Expression of prostaglandin E2 receptor subtypes on cells in sputum from patients with asthma and controls: Effect of allergen inhalational challenge

Sun, Yu; O’Connor, Brian; Meng, Qiu; Woodman, Natalie; Greenaway, Steven; Wong, Hai Ming; Mallett, Kirsty; Lee, Tak H.; Corrigan, Christopher

doi:10.1016/j.jaci.2004.08.034

Cited by 16 publications

(27 citation statements)

References 29 publications

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“…The individual cell types, activated by various intercellular signal mechanisms, follow specific traffic patterns on various levels in the blood and bronchial tissue (epithelium, mucosal and submucosal layers, smooth muscles and secretory glands), leading to a variety of inflammatory processes, bronchoconstriction, increased sputum production and airway remodeling [2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,47,48,49,50,51,52,53,54,55,56,57,58]. …”

Section: Discussionmentioning

confidence: 99%

“…Such an approach resulted in the collection of data which cannot be properly related to specific and well-defined types of hypersensitivity and the underlying immunologic processes. The BPT with allergen is the only method demonstrating the existence and participation of a certain type of asthmatic response in the individual patient to which the other in vivo and in vitro diagnostic parameters and immunologic aspects can be related [4,5,6,7,8,10,14,15,16,19,20,21,22,23,24,25,30,32,52,53,54,55,56,57]. …”

Section: Discussionmentioning

confidence: 99%

“…In most of the in vivo studies, either the single estimation of these factors has been performed in the (induced) sputum [19,26,47,51,61,62,63,64,65,66,67], bronchoalveolar lavage (BAL) fluid [18,50], blood [14,35,40,41,51,59,65,67], lung biopsy [26,43], urine [35] or exhaled breath condensate [58], or their concentrations were measured repeatedly in BAL fluid [8,14,15,20,21,42,53,54], induced sputum [22,28,31,55], blood [7,15,16,30,39,52], exhaled breath condensate [56], urine [23,24,30,32,57] or lung biopsy [15] after a segmental/endobronchial provocation with allergen. However, the changes of these factors in sputum, BAL fluid, urine or exhaled breath condensate were usually measured within a relatively short period of time, usually 1–2 h [8,53,54], and exceptionally up to 12 h [16,20,23] or 24 h [15,21,22,52] after the allergen provocation.…”

Section: Discussionmentioning

confidence: 99%

“…Relatively few studies deal with the determination of these factors in BAL fluid [8,21,42], induced sputum [22,28,31,55], blood [16,25,52,68], urine [23,24,32,57] or exhaled breath condensate [56] after a BPT performed by inhalation of allergen. In some of these studies, the recorded factor changes are related to the particular types of the asthmatic response, such as an IAR [4,16,23,24,25,28,42,53,57] or LAR [5,15,16,21,22,23,24,25,31,55,56].…”

Section: Discussionmentioning

confidence: 99%

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Delayed Asthmatic Response to Bronchial Challenge with Allergen-Mediators, Eicosanoids, Eosinophil and Neutrophil Constituents in the Blood and Urine

Pelikán¹

2011

Respiration

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Background: In patients with allergic bronchial asthma, different immunologic mechanisms may participate and lead to different types of asthmatic response to allergen challenge, such as immediate/early (IAR/EAR), late (LAR) or delayed asthmatic response (DYAR). Objectives: In 55 of 397 asthmatics, DYAR has been recorded (p < 0.001) and confirmed by repeated bronchial challenge with the same allergen (p < 0.001). DYAR began between 26 and 32 h, reached a maximum between 32 and 48 h and resolved within 56 h after the challenge. DYAR was associated with various clinical symptoms and diagnostic parameters having diverged from those recorded during the IARs/EARs and LARs. Methods: In 25 of 55 patients, repeated DYAR has been supplemented with the recording of leukotriene B₄ (LTB₄), LTC₄, LTE₄, prostaglandin D₂ (PGD₂), PGE₂, PGF₂_α, thromboxane B₂, lipoxin A₄, eosinophil cationic protein, eosinophil-derived neurotoxin/eosinophil protein X, eosinophilic peroxidase, myeloperoxidase, histamine and tryptase in peripheral blood, and of LTC₄, thromboxane B₂, eosinophil-derived neurotoxin and 9α,11β-PGF₂ in urine, before and up to 72 h after the bronchial allergen challenge, by means of enzyme-linked immunoassay (ELISA/EIA) or ImmunoCAP. Results: DYAR was accompanied by a significant increase in the plasma concentrations of LTB₄ (p < 0.05) and myeloperoxidase (p < 0.05) at 24, 36 and 48 h after the challenge, whereas the plasma/serum or urine concentrations of the other factors did not demonstrate any significant changes (p > 0.05). Conclusions: These results would indicate an active and prominent involvement of neutrophils, in addition to the previously demonstrated role of the Th1 lymphocytes, in the clinical DYAR.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Delayed Asthmatic Response to Bronchial Challenge with Allergen-Mediators, Eicosanoids, Eosinophil and Neutrophil Constituents in the Blood and Urine

