Depletion of circulating allergen-specific TH2 T lymphocytes after allergen exposure in asthma1

Crimi, Emanuele; Gaffi, Davide; Frittoli, Emanuela; Borgonovo, Barbara; Burastero, Samuele E.

doi:10.1016/s0091-6749(97)80013-9

Cited by 34 publications

(28 citation statements)

References 19 publications

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“…Infiltrating eosinophils, macrophages, Th2 cells, and monocytes comprise the largest proportion of cell-types within the airways of patients with allergic asthma. In addition, these cell-types are associated with airway hyper-reactivity [2]. T helper cell-type 2 (Th2) immunoregulatory cytokines play a central role in the pathogenesis of allergic asthma [2].…”

Section: Introductionmentioning

confidence: 99%

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Effects of All-Trans Retinoic Acid on Th1- and Th2-Related Chemokines Production in Monocytes

Tsai¹,

Chang²,

Chang³

et al. 2008

Inflammation

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Low vitamin C and reduced alpha-carotene intake are associated with increased asthma risk in children. In addition, mean serum vitamin A concentrations are significantly lower in asthmatic children than in controls. All-trans retinoic acid (ATRA) is a derivative of vitamin A. Macrophage-derived chemokine (MDC) is a T helper cell-type 2 (Th2)-related chemokine involved in the recruitment of Th2 cells toward inflammatory sites. On the other hand, Th1-related chemokine, interferon-inducible protein 10 (IP-10)/CXCL10 is also important in allergic inflammation. Both Th1- and Th2-related chemokines play an important role in allergic asthma. To survey whether ATRA and ascorbic acid effect Th1- and Th2-related chemokine expression in monocytes. To test this, THP-1 cells were pre-treated with ATRA or ascorbic acid and stimulated by lipopolysaccharide (LPS) or poly I:C. Supernatants were measured for Th2-related (MDC) and Th1-related (IP-10) chemokine concentrations by ELISA. The effects of ATRA on mitogen-activated protein kinase (MAPK) and NFkb were evaluated with Western blotting. After stimulation, ATRA significantly down-regulated MDC and IP-10 in a dose-dependent manner. Similarly, ascorbic acid reduced the LPS-induced changes in MDC but only with a high dose. However, asorbic acid had no effect on IP-10 changes either induced by LPS or poly I:C. RT-PCR showed ATRA inhibited IP-10 expression through decreasing the level of transcription. Furthermore, ATRA suppressed the expression of LPS-stimulated c-Raf, MKK1/2 and ERK expression of THP-1 cells. In conclusion, ATRA suppressed Th2- and Th1-related chemokines expression in THP-1 cells, at least in part via the c-Raf-MKK1/2-ERK/MAPK pathway.

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Section: Introductionmentioning

confidence: 99%

“…In addition, these cell-types are associated with airway hyper-reactivity [2]. T helper cell-type 2 (Th2) immunoregulatory cytokines play a central role in the pathogenesis of allergic asthma [2]. In addition, low vitamin C and alpha-carotene intake are associated with increased asthma risk in children [3].…”

Section: Introductionmentioning

confidence: 99%

Effects of All-Trans Retinoic Acid on Th1- and Th2-Related Chemokines Production in Monocytes

Tsai¹,

Chang²,

Chang³

et al. 2008

Inflammation

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“…In the process of airway inflammation, many kinds of inflammatory cells, such as mast cells (Ying et al, 1997), eosinophils (Lamkhioued et al, 1997), and T lymphocytes (Crimi et al, 1997;De Sanctis et al, 1997), are involved. In addition, various cytokines and growth factors produced by these cells, such as interleukin (IL)-4 (Leonard et al, 1997;Shi et al, 1998a), IL-5 (Shi et al, 1998b;Till et al, 1998), IL-10 (Borish et al, 1996;Robinson et al, 1996), IL-12 (Van Der Pouw Kraan et al, 1997), and IL-13 , may play important roles in the disease process.…”

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confidence: 99%

Early Interleukin 4–Dependent Response Can Induce Airway Hyperreactivity before Development of Airway Inflammation in a Mouse Model of Asthma

