Airway epithelial cells promote transmigration of eosinophils in a new three‐dimensional chemotaxis model

Kato, Yoshiko; Fujisawa, Takao; Shibano, Michiko; Saito, Takuya; Gatto, W.; Kamiya, Hitoshi; Hirai, Koichi; Sumida, Michihiro; Yoshie, Osamu

doi:10.1046/j.1365-2222.2002.01362.x

Cited by 17 publications

(9 citation statements)

References 44 publications

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“…A similar function has also been suggested for Fc mediated binding [34]. Epithelial cells may further facilitate a luminal influx leukocytes through release of migrationpromoting matrix proteins, as recently demonstrated in a three-dimensional chemotaxis model [35].…”

Section: Mechanisms Of Transepithelial Migrationsupporting

confidence: 60%

“…basal to luminal) migration of granulocytes come from in vitro experiments using cultured epithelial cells. Eotaxin, PAF, and C5a are examples of factors that have been implicated in transepithelial migration of eosinophils [35][36][37]. Similarly, luminal migration of neutrophils in vitro is promoted by mediators like IL-8, fMLP, LTB 4 and PAF [31,33,38,39].…”

Section: Mechanisms Of Transepithelial Migrationmentioning

confidence: 99%

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Transepithelial Migration, Necrosis and Apoptosis as Silent and Pro- Inflammatory Fates of Airway Granulocytes

Erjefält

2005

CDTIA

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In inflammatory airway diseases, granulocytes such as eosinophils and neutrophils infiltrate the tissue where they are thought to exert pathogenic activities. To avoid a catastrophic accumulation of activated granulocytes, their recruitment must be balanced by efficient cell clearance mechanisms. In this regard, the focus has been on elimination through apoptosis and subsequent engulfment of apoptotic cells by phagocytes. However, novel data suggest that in the airways, powerful non-apoptotic mechanisms are also critically involved in cell clearance. One such mechanism is transepithelial migration into the airway lumen where the mucociliary escalator executes the final elimination. The physiological clearance of tissue granulocytes is normally silent, but can under certain situations shift to become a pro-inflammatory event. For example, apoptotic cells that escape phagocytosis, disintegrate in a pro-inflammatory process called secondary necrosis. In other situations, granulocytes are triggered to undergo an active and violent cytolytic death. This delicate balance in vivo, between silent and violent properties of granulocyte demise, complicates the design of pro-apoptotic pharmacological interventions. On the other hand, this insight may also open possibilities to new exciting treatment strategies. In this context, promoting transepithelial migration, prevention of secondary necrosis, and boosting the macrophage phagocytic system appear as exciting treatment avenues.

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Section: Mechanisms Of Transepithelial Migrationsupporting

confidence: 60%

Section: Mechanisms Of Transepithelial Migrationmentioning

confidence: 99%

Transepithelial Migration, Necrosis and Apoptosis as Silent and Pro- Inflammatory Fates of Airway Granulocytes

Erjefält

2005

CDTIA

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“…Lumen levels of CCL11 may contribute to non-injurious loss of airway wall eosinophils,54 55 and tumour necrosis factor α (TNFα) may promote transmigration of both eosinophils and neutrophils 55. It is widely assumed that the clearance of CCR7+ memory and effector lymphocytes from inflamed airway tissues involves apoptosis, thus ‘ignoring a potentially very important exit pathway across the bronchial epithelial barrier’ according to Porter and colleagues 52 56.…”

Section: Mechanisms Involved In Transepithelial Egressionmentioning

confidence: 99%

Transepithelial exit of leucocytes: inflicting, reflecting or resolving airway inflammation?

Persson

Uller

2010

Thorax

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“…These therapies include CC chemokine receptor 3 antagonists; anti-chemokine (eotaxin) antibodies [121,122]; antagonists against the Th2 cytokines IL-4 and IL-13, which play important roles in the development of airway inflammation [123], and immune-suppressive agents [18]. …”

Section: Resultsmentioning

confidence: 99%

Evidence-Based Management of Nasal Polyposis by Intranasal Corticosteroids: From the Cause to the Clinic

Bachert¹

2011

Int Arch Allergy Immunol

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Background: Nasal polyposis is an inflammatory disorder involving the mucosa of the nose and paranasal sinuses and affecting approximately 2–4% of the general population. Methods: A literature search of Medline and Embase was conducted to obtain an overview of the epidemiology, pathophysiology, and current treatment of nasal polyposis, focusing on evidence-based efficacy of intranasal corticosteroids (INSs) as primary and postoperative therapy. Recent research on INSs in nasal polyp treatment, along with notable historic findings, was reviewed. Results: Nasal polyps are mostly characterized by eosinophil infiltration, a complex inflammation of nasal mucosa, and possibly production of polyclonal IgE. Current treatment modalities include INSs, oral corticosteroids, and surgery; surgery is generally limited to those with an insufficient response to medical treatment. Because of their effects on eosinophil-dominated inflammation, INSs and oral corticosteroids are the primary medical treatment strategies. The very low (≤1%) systemic bioavailability of newer INSs minimizes the systemic adverse effects seen with oral corticosteroids. Conclusion:Based on randomized, controlled trials, guidelines recommend INSs as first-line therapy for nasal polyps and for care after polypectomy. Clinical data suggest INSs are effective in reducing polyp size and relieving nasal symptoms. INS treatment has also reduced nasal polyp recurrence in patients undergoing functional endoscopic sinus surgery. Treatment with these mainstay options has been found to improve quality of life, which, along with symptom improvement, is a key factor in disease treatment.

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Airway epithelial cells promote transmigration of eosinophils in a new three‐dimensional chemotaxis model

Cited by 17 publications

References 44 publications

Transepithelial Migration, Necrosis and Apoptosis as Silent and Pro- Inflammatory Fates of Airway Granulocytes

Transepithelial Migration, Necrosis and Apoptosis as Silent and Pro- Inflammatory Fates of Airway Granulocytes

Transepithelial exit of leucocytes: inflicting, reflecting or resolving airway inflammation?

Evidence-Based Management of Nasal Polyposis by Intranasal Corticosteroids: From the Cause to the Clinic

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