Mediators of inflammation in nasal lavage from aspirin intolerant patients after aspirin challenge

Kupczyk, Maciej; Kurmanowska, Zofia; Kupryś‐Lipińska, Izabela; Bocheńska-Marciniak, Małgorzata; Kuna, Piotr

doi:10.1016/j.rmed.2010.04.017

Cited by 35 publications

(27 citation statements)

References 25 publications

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“…Expression of alternatively spliced variants of COX-1 mRNA is increased and correlates with aspirin-triggered 15-HETE generation (49). Furthermore, MCP-3 and RANTES are overproduced in AERD (50). In addition, bronchial challenge with aspirin involves systemic reactions and is associated with the mobilization of leukocyte and eosinophil progenitor cells from the bone marrow (51).…”

Section: Aspirin-intolerant Asthmamentioning

confidence: 99%

Untangling asthma phenotypes and endotypes

Agache

Akdiş

Jutel

et al. 2012

Allergy

292

235

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Asthma phenotypes have been developed to address the complexities of the disease. However, owing to a lack of longitudinal studies, little is known about the onset as well as the stability of phenotypes. Distinguishing phenotypes with regard to the severity or duration of the disease is essential. A phenotype covers the clinically relevant properties of the disease, but does not show the direct relationship to disease etiology and pathophysiology. Different pathogenetic mechanisms might cause similar asthma symptoms and might be operant in a certain phenotype. These putative mechanisms are addressed by the term 'endotype'. Classification of asthma based on endotypes provides advantages for epidemiological, genetic, and drug-related studies. A successful definition of endotypes should link key pathogenic mechanisms with the asthma phenotype. Thus, the identification of corresponding molecular biomarkers for individual pathogenic mechanism underlying phenotypes or subgroups within a phenotype is important. Whether newly defined asthma endotypes predict the individual course of asthma has to be validated in longitudinal studies. The accurate endotyping reflects natural history of asthma and should help to predict treatment response. Thus, understanding asthma endotypes might be useful in clinical practice.

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Section: Aspirin-intolerant Asthmamentioning

confidence: 99%

Untangling asthma phenotypes and endotypes

Agache

Akdiş

Jutel

et al. 2012

Allergy

292

235

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“…at the protein level, CCL5/RANTES and CCL7/MCP3 were found significantly elevated in nasal lavages from patients with AERD in comparison with patients with Aspirin-tolerant asthma (ATA) [7].…”

mentioning

confidence: 99%

CCL4 Levels Differ between Aspirin-Tolerant and Aspirin-Intolerant Patients with Asthma

Velázquez¹,

Soid-Raggi²,

Terán³

et al. 2017

Health

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Aspirin-exacerbated respiratory disease (AERD) is an asthma phenotype characterized by nasal polyps, chronic hypertrophic eosinophilic sinusitis, asthma, and sensitivity to aspirin. Unawareness of this disease by patients and their physicians may have serious consequences because of the risk of near-fatal asthma. Its confirmative diagnosis can be established only by provocative aspirin challenge, which represents a potential risk for patient health. Purpose: Because CCL4 plays an important role in several pulmonary conditions, we tested its immunoreactivity in nasal lavages and sera from control subjects, and from aspirin-sensitive and non-aspirin-sensitive patients. Method: Immunoreactivity of CCL4 was measured in serum and nasal lavages from 30 healthy controls (HC), 23 patients with AERD, and 20 patients with aspirin-tolerant asthma (ATA). Additionally, a serum biobank contained sera from 90 HC, 83 patients with AERD, and 69 patients with ATA was employed. Results: The serum immunoreactivity of CCL4 could distinguish both types of asthma phenotypes. Conclusion: CCL4 may play an unexpected role in thephysiopathology of AERD.

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“…CCL7 was shown to activate monocytes, basophils, and eosinophils, and it acts as a chemoattractant for a variety of cells, including those associated with allergy (e.g., monocytes, memory T lymphocytes, eosinophils, basophils, dendritic cells, and NK cells) (28)(29)(30). CCL7 was further linked to the pathology of a variety of allergic and inflammatory disease, including asthma (31,32), airway inflammation in response to oxidative stress (33), aspirin allergy (34), and allergic rhinitis (35). CCL7 production is increased in mice that develop allergic lung inflammation in response to Arizona sand dust (36) and in mice challenged with respiratory allergens (37).…”

mentioning

confidence: 99%

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Kuo

Collins

Boettner

et al. 2017

The Journal of Immunology

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Molecules that are necessary for ocular hypersensitivity reactions include the receptors CCR1 and CCR3; CCL7 is a ligand for these receptors. Therefore, we explored the role of CCL7 in mast cell activity and motility in vitro and investigated the requirement for CCL7 in a murine model of IgE-mediated allergic conjunctivitis. For mast cells treated with IgE and Ag, the presence of CCL7 synergistically enhanced degranulation and calcium influx. CCL7 also induced chemotaxis in mast cells. CCL7-deficient bone marrow–derived mast cells showed decreased degranulation following IgE and Ag treatment compared with wild-type bone marrow–derived mast cells, but there was no difference in degranulation when cells were activated via an IgE-independent pathway. In vivo, CCL7 was upregulated in conjunctival tissue during an OVA-induced allergic response. Notably, the early-phase clinical symptoms in the conjunctiva after OVA challenge were significantly higher in OVA-sensitized wild-type mice than in control challenged wild-type mice; the increase was suppressed in CCL7-deficient mice. In the OVA-induced allergic response, the numbers of conjunctival mast cells were lower in CCL7-deficient mice than in wild-type mice. Our results demonstrate that CCL7 is required for maximal OVA-induced ocular anaphylaxis, mast cell recruitment in vivo, and maximal FcεRI-mediated mast cell activation in vitro. A better understanding of the role of CCL7 in mediating ocular hypersensitivity reactions will provide insights into mast cell function and novel treatments for allergic ocular diseases.

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Mediators of inflammation in nasal lavage from aspirin intolerant patients after aspirin challenge

Cited by 35 publications

References 25 publications

Untangling asthma phenotypes and endotypes

Untangling asthma phenotypes and endotypes

CCL4 Levels Differ between Aspirin-Tolerant and Aspirin-Intolerant Patients with Asthma

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

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