Basophils, eosinophils, and mast cells in atopic and nonatopic asthma and in late-phase allergic reactions in the lung and skin

Macfarlane, Alison; Kon, Onn Min; Smith, Susan J.; Zeibecoglou, Kyriaki; Khan, L N; Taborda-Barata, Luís; McEuen, Alan R.; Buckley, Mark G.; Walls, Andrew F.; Meng, Qiu; Humbert, Marc; Barnes, Neil; Robinson, Douglas S.; Ying, Sun; Kay, A. B.

doi:10.1016/s0091-6749(00)90184-2

Cited by 169 publications

(109 citation statements)

References 29 publications

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“…For example, in allergen-induced, late-phase cutaneous reactions, basophil accumulation peaks at 24 h postchallenge, whereas eosinophil infiltration is maximal at 6 h, and basophil numbers do not correlate with the expression of eotaxin-1/CCL11, eotaxin-2/CCL24, RANTES/CCL5, MCP-3/CCL7, or MCP-4/CCL13 (13,14). Furthermore, basophils can be the major leukocyte type seen in an inflammatory infiltrate, such as in contact dermatitis (15) and responses to ticks (16), suggesting selective recruitment of basophils from the blood.…”

Section: Identification Of Selective Basophil Chemoattractants Inmentioning

confidence: 99%

Identification of Selective Basophil Chemoattractants in Human Nasal Polyps as Insulin-Like Growth Factor-1 and Insulin-Like Growth Factor-2

Hartnell

Heinemann

Conroy

et al. 2004

The Journal of Immunology

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In a search for novel leukocyte chemoattractants at sites of allergic inflammation, we found basophil-selective chemoattractant activity in extracts of human nasal polyps. The extracts were fractionated by reverse phase HPLC, and the resulting fractions were tested for leukocyte-stimulating activity using sensitive shape change assays. The basophil-selective activity detected was not depleted by a poxvirus CC-chemokine-binding protein affinity column. This activity was further purified by HPLC, and proteins in the bioactive fractions were analyzed by tandem electrospray mass spectrometry. Insulin-like growth factor-2 (IGF-2) was identified in these HPLC fractions, and the basophil-stimulating activity was inhibited by an anti-IGF-2-neutralizing Ab. Recombinant IGF-2 induced a substantial shape change response in basophils, but not eosinophils, neutrophils, or monocytes. IGF-2 stimulated chemokinesis of basophils, but not eosinophils or neutrophils, and synergized with eotaxin-1/CCL11 in basophil chemotaxis. IGF-2 also caused up-regulation of basophil CD11b expression and inhibited apoptosis, but did not stimulate degranulation or Ca2+ flux. Recombinant IGF-1 exhibited similar basophil-selective effects as IGF-2, and both growth factors were detected in nasal polyp extracts by ELISA. This is the first demonstration of chemokinetic factors that increase the motility of basophils, but do not act on other granulocytes or monocytes. IGF-1 and IGF-2 could play a role in the selective recruitment of basophils in vivo.

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Section: Identification Of Selective Basophil Chemoattractants Inmentioning

confidence: 99%

Identification of Selective Basophil Chemoattractants in Human Nasal Polyps as Insulin-Like Growth Factor-1 and Insulin-Like Growth Factor-2

Hartnell

Heinemann

Conroy

et al. 2004

The Journal of Immunology

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“…These cells are directed by chemotactic factors, chemokines particularly, to sites of inflammation where they release proinflammatory mediators and toxic granule products. Although exceeded in numbers by eosinophils, basophils are a constituent of the cellular infiltrate in bronchial tissue of atopic asthmatic patients (4,5) and are further increased after allergen challenge (6). More prominently, basophils are a major constituent of the cellular infiltrate in the cutaneous late-phase reaction to allergens (6,7) and dominate some T cell-mediated delayed-type hypersensitivity responses, such as cutaneous basophil hypersensitivity (8), contact dermatitis (9,10), and late-phase IgG1- (11,12), IgE- (13), and other T cell-mediated responses (14,15).…”

Section: Basophil Responses To Chemokinesmentioning

confidence: 99%

“…Major phenotypic similarities with respect to the expression of chemokine receptors (CCR3 in particular) and adhesion molecules (28) by eosinophils and basophils suggest common pathways of recruitment. However, although there is growing evidence for a crucial role of CCR3 in allergy-related tissue eosinophilia (29 -33), the magnitude and kinetics of basophil influx after allergen challenge parallel neither eosinophil recruitment (6, 8 -11, 13-15, 32), nor generation of eotaxin or eotaxin-2 at the inflammatory site (6,32). Thus, the existence of basophil-specific chemoattractants or mechanisms of recruitment need to be given serious consideration.…”

Section: Basophil Responses To Chemokinesmentioning

confidence: 99%

“…Eosinophils dominate helminth responses (1) and allergen late phase responses (6,32), whereas basophils dominate cutaneous basophil reactions (8,(11)(12)(13)(14)(15) and tick (3), as well as contact dermatitis responses (9,10). Differential basophil signaling via sequential and cooperatively acting chemokines could be a mechanism explaining these in vivo differences.…”

Section: Cooperation Of Chemokine Receptor Signalingmentioning

confidence: 99%

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Basophil Responses to Chemokines Are Regulated by Both Sequential and Cooperative Receptor Signaling

