Eotaxin-3 is involved in Churg-Strauss syndrome - a serum marker closely correlating with disease activity

Polzer, K; Karonitsch, Thomas; Neumann, Thomas; Eger, G.; Haberler, Christine; Soleiman, Aron; Hellmich, Bernhard; Csernok, Elena; Distler, Jörg H W; Manger, Bernhard; Redlich, Kurt; Schett, Georg; Zwerina, Jochen

doi:10.1093/rheumatology/ken033

Cited by 102 publications

(63 citation statements)

References 25 publications

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“…Eosinophil depletion with anti-IL-5 monoclonal antibodies has shown promising preliminary results in treating CSS, emphasizing the mechanistic importance of IL-5 in the disorder (82). Circulating biomarkers of CSS include IL-25 and the chemokines eotaxin-3 (CCL26) and TARC (thymus and activation-regulated chemokine; also called CCL17), suggesting a potential role for these proteins in CSS pathogenesis (34,146,189,221). Several medications used in the treatment of asthma, including leukotriene modifiers, inhaled corticosteroids, and omalizumab, have been associated with the development of CSS (95,(204)(205)(206).…”

Section: Cssmentioning

confidence: 99%

Eosinophilic Pneumonias

2012

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SUMMARY This review starts with discussions of several infectious causes of eosinophilic pneumonia, which are almost exclusively parasitic in nature. Pulmonary infections due specifically to Ascaris , hookworms, Strongyloides , Paragonimus , filariasis, and Toxocara are considered in detail. The discussion then moves to noninfectious causes of eosinophilic pulmonary infiltration, including allergic sensitization to Aspergillus , acute and chronic eosinophilic pneumonias, Churg-Strauss syndrome, hypereosinophilic syndromes, and pulmonary eosinophilia due to exposure to specific medications or toxins.

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Section: Cssmentioning

confidence: 99%

Eosinophilic Pneumonias

2012

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“…In a recent study comparing patients with EGPA ANCA-negative and HES FIP1L1-PDGFRA-negative, none of the analyzed serum biomarkers (sIL2R, IL-5, IL-6, IL-8, IL-10, CCL17, eotaxin-1) could differentiate between the two groups of patients [80]. As previously mentioned, eotaxin-3 could differentiate active EGPA from various forms of HES, as well as from other allergic or immune diseases associated with eosinophilia [11,82].…”

Section: Hypereosinophilic Syndrome (Hes)mentioning

confidence: 90%

Churg-Strauss Syndrome or Eosinophilic Granulomatosis with Polyangiitis

et al. 2015

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Eosinophilic granulomatosis with polyangiitis (Churg-Strauss, EGPA) is a systemic small-to-medium-sized vasculitis associated with asthma and eosinophilia. Histologically EGPA presents tissue eosinophilia, necrotizing vasculitis, and granulomatous inflammation with eosinophil tissue infiltration. EGPA commonly involves the upper airway and lung parenchyma, peripheral neuropathy, cardiac disorders, and skin lesions. The anti-neutrophil cytoplasmic antibodies (ANCA) are positive in 40% of cases, especially in those patients with clinical signs of vasculitis. The pathogenesis of EGPA is multifactorial. The disease can be triggered by exposure to a variety of allergens and drugs, but a genetic background has also been described, particularly an association with HLA-DRB4. Th2 response is of special importance in the upregulation of different interleukins such as IL-4, IL-13, and IL-5. Th1 and Th17 responses are also of significance. Activated eosinophils have a prolonged survival and probably cause tissue damage by releasing eosinophil granule proteins, while their tissue recruitment can be regulated by chemokines such as eotaxin-3 and CCL17. Humoral immunity is also OPEN ACCESSSinusitis 2016, 1 25 abnormally regulated, as demonstrated by excessive responses of IgG4 and IgE. EGPA has a good respond to glucocorticoids, although the combination of glucocorticoids and immunosuppressants (e.g., cyclophosphamide, azathioprine) is needed in most of cases. Newer treatment options include anti-IL-5 antibodies (mepolizumab), whose efficacy has been described in clinical trials, and anti-CD-20, a B cell-depleting agent (rituximab), reported in several case series.

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“…Eotaxin-3 is an eotactic chemokine that induces chemotaxis and activation of eosinophilic granulocytes in vitro, and may be involved in the pathogenesis of EGPA. Polzer, et al suggested that elevated eotaxin-3 expression was associated with high disease activity in EGPA 6 , while Dejaco, et al proposed that eotaxin-3 levels could not reliably discriminate between active and inactive disease in established EGPA 7 . In our current study, we investigated the clinical utility of eotaxin-3 as a possible biomarker of EGPA relapse.…”

Section: To the Editormentioning

confidence: 99%

“…Worsening asthma and/or rhinosinusitis without other organ involvement was not sufficient to classify a patient as having active EGPA. Serum eotaxin-3 and interleukin (IL)-6 were analyzed by ELISA (R&D Systems) 6 . Laboratory variables were compared using the Mann-Whitney U test.…”

Section: To the Editormentioning

confidence: 99%