Effect of Interleukin-2 on the Airway Response to Antigen in the Rat

Renzi, Paolo; Sapienza, S.; Waserman, Susan; Du, Tao; Olivenstein, Ron; Wang, Nai San; Martin, James G.

doi:10.1164/ajrccm/146.1.163

Cited by 49 publications

(28 citation statements)

References 17 publications

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“…IL-2 causes lymphocyte activation and proliferation and affects the regulation of immunoglobulin production and lymphokine expression related to the activation of other cells. It has been reported that IL-2 administration induced OVA-specific IgG production and airway inflammation [26]. In addition, T-cells from eosinophilic patients produce IL-5 after IL-2 stimulation [27].…”

Section: Discussionmentioning

confidence: 99%

Murine strain differences in airway inflammation caused by diesel exhaust particles

Miyabara¹,

Yanagisawa²,

Shimojo³

et al. 1998

Eur Respir J

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aaUrban areas have been polluted heavily by nitrogen dioxide (NO 2 ) and suspended particulate matters (SPM) [1]. The primary source of NO 2 and SPM in urban areas is vehicle emissions. The ratio of vehicle emission to total oxides of nitrogen (NO x ) exhausts in Tokyo and Osaka in 1990 were 70% and 56%, respectively [2]. The number of diesel-powered cars has been increasing, and diesel vehicles emit more NO 2 and particulates than petrol-engined cars. Therefore, the ratio of diesel exhaust particles (DEP) to SPM is very high in urban air; in Tokyo in 1989 it was at least 40% [2]. DEP contains elemental carbon nuclei that adsorb a variety of organic compounds and a trace amount of heavy metals. Some of these organic compounds are strong mutagens and carcinogens [3][4][5]. It has been established that DEP causes lung tumours in a dosedependent manner [6].It has been shown that the prevalence of allergic rhinitis among schoolchildren is significantly higher in districts polluted by automobile exhaust than in nonpolluted districts [7]. Although, there have been numerous attempts to demonstrate the relationship between NO 2 and bronchial asthma, no direct link has been demonstrated experimentally. Furthermore, no experimental study has addressed the relationship between DEP and asthma. A previous report from our laboratory showed that repeated intratracheal instillations of DEP in mice induced chronic airway inflammation with infiltration of eosinophils and lymphocytes, and airway hyperresponsiveness with hypersecretion of mucus [8].It is clear in allergic diseases such as asthma that allergen-specific immunoglobulin (Ig) E plays a central role in hypersensitivity reactions, and that the IgE-mediated reactions are followed by chronic inflammation leading to increased airway responsiveness. It has also been shown that DEP has adjuvant effects on IgE production in mice in cases of allergic rhinitis [9]. Intranasal instillation of DEP and antigen induced an increase of antigen-specific IgE antibody in mouse sera [10]. However, some observations suggest the existence of alternative and/or additional pathways of hypersensitivity reactions. Firstly, allergeninduced bronchial hyperreactivity and eosinophilic inflammation occur in IgE and mast cell-deficient mice [11,12]. Secondly, immediate hypersensitivity and airway hyperresponsiveness were induced by the administration of ovalbumin (OVA)-specific IgE or IgG1, but not IgG2a or IgG3 [13]. We developed a murine asthma model by intratracheal instillation of DEP and OVA, and found that DEP enhanced the production of allergen specific IgG1, airway inflammation and airway hyperresponsiveness, before it enhanced IgE production [14]. Thus, both IgG and IgE antibodies are involved in allergic airway inflammation and airway hyperresponsiveness in that murine model of asthma. Both mouse strains received DEP intratracheally once a week for 5 weeks. After the second injection of DEP, ovalbumin and aluminium hydroxide were injected intraperitoneally. After the last DEP administration,...

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Section: Discussionmentioning

confidence: 99%

Murine strain differences in airway inflammation caused by diesel exhaust particles

Miyabara¹,

Yanagisawa²,

Shimojo³

et al. 1998

Eur Respir J

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“…Firstly, administration of exogenous IL-2, a potent T cell growth factor, resulted in enhancement of LARs in the Brown Norway (BN) rat (14). This study suggested that the activation of T cells by IL-2 and the subsequent release of other T cell cytokines might directly modulate the LAR.…”

Section: Introductionmentioning

confidence: 99%

Transfer of allergic airway responses with antigen-primed CD4+ but not CD8+ T cells in brown Norway rats.

