Navegando por Palavras-chave "Th1/Th2 cytokines"

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    Beneficial effect of annexin A1 in a model of experimental allergic conjunctivitis
    (Elsevier B.V., 2015-05-01) Gimenes, Alexandre D. [UNIFESP]; Andrade, Teresa Raquel M. [UNIFESP]; Mello, Claudia B.; Ramos, Lisandra [UNIFESP]; Gil, Cristiane D. [UNIFESP]; Oliani, Sonia M. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Estadual Paulista
    Annexin A1 (ANXA1), a 37 kDa glucocorticoid-regulated protein, is a potent anti-inflammatory mediator effective in terminating acute inflammatory response, and its role in allergic settings has been poorly studied. the aim of this investigation was to evaluate the mechanism of action of ANXA1 in intraocular inflammation using a classical model of ovalbumin (OVA)-induced allergic conjunctivitis (AC). OVA-immunised Balb/c mice, wild-type (WT) and ANXA1-deficient (AnxA1(-/-)), were challenged with eye drops containing OVA on days 14-16 with a subset of WT animals pretreated intraperitoneally with the peptide AC(2-26) (N-terminal region of ANXA1) or dexamethasone (DEX). After 24 h of the last ocular challenge, WT mice treated with Ac2-26 and DEX had significantly reduced clinical signs of conjunctivitis (chemosis, conjunctival hyperaemia, lid oedema and tearing), plasma IgE levels, leukocyte (eosinophil and neutrophil) influx and mast cell degranulation in the conjunctiva compared to WT controls. These anti-inflammatory effects of DEX were associated with high endogenous levels of ANXA1 in the ocular tissues as detected by immunohistochemistry. Additionally, AC(2-26) administration was effective to reduce IL-2, IL-4, IL-10, IL-13, eotaxin and RANTES in the eye and lymph nodes compared to untreated WT animals. the lack of ANXA1 produced an exacerbated allergic response as detected by the density of the inflammatory cell influx to the conjunctiva and the cytokine/chemokine release. These different effects observed for Ac2-26 were correlated with diminished level of activated ERK at 24 h in the ocular tissues compared to untreated OVA group. Our findings demonstrate the protective effect of ANXA1 during the inflammatory allergic response suggesting this protein as a potential target for new ocular inflammation therapies. (C) 2015 Elsevier B.V. All rights reserved.
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    Influence of TH1/TH2 switched immune response on renal ischemia-reperfusion injury
    (Karger, 2006-01-01) Marques, Vilmar Paiva [UNIFESP]; Gonçalves, Giselle Martins [UNIFESP]; Feitoza, Carla Quarin [UNIFESP]; Cenedeze, Marcos Antonio [UNIFESP]; Bertocchi, Ana Paula Fernandes [UNIFESP]; Damiao, Marcio Jose [UNIFESP]; Pinheiro, Helady Sanders; Teixeira, Vicente Paula Antunes; Reis, Marlene Antonia dos; Pacheco-Silva, Alvaro [UNIFESP]; Camara, Niels Olsen Saraiva [UNIFESP]; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    Background/Aims: Recent evidence shows a critical role of the CD4+ T cell with the Th1/Th2 paradigm as a possible effector mechanism in ischemia and reperfusion injury. We hypothesize that a polarized Th1 activation response may negatively influence the renal IRI through its relationship with chemokine production (MCP-1) and with a protective tissue response (HO-1). Methods: We subjected mice to renal ischemia for 45 min using IL-4 and IL-12 knockout C57BL/6. We then measured serum urea levels, performed histomorphometric analysis for tubular necrosis and regeneration, and evaluated the mRNA expression of HO-1, t-bet, Gata-3 and MCP-1 by real-time PCR at 24,48 and 120 h after surgery. Results/Conclusions: the IL-4 knockout mice had a statistically significant rise in serum urea levels post IRI compared with control animals. the IL-12-deficient mice were not affected. the IL-4-deficient mice had a statistically significant increase in tubular injury and impairment in cell regeneration. the IRI in IL-4-deficient mice was accompanied by higher levels of HO-1, t-bet and later up-regulation of MCP-1. These findings suggest that the deleterious effects of the Th1 cell involve increased production of chemokines such as MCP-1. Copyright (c) 2006 S. Karger AG, Basel.
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    Role of interplay between IL-4 and IFN-gamma in the in regulating M1 macrophage polarization induced by Nattectin
    (Elsevier B.V., 2012-12-01) Ishizuka, Edson Kiyotaka; Ferreira, Marcio Jose; Grund, Lidiane Zito; Coutinho, Erica Maria Martins; Komegae, Evilin Naname; Cassado, Alexandra dos Anjos [UNIFESP]; Bortoluci, Karina Ramalho [UNIFESP]; Lopes-Ferreira, Monica; Lima, Carla; Inst Butantan; Universidade Federal de São Paulo (UNIFESP)
    Recently our group described that Nattectin, a C-type lectin of the venom of Thalassophryne nattereri shows a potent pro-inflammatory capacity. Here, we demonstrated that Nattectin is able to induce M1 macrophage marker iNOS, and up-regulate the expression of MHC class II, CD80, CD86 and CD40 molecules. the increase in MHC class II and CD49a integrin expression with MMP-9 production and endocytic capacity depend on lectin function of Nattectin. Moreover, the polarization of peritoneal and bone marrow-derived macrophages induced by Nattectin to M1 profile is dependent on Th1 cytokines (IL-12 and IFN-gamma), and negatively regulated by Th2 cytokines (IL-4, IL-10 and IL-13). Also we reveal that IL-4 play a dual role in this polarization: a regular action of IL-4 was seen in the negative regulation of the CD40 expression, but an unexpected positive regulation was seen in the expression of CCR7 and MHC class II. Finally, our in vivo studies showed that the influx of neutrophils and small peritoneal macrophage - F4/80(low)MHCII(hi) induced by Nattectin is totally dependent on IL-4 and IFN-gamma cytokines. Furthermore, the induction of IL-6 release is negatively regulated by IL-4 and positively regulated by IL-12 and IFN-gamma. Together, the results allowed us to expand the knowledge about the regulation of macrophage activation, as well as confirmed the ability of Nattectin, a fish C-type lectin, as an important immunomodulatory agent. (c) 2012 Elsevier B.V. All rights reserved.