasts and alternatively activated macrophages enhances anti‐inflammatory phenotype in both cells