Expression of interleukin‐13 receptor α 1‐subunit on peripheral blood eosinophils is regulated by cytokines

Myrtek, Daniel; Knoll, Mathias; Matthiesen, T; Krause, Sebastian; Lohrmann, Jens; Schillinger, Dirk; Idzko, Marco; Virchow, J. Christian; Friedrich, Karlheinz; Luttmann, Werner

doi:10.1046/j.1365-2567.2004.01897.x

Cited by 30 publications

(29 citation statements)

References 41 publications

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“…Thus, we determined whether other receptor chains specific for eosinophilderived cytokines were present preformed within eosinophils. IL-13R␣ 1 expression has been detected on human eosinophils (27), and as noted above, we identified an intracellular pool of IL-13R␣ 1 (Fig. 1C).…”

Section: Eosinophils Contain Preformed Intracellular Stores Of Il-6 Rsupporting

confidence: 82%

Cytokine receptor-mediated trafficking of preformed IL-4 in eosinophils identifies an innate immune mechanism of cytokine secretion

Spencer¹,

Melo

Perez

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

122

130

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Section: Eosinophils Contain Preformed Intracellular Stores Of Il-6 Rsupporting

confidence: 82%

Cytokine receptor-mediated trafficking of preformed IL-4 in eosinophils identifies an innate immune mechanism of cytokine secretion

Spencer¹,

Melo

Perez

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

122

130

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“…Also, IL-13 is an important growth factor for IgE-producing B lymphocytes (49). Although we do not measure IL-13 in our model, we may suggest that the level of this cytokine is also decreased in MK886-treated mice, because this drug decreases eosinophil numbers, a relevant source of IL-13 in Th2 immune response (50,51). Thus, in our model, besides the fact that MK886 did not change IL-4 production, the decrease of IgE levels could be related with inhibition of IL-5 and IL-13 levels.…”

Section: Discussionmentioning

confidence: 94%

Leukotrienes Play a Role in the Control of Parasite Burden in Murine Strongyloidiasis

Machado

Ueta

Lourenço

et al. 2005

The Journal of Immunology

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It is clear that leukotrienes mediate inflammatory response; new aspects of leukotriene function have recently been described. In this study, we demonstrate that leukotrienes are key chemical mediators in the control of parasite burdens in mice infected with Strongyloides venezuelensis. High leukotriene levels were detected in the lungs and small intestines of Swiss mice. In infected Swiss mice treated with MK886, a leukotriene synthesis inhibitor, numbers of adult worms, and eggs/g/feces were greater than in infected-only animals. The MK886 treatment inhibited leukotriene B4 production in the lungs and small intestines, albeit on different postinfection days. Similarly, parasite burdens and eggs/g/feces were greater in 5-lipoxygenase−/− mice than in wild-type animals. These observation were confirmed by histopathological study of the duodena. We subsequently observed significant lower numbers of eosinophils and mononuclear cells in the blood, peritoneal cavity fluid, and bronchoalveolar lavage fluid of Swiss mice treated with MK886. In the lung parenchyma of infected animals, MK886 significantly inhibited synthesis of IL-5 at the beginning of infection, whereas levels of IL-12 increased progressively throughout the postinfection period. However, levels of leukotriene C4, PGE2, TNF-α, IL-3, IL-4, IFN-γ, and IL-10 were comparable between the treated and untreated groups. Nevertheless, IgE and IgG1 (but not IgG2a) synthesis was also significantly inhibited by MK886 administration. Therefore, in S. venezuelensis-infected mice, adult worm and egg burdens are leukotriene dependent. These findings indicate potential immunostimulatory strategies involving leukotriene administration, and may serve as an alert to physicians treating Strongyloides stercoralis-infected patients presenting asthma-like symptoms because use of 5-lipoxygenase inhibitors may worsen the infection.

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“…In this study, we used Il13ra1 −/− mice from two genetic backgrounds (BALB/c and C57BL/6) to demonstrate that the phenotype of abolished airway eosinophilia in Il13ra1 −/− mice is observed across two mouse strains. The Il13ra1 −/− recipient mice results demonstrate that the previously observed airway eosinophil migration deficit (23) was primarily due to the IL-13RA1 receptor expressed on recipient cells (likely respiratory epithelium) rather than to IL-13RA1 expressed on the eosinophils themselves (25,26) or to an altered eosinophil developmental property driven by IL-13RA1. These findings not only confirm the Il13ra1 −/− recipient phenotype but also substantiate the utility of these systems in that eosinophil migration phenotype detection can be readily performed using these two common genetic backgrounds in the allergy/eosinophil field, namely BALB/c and C57BL/6.…”

Section: Discussionmentioning

confidence: 61%

Eosinophil adoptive transfer system to directly evaluate pulmonary eosinophil trafficking in vivo

Wen

Besse

Mingler

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Most in vivo studies of granulocytes draw conclusions about their trafficking based on examination of their steady-state tissue/blood levels, which result from a combination of tissue homing, survival, and egress, rather than direct examination of cellular trafficking. Herein, we developed a unique cell transfer system involving the adoptive transfer of a genetically labeled, bone-marrow-derived unique granulocyte population (eosinophils) into an elicited inflammatory site, the allergic lung. A dual polychromatic FACS-based biomarker-labeling system based on the IL4-eGFP transgene (4get) or Cd45.1 allele was used to track i.v. transferred eosinophils into the airway following allergen or T H 2-associated stimuli in the lung in multiple mouse strains. The system was amenable to reverse tagging of recipients, thus allowing transfer of nonlabeled eosinophils and competitive tracking of multiple populations of eosinophils in vivo. The half-life of eosinophils in the blood was 3 h, and migration to the lung was dependent upon the dosage of transferred eosinophils, sensitive to pertussis toxin pretreatment, peaked at ∼24 h after adoptive transfer, and revealed a greater than 8-d eosinophil half-life in the lung. Eosinophil migration to the lung was dependent upon recipient IL-5 and IL-13 receptor α1 and donor eosinophil C-C chemokine receptor type 3 (CCR3) and interleukin 1 receptor-like 1 (ST2) in vivo. Taken together, this unique eosinophil transfer system provides an unprecedented opportunity to examine airway eosinophil migration without the need for extensive efforts to acquire donor source and timeconsuming genetic crossing and has already been used to identify a long eosinophil half-life in the allergic lung and a definite role for ST2 in regulating eosinophil trafficking.asthma | allergy | eosinophilia | chemoattraction

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Expression of interleukin‐13 receptor α 1‐subunit on peripheral blood eosinophils is regulated by cytokines

Cited by 30 publications

References 41 publications

Cytokine receptor-mediated trafficking of preformed IL-4 in eosinophils identifies an innate immune mechanism of cytokine secretion

Cytokine receptor-mediated trafficking of preformed IL-4 in eosinophils identifies an innate immune mechanism of cytokine secretion

Leukotrienes Play a Role in the Control of Parasite Burden in Murine Strongyloidiasis

Eosinophil adoptive transfer system to directly evaluate pulmonary eosinophil trafficking in vivo

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