Adhesion molecules and their ligands in nasal polyps of aspirin-hypersensitive patients

Kupczyk, Maciej; Kupryś, Izabela; Danilewicz, Marian; Bocheńska-Marciniak, Małgorzata; Murlewska, A; Górski, Paweł; Kuna, Piotr

doi:10.1016/s1081-1206(10)61048-4

Cited by 11 publications

(6 citation statements)

References 28 publications

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“…In our study we found that AIA patients have diminished ability to synthesize LXs in vivo after exposure to ASA. Lack of LXs may results in impairment of healing processes thus leading to the development of vicious circle of persistent inflammation which may in part explain our clinical observations that aspirin sensitivity syndrome is characterized by chronic inflammation in the airways even in subjects avoiding triggering factors such as ASA and other NSAIDs (17, 18). Clinically positive allergen challenge had no impact on LXs levels in atopic patients.…”

Section: Discussionmentioning

confidence: 88%

Lipoxin A₄ generation is decreased in aspirin‐sensitive patients in lysine‐aspirin nasal challenge in vivo model

Kupczyk¹,

Antczak

Kupryś‐Lipińska³

et al. 2009

Allergy

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Section: Discussionmentioning

confidence: 88%

Lipoxin A₄ generation is decreased in aspirin‐sensitive patients in lysine‐aspirin nasal challenge in vivo model

Kupczyk¹,

Antczak

Kupryś‐Lipińska³

et al. 2009

Allergy

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“…5 However, it is still unclear why in the airways of ASA intolerant patients despite avoiding triggering factors, like ASA and other NSAIDs, we can still find signs of persistent, severe inflammation with marked eosinophilia, epithelial disruption, cytokine production and upregulation of several adhesion molecules. 6,7 The goal of our study was to evaluate levels of several proinflammatory mediators, including MCP-3, RANTES, eotaxin, Il-5 and Il-3 in nasal lavage fluid from AIA patients in nasal lysineeaspirin (LyseASA) challenge in vivo model. The results of such tests should add to our understanding of chronic inflammation in ASA intolerance.…”

Section: Introductionmentioning

confidence: 99%

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

Kupczyk

Kurmanowska

Kupryś‐Lipińska

et al. 2010

Respiratory Medicine

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The pathogenetic mechanisms underlying development of persistent inflammation in aspirin (ASA) intolerance are not fully understood. The aim of this study was to determine levels of MCP-3, RANTES, eotaxin, Il-5 and Il-3 in aspirin intolerant asthmatics (AIA) after nasal lysine-aspirin (Lys-ASA) challenge. Twenty AIA and 10 aspirin tolerant controls (ATC) were challenged with saline or 14.4mg of Lys-ASA. Lys-ASA challenge induced clinical symptoms and influx of eosinophils and basophils only in AIA group. Statistically significant higher levels of MCP-3 and RANTES were found in lavages from AIA as compared with ATC (p<0.05 in all time points). Before challenge the average level of MCP-3 was 86.95pg/ml in AIA and 47.61pg/ml in ATC, RANTES levels were 34.20pg/ml in AIA and 17.21pg/ml in ATC and did not change after the challenge in both group. The mean eotaxin's level was 11.01pg/ml in AIA and 8.03pg/ml in ATC before and increased to 20.06, 26.22pg/ml (4 and 24h in AIA) as compared to 10.51, 14.76pg/ml (4 and 24h in ATC) after the challenge (p<0.05). Interleukin-3 and Il-5 were not detectable. The highest inhibition of eosinophils' chemotaxis was induced by anti-eotaxin (47% of inhibition), followed by anti-RANTES (29%), anti-MCP-3 (19%) and anti-Il-5 (9%). In summary, we found that persistent inflammation in AIA patients is characterized by overproduction of MCP-3 and RANTES. Lack of increase in MCP-3 and RANTES levels after Lys-ASA challenge suggest that those mediators are involved in chronic rather than acute phase of ASA induced inflammation.

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“…There is also locally an increase in the oxidative metabolism of these Eo . In addition, adhesion molecules, such as vascular cell adhesion molecule 1 (VCAM‐1), lymphocyte‐associated antigen 1 (LFA‐1), and intracellular adhesion molecule 1 (ICAM‐1), have demonstrated importance in local recruitment of cells …”

mentioning

confidence: 99%

Activation state of circulating eosinophils in nasal polyposis

Dupuch¹,

Tridon

Ughetto

et al. 2018

Int Forum Allergy Rhinol

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This study demonstrates a priming state of circulating eosinophils in CRSwNP patients when compared with healthy controls, as evidenced by the extent of oxidative metabolism, with increased sensitivity to IL-5 and by the observed variations of percent and MFI of CD49d, CCR3, and CD25. This priming is thus found at the peripheral level and occurs before the migration of eosinophils to polyps, reflecting the systemic and not just local nature of abnormalities in CRSwNP.

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Adhesion molecules and their ligands in nasal polyps of aspirin-hypersensitive patients

Cited by 11 publications

References 28 publications

Lipoxin A₄ generation is decreased in aspirin‐sensitive patients in lysine‐aspirin nasal challenge in vivo model

Lipoxin A₄ generation is decreased in aspirin‐sensitive patients in lysine‐aspirin nasal challenge in vivo model

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

Activation state of circulating eosinophils in nasal polyposis

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Adhesion molecules and their ligands in nasal polyps of aspirin-hypersensitive patients

Cited by 11 publications

References 28 publications

Lipoxin A4 generation is decreased in aspirin‐sensitive patients in lysine‐aspirin nasal challenge in vivo model

Lipoxin A4 generation is decreased in aspirin‐sensitive patients in lysine‐aspirin nasal challenge in vivo model

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

Activation state of circulating eosinophils in nasal polyposis

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Lipoxin A₄ generation is decreased in aspirin‐sensitive patients in lysine‐aspirin nasal challenge in vivo model

Lipoxin A₄ generation is decreased in aspirin‐sensitive patients in lysine‐aspirin nasal challenge in vivo model