Wound healing in cutaneous leishmaniasis: A double edged sword of IL-10 and TGF-β

Abdoli, Amir; Maspi, Nahid; Ghaffarifar, Fatemeh

doi:10.1016/j.cimid.2017.02.001

Cited by 47 publications

(42 citation statements)

References 165 publications

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“…Promastigote forms of Leishmania are regurgitated by the phlebotomine at the moment of blood meal and immediately get in touch with the extracellular microenvironment interacting with ECM constituents ( Ghosh et al, 1999 ). Skin is the largest organ of the body and acts not only as a physical barrier against infection but also as an important immunological organ ( Nylén and Eidsmo, 2012 ; Abdoli et al, 2017 ). After the skin injury produced by sandfly bites and Leishmania deposition, several growth factors and cytokines, including TGF-β, are released to attract immune (e.g., neutrophils, macrophages, and eosinophil) and non-immune cells (e.g., fibroblasts and endothelial cells; Gauglitz, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

“…After the skin injury produced by sandfly bites and Leishmania deposition, several growth factors and cytokines, including TGF-β, are released to attract immune (e.g., neutrophils, macrophages, and eosinophil) and non-immune cells (e.g., fibroblasts and endothelial cells; Gauglitz, 2013 ). Neutrophils rapidly infiltrate the wounded skin and take up the parasites ( Laskay et al, 2008 ; Peters et al, 2008 ; Abdoli et al, 2017 ). Posteriorly, within 2 days, monocytes/macrophages infiltrate to infection site and act as the main host cells for Leishmania amastigotes ( Ribeiro-Gomes et al, 2004 ; van Zandbergen et al, 2004 ; Peter et al, 2007 ; Abdoli et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

“…Neutrophils rapidly infiltrate the wounded skin and take up the parasites ( Laskay et al, 2008 ; Peters et al, 2008 ; Abdoli et al, 2017 ). Posteriorly, within 2 days, monocytes/macrophages infiltrate to infection site and act as the main host cells for Leishmania amastigotes ( Ribeiro-Gomes et al, 2004 ; van Zandbergen et al, 2004 ; Peter et al, 2007 ; Abdoli et al, 2017 ). During the early phase of infection, no macroscopic alterations occur in the epidermis.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies showed that L. amazonensis induces TGF-β production early in infection. It is frequently seen in the literature that TGF-β acts suppressing the immune response and macrophage activation ( Tsunawaki et al, 1988 ), increasing the susceptibility to CL ( Maspi et al, 2016 ; Abdoli et al, 2017 ). Consistent with this view, Barral-Netto et al (1992) showed an increased production of TGF-β in L. amazonensis -infected BALB/c footpads and peritoneal macrophages.…”

Section: Discussionmentioning

confidence: 99%

“…At the same time that these cytokines increase the susceptibility to CL, suppressing the immune responses against Leishmania parasite ( Maspi et al, 2016 ), they exert a critical role in the acceleration of the wound healing process. IL-10 and TGF-β stimulates the granulation tissue formation, angiogenesis, and extracellular matrix (ECM) synthesis ( Gauglitz, 2013 ; Abdoli et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

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Modulation of Cytokines and Extracellular Matrix Proteins Expression by Leishmania amazonensis in Susceptible and Resistant Mice

et al. 2020

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Leishmaniases are a complex of diseases with a broad spectrum of clinical forms, which depend on the parasite species, immunological status, and genetic background of the host. In the Leishmania major model, susceptibility is associated with the Th2 pattern of cytokines production, while resistance is associated with Th1 response. However, the same dichotomy does not occur in L. amazonensis -infected mice. Cytokines are key players in these diseases progression, while the extracellular matrix (ECM) components participate in the process of parasite invasion as well as lesion healing. In this article, we analyzed the influence of host genetics on the expression of cytokines, inducible nitric oxide synthase (iNOS), and ECM proteins, as well as the parasite load in mice with different genetic backgrounds infected by L. amazonensis . C57BL/10 and C3H/He mice were subcutaneously infected with 10 6 L. amazonensis promastigotes. Lesion kinetics, parasite load, cytokines, iNOS, and ECM proteins expression were measured by quantitative PCR (qPCR) in the footpad, draining lymph nodes, liver, and spleen at early (24 h and 30 days) and late phase (120 and 180 days) of infection. Analysis of lesion kinetics showed that C57BL/10 mice developed ulcerative lesions at the inoculation site after L. amazonensis infection, while C3H/He showed slight swelling in the footpad 180 days after infection. C57BL/10 showed progressive enhancement of parasite load in all analyzed organs, while C3H/He mice showed extremely low parasite loads. Susceptible C57BL/10 mice showed high levels of TGF-β mRNA in the footpad early in infection and high levels of proinflammatory cytokines mRNA (IL-12, TNF-α, and IFN-γ) and iNOS in the late phase of the infection. There is an association between increased expression of fibronectin, laminin, collagen III and IV, and TGF-β. On the other hand, resistant C3H/He mice presented a lower repertory of cytokines mRNA expression when compared with susceptible C57BL/10 mice, basically producing TNF-α, collagen IV, and laminin early in infection. The findings of our study indicate that L. amazonensis infection induces different cytokine expression in resistant and susceptible mice but not like the L. major model. An organ-compartmentalized cytokine response was observed in our model. Host genetics determine this response, which modulates ECM proteins expression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Modulation of Cytokines and Extracellular Matrix Proteins Expression by Leishmania amazonensis in Susceptible and Resistant Mice

et al. 2020

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Targeting inflammation with collagen

Schwarz

Lipoldová

Reinecke

et al. 2022

Clinical & Translational Med

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Tissue damage caused by an infection or an autoimmune disease triggers degradation of collagen in the extracellular matrix (ECM), which further enhances inflammation. Therefore, improving ECM in an inflamed tissue can be exploited as a potential therapeutic target. A recent study emphasised an innovative approach against COVID‐19 using polymerised type I collagen (PTIC) that improves disease severity through a hitherto unknown mechanism. In this paper, we provide an overview of potential mechanism that may explain the anti‐inflammatory effect of collagen peptides. In addition,the paper includes a brief summary of possible side effect of collagen deposition in inflammatory diseases. Altogether, current knowledge suggests that collagen may potentially reduce the residual risk in inflammatory diseases; however, the detailed mechanism remains elusive.

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Einzeller beim Menschen

Mehlhorn

2022

Die Parasiten Des Menschen

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Wound healing in cutaneous leishmaniasis: A double edged sword of IL-10 and TGF-β

Cited by 47 publications

References 165 publications

Modulation of Cytokines and Extracellular Matrix Proteins Expression by Leishmania amazonensis in Susceptible and Resistant Mice

Modulation of Cytokines and Extracellular Matrix Proteins Expression by Leishmania amazonensis in Susceptible and Resistant Mice

Targeting inflammation with collagen

Einzeller beim Menschen

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