Pelikán¹

2011

Respiration

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“…Expression of EP2 and EP4 receptors in eosinophils has been demonstrated at mRNA and protein levels, whereas data on EP1 and EP3 receptor expression have remained inconclusive (42,43). Functionally, stimulation of EP4 but not EP2 receptors inhibits leukotriene C 4 biosynthesis in human eosinophils (42).…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 Inhibits Eosinophil Trafficking through E-Prostanoid 2 Receptors

Sturm

Schratl

Schuligoi

et al. 2008

The Journal of Immunology

108

110

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The accumulation of eosinophils in lung tissue is a hallmark of asthma, and it is believed that eosinophils play a crucial pathogenic role in allergic inflammation. Prostaglandin (PG) E2 exerts anti-inflammatory and bronchoprotective mechanisms in asthma, but the underlying mechanisms have remained unclear. In this study we show that PGE2 potently inhibits the chemotaxis of purified human eosinophils toward eotaxin, PGD2, and C5a. Activated monocytes similarly attenuated eosinophil migration, and this was reversed after pretreatment of the monocytes with a cyclooxygenase inhibitor. The selective E-prostanoid (EP) 2 receptor agonist butaprost mimicked the inhibitory effect of PGE2 on eosinophil migration, whereas an EP2 antagonist completely prevented this effect. Butaprost, and also PGE2, inhibited the C5a-induced degranulation of eosinophils. Moreover, selective kinase inhibitors revealed that the inhibitory effect of PGE2 on eosinophil migration depended upon activation of PI3K and protein kinase C, but not cAMP. In animal models, the EP2 agonist butaprost inhibited the rapid mobilization of eosinophils from bone marrow of the in situ perfused guinea pig hind limb and prevented the allergen-induced bronchial accumulation of eosinophils in OVA-sensitized mice. Immunostaining showed that human eosinophils express EP2 receptors and that EP2 receptor expression in the murine lungs is prominent in airway epithelium and, after allergen challenge, in peribronchial infiltrating leukocytes. In summary, these data show that EP2 receptor agonists potently inhibit eosinophil trafficking and activation and might hence be a useful therapeutic option in eosinophilic diseases.

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EP4 receptor stimulation down-regulates human eosinophil function

Luschnig-Schratl

Sturm

Kónya

et al. 2011

Cell. Mol. Life Sci.

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Accumulation of eosinophils in tissue is a hallmark of allergic inflammation. Here we observed that a selective agonist of the PGE2 receptor EP4, ONO AE1-329, potently attenuated the chemotaxis of human peripheral blood eosinophils, upregulation of the adhesion molecule CD11b and the production of reactive oxygen species. These effects were accompanied by the inhibition of cytoskeletal rearrangement and Ca2+ mobilization. The involvement of the EP4 receptor was substantiated by a selective EP4 antagonist, which reversed the inhibitory effects of PGE2 and the EP4 agonist. Selective kinase inhibitors revealed that the inhibitory effect of EP4 stimulation on eosinophil migration depended upon activation of PI 3-kinase and PKC, but not cAMP. Finally, we found that EP4 receptors are expressed by human eosinophils, and are also present on infiltrating leukocytes in inflamed human nasal mucosa. These data indicate that EP4 agonists might be a novel therapeutic option in eosinophilic diseases.Electronic supplementary materialThe online version of this article (doi:10.1007/s00018-011-0642-5) contains supplementary material, which is available to authorized users.

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Expression of prostaglandin E2 receptor subtypes on cells in sputum from patients with asthma and controls: Effect of allergen inhalational challenge

Cited by 16 publications

References 29 publications

Delayed Asthmatic Response to Bronchial Challenge with Allergen-Mediators, Eicosanoids, Eosinophil and Neutrophil Constituents in the Blood and Urine

Delayed Asthmatic Response to Bronchial Challenge with Allergen-Mediators, Eicosanoids, Eosinophil and Neutrophil Constituents in the Blood and Urine

Prostaglandin E2 Inhibits Eosinophil Trafficking through E-Prostanoid 2 Receptors

EP4 receptor stimulation down-regulates human eosinophil function

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