Heinemann

Hartnell

Stubbs

et al. 2000

The Journal of Immunology

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To investigate human basophil responses to chemokines, we have developed a sensitive assay that uses flow cytometry to measure leukocyte shape change as a marker of cell responsiveness. PBMC were isolated from the blood of volunteers. Basophils were identified as a single population of cells that stained positive for IL-3Rα (CDw123) and negative for HLA-DR, and their increase in forward scatter (as a result of cell shape change) in response to chemokines was measured. Shape change responses of basophils to chemokines were highly reproducible, with a rank order of potency: monocyte chemoattractant protein (MCP) 4 (peak at <1 nM) ≥ eotaxin-2 = eotaxin-3 ≥ eotaxin > MCP-1 = MCP-3 > macrophage-inflammatory protein-1α > RANTES = MCP-2 = IL-8. The CCR4-selective ligand macrophage-derived chemokine did not elicit a response at concentrations up to 10 nM. Blocking mAbs to CCR2 and CCR3 demonstrated that responses to higher concentrations (>10 nM) of MCP-1 were mediated by CCR3 rather than CCR2, whereas MCP-4 exhibited a biphasic response consistent with sequential activation of CCR3 at lower concentrations and CCR2 at 10 nM MCP-4 and above. In contrast, responses to MCP-3 were blocked only in the presence of both mAbs, but not after pretreatment with either anti-CCR2 or anti-CCR3 mAb alone. These patterns of receptor usage were different from those seen for eosinophils and monocytes. We suggest that cooperation between CCRs might be a mechanism for preferential recruitment of basophils, as occurs in tissue hypersensitivity responses in vivo.

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“…During allergic inflammation, such as bronchial asthma and atopic dermatitis, basophils infiltrate into peripheral tissues. 16,17 Several lines of evidence have shown that basophils play a major role in allergic reactions and/or immune responses. 18 -21 Basophils initiate IgE-mediated, chronic, cutaneous allergic inflammation (IgE-CAI).…”

mentioning

confidence: 99%

FcεRI, but Not FcγR, Signals Induce Prostaglandin D2 and E2 Production from Basophils

Ugajin

Satoh

Kanamori

et al. 2011

The American Journal of Pathology

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Prostaglandin (PG) D2 and PGE2 are arachidonic acid metabolites that are generated though an isomerization reaction catalyzed by PG synthases. PGs have been implicated in immunologic reactions in addition to a wide range of physiological functions. It has long been thought that basophils, in contrast to mast cells, do not synthesize PGs, although they do release leukotrienes and platelet-activating factor. Here, we show that basophils function as a source of PGD2 and PGE2. In vitrocultured basophils from mouse bone marrow produced both PGD2 and PGE2 in response to IgE ؉ antigen (Ag), but not to IgG ؉ Ag. Release of PGs was almost completely abrogated in cultured basophils from FcR␥-chain ؊/؊ mice, indicating the involvement of Fc RI. Basophils freshly isolated from bone marrow cells (primary basophils) were also capable of secreting PGD2 and PGE2. Although the amount of PGD2 released from primary basophils was lower than that from mast cells, the capability of primary basophils to generate PGE2 was more potent than that of mast cells. Transcripts and proteins for both hematopoietic-type PGD synthase and PGE synthase were detected in basophils. In addition, human basophils, like mouse basophils, also produced PGD2 through IgE-mediated stimulation. Thus, basophils could be an important source of PGD2/ PGE2 and may contribute to allergic inflammation and immune responses. Prostaglandins, such as PGD2 and PGE2, are cyclooxygenase (COX) metabolites of arachidonic acids. They have a wide range of biological activities, including relaxation and contraction of smooth muscles, and modulation of neuronal activity. 1 PGD2 is principally produced by activated mast cells and, to a lesser extent, by T helper cell 2 (Th2) cells and dendritic cells 2-4 and exerts its effect through D prostanoid 5 and chemoattractant receptor-homologous molecule receptors expressed onTh2 lymphocytes (CRTH2). 6 A number of recent studies have shown that PGD2 is involved in inflammatory reactions. Mast cell-derived PGD2 suppresses IL-12 production by dendritic cells that induce Th2 responses in vivo. 7 PGD2 both activates and induces chemotaxis of Th2 cells, eosinophils, and basophils. 6 A large amount of PGD2 is detected in broncho-alveolar lavage fluid during allergen-induced airway inflammation. 8 Transgenic mice overexpressing human PGD synthase showed exacerbation of ovalbumin (OVA)-induced lung inflammation associated with pronounced eosinophilia and increased Th2 cytokine production. 9 In our previous studies, mice deficient in the CRTH2 gene were characterized by alleviated IgE-mediated cutaneous responses, contact hypersensitivity reactions, 10 and cedar pollen dermatitis. 11 However, PGE2 is produced by a variety of cells, including fibroblasts and macrophages, and exerts its effects via prostaglandin E2 (EP)1, EP2, EP3, and EP4 receptors. 12 PGE2 acts on T cells to enhance production of Th2-type cytokines and to inhibit production of Th1 cytokines in vitro, 13 whereas another study showed that PGE2 facilitates Th1 differentiation via EP...

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Basophils, eosinophils, and mast cells in atopic and nonatopic asthma and in late-phase allergic reactions in the lung and skin

Cited by 169 publications

References 29 publications

Identification of Selective Basophil Chemoattractants in Human Nasal Polyps as Insulin-Like Growth Factor-1 and Insulin-Like Growth Factor-2

Identification of Selective Basophil Chemoattractants in Human Nasal Polyps as Insulin-Like Growth Factor-1 and Insulin-Like Growth Factor-2

Basophil Responses to Chemokines Are Regulated by Both Sequential and Cooperative Receptor Signaling

FcεRI, but Not FcγR, Signals Induce Prostaglandin D2 and E2 Production from Basophils

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