Dohi

Tanaka

et al. 2001

Laboratory Investigation

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SUMMARY:In experimental models of bronchial asthma with mice, airway inflammation and increase in airway hyperreactivity (AHR) are induced by a combination of systemic sensitization and airway challenge with allergens. In this report, we present another possibility: that systemic antigen-specific sensitization alone can induce AHR before the development of inflammation in the airway. Male BALB/c mice were sensitized with ovalbumin (OVA) by a combination of intraperitoneal injection and aerosol inhalation, and various parameters for airway inflammation and hyperreactivity were sequentially analyzed. Bronchial response measured by a noninvasive method (enhanced pause) and the eosinophil count and interleukin (IL)-5 concentration in bronchoalveolar lavage fluid (BALF) gradually increased following the sensitization, and significant increase was achieved after repeated OVA aerosol inhalation along with development of histologic changes of the airway. In contrast, AHR was already significantly increased by systemic sensitization alone, although airway inflammation hardly developed at that time point. BALF IL-4 concentration and the expression of IL-4 mRNA in the lung reached maximal values after the systemic sensitization, then subsequently decreased. Treatment of mice with anti-IL-4 neutralizing antibody during systemic sensitization significantly suppressed this early increase in AHR. In addition, IL-4 gene-targeted mice did not reveal this early increase in AHR by systemic sensitization. These results suggest that an immune response in the lung in an early stage of sensitization can induce airway hyperreactivity before development of an eosinophilic airway inflammation in BALB/c mice and that IL-4 plays an essential role in this process. If this early increase in AHR does occur in sensitized human infants, it could be another therapeutic target for early prevention of the future onset of asthma. (Lab Invest 2001, 81:1385-1396.A fter exposure to allergen(s), atopic bronchial asthma is characterized by airway inflammation and increased serum immunoglobulin (Ig) E levels together with increased airway hyperreactivity (AHR) in response to specific allergens and nonspecific stimuli (Burrows et al, 1989;Sears et al, 1991). In the process of airway inflammation, many kinds of inflammatory cells, such as mast cells (Ying et al, 1997), eosinophils (Lamkhioued et al, 1997), and T lymphocytes (Crimi et al, 1997;De Sanctis et al, 1997), are involved. In addition, various cytokines and growth factors produced by these cells, such as interleukin (IL)-4 (Leonard et al, 1997;Shi et al, 1998a), IL-5 (Shi et al, 1998b;Till et al, 1998), IL-10 (Borish et al, 1996;Robinson et al, 1996), IL-12 (Van Der Pouw Kraan et al, 1997), and IL-13 , may play important roles in the disease process. IL-5 and eosinophils have been recently specifically implicated as key contributors to the development of allergic airway inflammation.The predominance of Th2 phenotype of lymphocyte over Th1 phenotype from a very early stage of life has recently bee...

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“…In allergic asthma, CD4 + T lymphocytes are a fundamental component of local chronic inflammation (17). The circulating cytokine profile of these cells is oriented towards a Th2 phenotype, characterized by the production of IL-4, IL-5 and IL-13.…”

Section: Discussionmentioning

confidence: 99%

Up-regulation of CD44 expression by interleukin-13 in a murine model of asthma

Liang

Jiang

2011

Mol Med Report

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Abstract. Allergic asthma is a chronic inflammatory disease characterized by the infiltration of inflammatory cells, the elevated production of cytokines and enhanced airway hyperreactivity (AHR). CD44 is a widely expressed cell adhesion molecule that is involved in lymphocyte adhesion to inflamed endothelium. Previous studies showed that pulmonary eosinophils and CD4 + T cells express high levels of CD44 in bronchoalveolar lavage fluid following antigen administration. The aim of this study was to investigate whether interleukin (IL)-13 is capable of modulating CD44 expression in lung tissue and lymphocytes, further promoting inflammatory cell recruitment into the lungs and exacerbating asthmatic responses. Six-to eight-week-old male Balb/c mice were used. Quantitative PCR and immunohistochemistry were employed to determine the effect on CD44 expression. Our findings showed that IL-13 may play a significant role during the challenge phase in that CD44 expression was up-regulated in lung tissue and lymphocytes following IL-13 treatment, resulting in inflammatory cells infiltrating into lungs and enhancing AHR.

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Depletion of circulating allergen-specific TH2 T lymphocytes after allergen exposure in asthma1

Cited by 34 publications

References 19 publications

Effects of All-Trans Retinoic Acid on Th1- and Th2-Related Chemokines Production in Monocytes

Effects of All-Trans Retinoic Acid on Th1- and Th2-Related Chemokines Production in Monocytes

Early Interleukin 4–Dependent Response Can Induce Airway Hyperreactivity before Development of Airway Inflammation in a Mouse Model of Asthma

Up-regulation of CD44 expression by interleukin-13 in a murine model of asthma

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