Watanabe

Mishima²,

Renzi³

et al. 1995

J. Clin. Invest.

122

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Activated CD4+ helper T cells have been demonstrated in asthmatic airways and postulated to play a central role in eliciting allergic inflammation; direct evidence of their involvement seems to be lacking. We hypothesized that CD4+ T cells have the potential to induce allergic responses to antigen challenge, and tested this hypothesis in a model of allergic bronchoconstriction, the Brown Norway rat, using the approach of adoptive transfer. Animals were actively sensitized to either ovalbumin (OVA) or BSA and were used as donors of T cells. W3/25 (CD4) + or OX8 (CD8) + T cells were isolated from the cervical lymph nodes of sensitized donors and transferred to naive BN rats. 2 d after adoptive transfer recipient rats were challenged by OVA inhalation, and changes in lung resistance (RL), bronchoalveolar lavage (BAL) cells, and serum levels of antigen-specific IgE were studied. After OVA challenge recipients of OVA-primed W3/25+ T cells exhibited sustained increases in RL throughout the entire 8-h observation period and had significant bronchoalveolar lavage eosinophilia, which was detected by immunocytochemistry using an antimajor basic protein mAb. Recipients of BSA-primed W3/25+ T cells or OVAprimed OX8+ T cells failed to respond to inhaled OVA. OVA-specific immunoglobulin E was undetectable by ELISA or skin testing in any of the recipient rats after adoptive transfer. In conclusion, antigen-induced airway bronchoconstriction and eosinophilia were successfully transferred by antigen-specific W3/25+ T cells in Brown Norway rats. These responses were dependent on antigenprimed W3/25+ T cells and appeared to be independent of IgE-mediated mast cell activation. This study provides clear evidence for T cell mediated immune mechanisms in allergic airway responses in this experimental model. (J. Clin. Invest.

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“…It is important to note that these effects were observed in vitro, but gedunin treatment also resulted in diminished numbers of activated T lymphocytes in draining lymph nodes and in the allergic tissue. During allergic responses, the number of T cells increase in the lymph nodes, as a consequence of antigen presentation and clonal expansion, which is followed by the migration of antigen-specific T lymphocytes into the inflamed site [47,48]. Resident T cells are activated at the site of allergen deposition and mediate the local response to allergen, which is amplified by the arrival of new T lymphocytes in the target tissue [49][50][51].…”

Section: Discussionmentioning

confidence: 99%

Gedunin, a natural tetranortriterpenoid, modulates T lymphocyte responses and ameliorates allergic inflammation

Ferraris

Moret

Figueiredo

et al. 2012

International Immunopharmacology

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T lymphocytes are critical cells involved in allergy. Here, we report that the natural tetranortriterpenoid gedunin impaired allergic responses primarily by modulating T lymphocyte functions. The intraperitoneal (i.p.) administration of gedunin inhibited pleural leukocyte accumulation triggered by intra-pleural (i.pl.) challenge with ovalbumin (OVA) in previously sensitized C57BL/6 mice; this inhibition was primarily due to the impairment of eosinophil and T lymphocyte influx. Likewise, i.pl. pre-treatment with gedunin inhibited eosinophil and T lymphocyte migration into mouse lungs 24 h after OVA intra-nasal (i.n.) instillation. Pre-treatment with gedunin diminished the levels of CCL2, CCL3, CCL5, CCL11, Interleukin-5 and leukotriene B(4) at the allergic site. In vitro pre-treatment with gedunin failed to inhibit T lymphocyte adhesion and chemotaxis towards pleural washes recovered from OVA-challenged mice, suggesting that gedunin inhibits T lymphocyte migration in vivo via the inhibition of chemotactic mediators in situ. In vivo pre-treatment with gedunin reduced the numbers of CD69(+) and CD25(+) T lymphocytes in the pleura and CD25(+) cells in the thoracic lymph nodes 24 h after OVA i.pl. challenge. In accordance, in vitro treatment of T lymphocytes with gedunin inhibited α-CD3 mAb-induced expression of CD69 and CD25, proliferation, Interleukin-2 production and nuclear translocation of NFκB and NFAT. Notably, post-treatment of mice with gedunin reverted OVA-induced lung allergic inflammation by decreasing the T lymphocyte and eosinophil counts and the levels of eosinophilotactic mediators in bronchoalveolar lavage fluid. Our results demonstrate a remarkable anti-allergic effect of gedunin due to its capability to modulate T cell activation and trafficking into the airways.

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Effect of Interleukin-2 on the Airway Response to Antigen in the Rat

Cited by 49 publications

References 17 publications

Murine strain differences in airway inflammation caused by diesel exhaust particles

Murine strain differences in airway inflammation caused by diesel exhaust particles

Transfer of allergic airway responses with antigen-primed CD4+ but not CD8+ T cells in brown Norway rats.

Gedunin, a natural tetranortriterpenoid, modulates T lymphocyte responses and ameliorates allergic inflammation

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