Mouse Eotaxin Expression Parallels Eosinophil Accumulation during Lung Allergic Inflammation but It Is Not Restricted to a Th2-Type Response

Gonzalo, José-Ángel; Jia, Gui-yan; Aguirre, Vincent; Friend, Daniel S.; Coyle, Anthony J.; Jenkins, Nancy A.; Lin, Gu‐Jiun; Katz, Howard R.; Lichtman, Andrew H.; Copeland, Neal G.; Köpf, Manfred; Gutierrez‐Ramos, José Carlos

doi:10.1016/s1074-7613(00)80293-9

Cited by 236 publications

(174 citation statements)

References 55 publications

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“…Using animal models of allergic airway inflammation, there is now considerable evidence to support the hypothesis that eotaxin plays an important role in eosinophil homing and tissue recruitment (28 -30). Indeed, eotaxin mRNA and/or protein expression is up-regulated in guinea pig and rodent models of allergic asthma that parallel eosinophil accumulation (31)(32)(33). It was further shown that a neutralizing Ab to eotaxin induced a significant inhibition of eosinophil infiltration following Ag challenge (32) and eotaxin knockout mice exhibited a significantly reduced eosinophil recruitment to the lung 18 h after allergen challenge (34,35).…”

Section: Discussionmentioning

confidence: 99%

Critical Role for T Cells in Sephadex-Induced Airway Inflammation: Pharmacological and Immunological Characterization and Molecular Biomarker Identification

Haddad¹,

Underwood²,

Dabrowski

et al. 2002

The Journal of Immunology

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Intratracheal instillation of Sephadex particles is a convenient model for assessing the impact of potential anti-inflammatory compounds on lung eosinophilia thought to be a key feature in asthma pathophysiology. However, the underlying cellular and molecular mechanisms involved are poorly understood. We have studied the time course of Sephadex-induced lung eosinophilia, changes in pulmonary T cell numbers, and gene and protein expression as well as the immunological and pharmacological modulation of these inflammatory indices in the Sprague Dawley rat. Sephadex increased T cell numbers (including CD4+ T cells) and evoked a pulmonary eosinophilia that was associated with an increase in gene/protein expression of the Th2-type cytokines IL-4, IL-5, and IL-13 and eotaxin in lung tissue. Sephadex instillation also induced airway hyperreactivity to acetylcholine and bradykinin. A neutralizing Ab (R73) against the αβ-TCR caused 54% depletion of total (CD2+) pulmonary T cells accompanied by a significant inhibition of IL-4, IL-13 and eotaxin gene expression together with suppression (65% inhibition) of eosinophils in lung tissue 24 h after Sephadex treatment. Sephadex-induced eosinophilia and Th2 cytokine gene and/or protein expression were sensitive to cyclosporin A and budesonide, compounds that inhibit T cell function, suggesting a pivotal role for T cells in orchestrating Sephadex-induced inflammation in this model.

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Section: Discussionmentioning

confidence: 99%

Critical Role for T Cells in Sephadex-Induced Airway Inflammation: Pharmacological and Immunological Characterization and Molecular Biomarker Identification

Haddad¹,

Underwood²,

Dabrowski

et al. 2002

The Journal of Immunology

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“…10C). Eotaxin is well recognized as a potent chemoattractant for eosinophils (46,47). Although eosinophil accumulation was not compared in WT versus Tbx21 2/2 mice, it has previously been reported that Ghanian pediatric patients with CM had uniformly low eosinophil counts because of tissue sequestration and destruction rather than decreased production during acute illness followed by eosinophilia 30 d after cure (48).…”

Section: Figurementioning

confidence: 99%

The Transcription Factor T-bet Regulates Parasitemia and Promotes Pathogenesis duringPlasmodium bergheiANKA Murine Malaria

Oakley

Sahu

Lotspeich-Cole

et al. 2013

The Journal of Immunology

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The pathogenesis of experimental cerebral malaria (ECM) is an immunologic process, mediated in part by Th1 CD4+ T cells. However, the role of the Th1 CD4+ T cell differentiation program on the ability to control parasitemia and susceptibility to ECM disease during blood stage malaria has never been assessed directly. Using the Plasmodium berghei ANKA murine model of ECM and mice deficient for the transcription factor T-bet (the master regulator of Th1 cells) on the susceptible C57BL/6 background, we demonstrate that although T-bet plays a role in the regulation of parasite burden, it also promotes the pathogenesis of ECM. T-bet−deficient (Tbx21−/−) mice had higher parasitemia than wild type controls did during the ECM phase of disease (17.7 ± 3.1% versus 10.9 ± 1.5%). In addition, although 100% (10/10) of wild type mice developed ECM by day 9 after infection, only 30% (3/10) of Tbx21−/− mice succumbed to disease during the cerebral phase of infection. Resistance to ECM in Tbx21−/− mice was associated with diminished numbers of IFN-γ–producing CD4+ T cells in the spleen and a lower accumulation of CD4+ and CD8+ T cells in the brain. An augmented Th2 immune response characterized by enhanced production of activated GATA-3+ CD4+ T cells and elevated levels of the eotaxin, MCP-1, and G-CSF cytokines was observed in the absence of T-bet. Our results suggest that in virulent malarias, immune modulation or therapy resulting in an early shift toward a Th2 response may help to ameliorate the most severe consequences of malaria immunopathogenesis and the prospect of host survival.

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“…Eotaxin is a fundamental regulator of physiological eosinophil trafficking during healthy states [23] and inflammation [24]. Ecalectin (galectin-9), which is produced by antigen-stimulated T cells, is a powerful eosinophil-specific chemoattractant in vitro and in vivo [25].…”

Section: Eosinophil Migration and Infiltration To Tissuesmentioning

confidence: 99%

Eosinophils and Trichinella infection: toxic for the parasite and the host?

Bruschi

Korenaga

Watanabe

2008

Trends in Parasitology

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Mouse Eotaxin Expression Parallels Eosinophil Accumulation during Lung Allergic Inflammation but It Is Not Restricted to a Th2-Type Response

Cited by 236 publications

References 55 publications

Critical Role for T Cells in Sephadex-Induced Airway Inflammation: Pharmacological and Immunological Characterization and Molecular Biomarker Identification

Critical Role for T Cells in Sephadex-Induced Airway Inflammation: Pharmacological and Immunological Characterization and Molecular Biomarker Identification

The Transcription Factor T-bet Regulates Parasitemia and Promotes Pathogenesis duringPlasmodium bergheiANKA Murine Malaria

Eosinophils and Trichinella infection: toxic for the parasite and the host?

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