Real-time differential tracking of human neutrophil and eosinophil migration in vivo

Lukawska, Joanna; Livieratos, Lefteris; Sawyer, B.; Lee, Tak H.; O’Doherty, Michael; Blower, Philip J.; Kofi, M.; Ballinger, James R.; Corrigan, Christopher; Gnanasegaran, Gopinath; Sharif‐Paghaleh, Ehsan; Mullen, Gregory

doi:10.1016/j.jaci.2013.06.031

Cited by 31 publications

(42 citation statements)

References 26 publications

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“…115 Sorely needed are ways of detecting organ-specific disease activity, such as the “string test” in EoE 116 and nuclear medicine-based scans of eosinophil trafficking and accumulation. 117–119 Reliable biomarkers of disease activity, remission and drug responsiveness other than blood eosinophil counts would improve disease management, including confidence and safety during tapering of treatment. 120, 121 Examples of such biomarkers might include the presence of an activated eosinophil surface phenotype as detected by flow cytometry, 122, 123 , and a variety of measurements in biological fluids such as serum periostin in IL-13-driven asthma; 124, 125 serum CCL17 in HES and atopic dermatitits; 29, 126 serum levels of soluble receptors such as for IL-5, EMR1 and Siglec-8 in various forms of HES; 16, 121, 127 and detection of EPX in biological fluids.…”

Section: Novel Therapies That May Indirectly Affect Eosinophils That mentioning

confidence: 99%

Novel Therapies for Eosinophilic Disorders

Bochner¹

2015

Immunology and Allergy Clinics of North America

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Synopsis Current therapies for eosinophilic disorders are limited. Most treatment approaches remain empirical, are not supported by data from controlled clinical trials, involve the off-label use of agents developed for treatment of other diseases, and tend to rely heavily on the use of glucocorticoids and other agents with significant toxicity. Also lacking are validated outcome metrics and clinically relevant biomarkers to help guide treatment choices, efficacy and assessment of disease activity. Over the last decade, great progress has been made in the discovery, preclinical development and clinical testing of a variety of biologics and small molecules that have the potential to directly or indirectly influence eosinophils, eosinophilic inflammation and the consequences of eosinophil activation. Particularly advanced are studies with biologics that target eosinophil-selective cytokines and their receptors. In addition, other therapies that have received FDA approval in recent years for non-eosinophil-related indications can be considered for testing in eosinophilic disorders. Overall, the landscape of therapeutic options for those suffering from eosinophilic disorders has never been brighter, with many new choices on the horizon.

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Section: Novel Therapies That May Indirectly Affect Eosinophils That mentioning

confidence: 99%

Novel Therapies for Eosinophilic Disorders

Bochner¹

2015

Immunology and Allergy Clinics of North America

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“…Although ROS production by neutrophils of asthmatics has been previously described (Kanazawa et al, 1991;Lavinskiene, 2012;Sartorelli et al, 2009;Teramoto et al, 1996), these studies utilized the Percoll or Ficoll gradients for separating neutrophils from peripheral blood -techniques that are known to cause a spontaneous activation of neutrophils (Kolaczkowska & Kubes, 2013;Lukawska et al, 2014) and therefore could affect ROS production. To date, no studies are available in the literature on the increased ROS production or elevated digestive activity exhibited by neutrophils isolated from peripheral blood of patients with allergic asthma using spontaneous sedimentation method that does not promote the unspecific cellular priming.…”

Section: Discussionmentioning

confidence: 99%

Chemotactic and Phagocytic Activity of Blood Neutrophils in Allergic Asthma

Mosca

Menezes

Silva

et al. 2015

Immunological Investigations

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Allergic asthma is a chronic inflammatory airway disease, and has been considered a T helper-2-biased response. Studies suggest that neutrophils may be associated with exacerbation and asthma severity. We sought to evaluate the chemotactic activity and phagocytic capacity by peripheral blood neutrophils from individuals with controlled and uncontrolled allergic asthma, and compare the results with non-asthmatic controls groups. Blood neutrophils were isolated from 95 patients: 24 with controlled asthma, 24 uncontrolled asthma, 24 healthy subjects and 23 patients with IgE-mediated allergies other than asthma. The neutrophil chemotaxis, stimulated with LPS, autologous serum or homologous serum, was determined using Boyden chambers. The phagocytic capacity was assessed by ingestion of zimosan particles, and digestion phase was analyzed by NBT test. The phagocytic digestion phase and chemotaxis by neutrophils from asthmatic patients was higher than in non-asthmatic controls (p < 0.05). Autologous serum-induced neutrophil chemotaxis in patients with uncontrolled asthma was greater (p < 0.05) than in other study groups. The ingestion phase of phagocytosis showed similar values in asthmatics and non-asthmatics. We conclude that the blood neutrophil from controlled and uncontrolled asthmatic patients exhibit activation markers, particularly phagocytic digestion and chemotactic activities.

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“…In in vitro conditions, blood eosinophils undergo spontaneous apoptosis in a few days but in a physiological situation they tend to migrate and accumulate into liver and spleen, where they are likely to live longer than a few days [12–15]. Apoptosis of eosinophils can be delayed or accelerated by various agents [14,15].…”

Section: Introductionmentioning

confidence: 99%

Mitochondria in the Center of Human Eosinophil Apoptosis and Survival

Ilmarinen

Moilanen

Kankaanranta

2014

IJMS

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Eosinophils are abundantly present in most phenotypes of asthma and they contribute to the maintenance and exacerbations of the disease. Regulators of eosinophil longevity play critical roles in determining whether eosinophils accumulate into the airways of asthmatics. Several cytokines enhance eosinophil survival promoting eosinophilic airway inflammation while for example glucocorticoids, the most important anti-inflammatory drugs used to treat asthma, promote the intrinsic pathway of eosinophil apoptosis and by this mechanism contribute to the resolution of eosinophilic airway inflammation. Mitochondria seem to play central roles in both intrinsic mitochondrion-centered and extrinsic receptor-mediated pathways of apoptosis in eosinophils. Mitochondria may also be important for survival signalling. In addition to glucocorticoids, another important agent that regulates human eosinophil longevity via mitochondrial route is nitric oxide, which is present in increased amounts in the airways of asthmatics. Nitric oxide seems to be able to trigger both survival and apoptosis in eosinophils. This review discusses the current evidence of the mechanisms of induced eosinophil apoptosis and survival focusing on the role of mitochondria and clinically relevant stimulants, such as glucocorticoids and nitric oxide.

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Real-time differential tracking of human neutrophil and eosinophil migration in vivo

Cited by 31 publications

References 26 publications

Novel Therapies for Eosinophilic Disorders

Novel Therapies for Eosinophilic Disorders

Chemotactic and Phagocytic Activity of Blood Neutrophils in Allergic Asthma

Mitochondria in the Center of Human Eosinophil Apoptosis and Survival

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