Skip to main content
Erschienen in: Inflammation 5/2017

04.02.2017 | LETTER TO THE EDITOR

Comment on “Potential Effects of Calcium Binding Protein S100A12 on Severity Evaluation and Curative Effect of Severe Acute Pancreatitis”

verfasst von: Vahid Bagheri, Carolyn L. Geczy

Erschienen in: Inflammation | Ausgabe 5/2017

Einloggen, um Zugang zu erhalten

Excerpt

Feng and colleagues recently investigated the role of the calcium binding protein, S100A12, in severe acute pancreatitis. They reported that this is induced by caerulein and lipopolysaccharide in mice and anti-recombinant S100A12 antibodies decreased severity [1]. They suggest that “S100A12 is a mediator, not a marker, of acute pancreatitis” and that inhibiting it may represent a novel therapeutic approach. Based on reagents used in this study (antibodies raised against human recombinant S100A12 as immunogen) and strong evidence for the absence of S100A12 in the mouse genome [2, 3], we found that conclusions drawn from this publication are misleading. …
Literatur
1.
Zurück zum Zitat Feng, Z., Z. Yinchu, S. Yinsheng, W. Fengqing, Z. Xiaoyang, L. Jin, and G. Xiaofei. 2015. Potential effects of calcium binding protein S100A12 on severity evaluation and curative effect of severe acute pancreatitis. Inflammation 38(1): 290–297.CrossRefPubMed Feng, Z., Z. Yinchu, S. Yinsheng, W. Fengqing, Z. Xiaoyang, L. Jin, and G. Xiaofei. 2015. Potential effects of calcium binding protein S100A12 on severity evaluation and curative effect of severe acute pancreatitis. Inflammation 38(1): 290–297.CrossRefPubMed
2.
Zurück zum Zitat Fuellen, G., D. Foell, W. Nacken, C. Sorg, and C. Kerkhoff. 2003. Absence of S100A12 in mouse: implications for RAGE-S100A12 interaction. Trends in Immunology 24(12): 622–623.CrossRefPubMed Fuellen, G., D. Foell, W. Nacken, C. Sorg, and C. Kerkhoff. 2003. Absence of S100A12 in mouse: implications for RAGE-S100A12 interaction. Trends in Immunology 24(12): 622–623.CrossRefPubMed
3.
Zurück zum Zitat Ravasi, T., K. Hsu, J. Goyette, K. Schroder, Z. Yang, F. Rahimi, L.P. Miranda, P.F. Alewood, D.A. Hume, and C. Geczy. 2004. Probing the S100 protein family through genomic and functional analysis. Genomics 84(1): 10–22.CrossRefPubMed Ravasi, T., K. Hsu, J. Goyette, K. Schroder, Z. Yang, F. Rahimi, L.P. Miranda, P.F. Alewood, D.A. Hume, and C. Geczy. 2004. Probing the S100 protein family through genomic and functional analysis. Genomics 84(1): 10–22.CrossRefPubMed
4.
Zurück zum Zitat Yan, W.X., C. Armishaw, J. Goyette, Z. Yang, H. Cai, P. Alewood, and C.L. Geczy. 2008. Mast cell and monocyte recruitment by S100A12 and its hinge domain. Journal of Biological Chemistry 283(19): 13035–13043.CrossRefPubMed Yan, W.X., C. Armishaw, J. Goyette, Z. Yang, H. Cai, P. Alewood, and C.L. Geczy. 2008. Mast cell and monocyte recruitment by S100A12 and its hinge domain. Journal of Biological Chemistry 283(19): 13035–13043.CrossRefPubMed
5.
Zurück zum Zitat Bowman, M.H., J. Wilk, A. Heydemann, G. Kim, J. Rehman, J.A. Lodato, J. Raman, and E.M. McNally. 2010. S100A12 mediates aortic wall remodeling and aortic aneurysm. Circulation Research 106(1): 145–154.CrossRef Bowman, M.H., J. Wilk, A. Heydemann, G. Kim, J. Rehman, J.A. Lodato, J. Raman, and E.M. McNally. 2010. S100A12 mediates aortic wall remodeling and aortic aneurysm. Circulation Research 106(1): 145–154.CrossRef
6.
Zurück zum Zitat Bowman, H., A. Heydemann, J. Gawdzik, R.A. Shilling, and B. Camoretti‐Mercado. 2011. Transgenic expression of human S100A12 induces structural airway abnormalities and limited lung inflammation in a mouse model of allergic inflammation. Clinical & Experimental Allergy 41(6): 878–889.CrossRef Bowman, H., A. Heydemann, J. Gawdzik, R.A. Shilling, and B. Camoretti‐Mercado. 2011. Transgenic expression of human S100A12 induces structural airway abnormalities and limited lung inflammation in a mouse model of allergic inflammation. Clinical & Experimental Allergy 41(6): 878–889.CrossRef
7.
Zurück zum Zitat Yan, L., L. Mathew, B. Chellan, B. Gardner, J. Earley, T.S. Puri, and M.A.H. Bowman. 2014. S100/Calgranulin-mediated inflammation accelerates left ventricular hypertrophy and aortic valve sclerosis in chronic kidney disease in a receptor for advanced glycation end products–dependent manner. Arteriosclerosis, Thrombosis, and Vascular Biology 34(7): 1399–1411.CrossRefPubMedPubMedCentral Yan, L., L. Mathew, B. Chellan, B. Gardner, J. Earley, T.S. Puri, and M.A.H. Bowman. 2014. S100/Calgranulin-mediated inflammation accelerates left ventricular hypertrophy and aortic valve sclerosis in chronic kidney disease in a receptor for advanced glycation end products–dependent manner. Arteriosclerosis, Thrombosis, and Vascular Biology 34(7): 1399–1411.CrossRefPubMedPubMedCentral
Metadaten
Titel
Comment on “Potential Effects of Calcium Binding Protein S100A12 on Severity Evaluation and Curative Effect of Severe Acute Pancreatitis”
verfasst von
Vahid Bagheri
Carolyn L. Geczy
Publikationsdatum
04.02.2017
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 5/2017
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-017-0529-1

Weitere Artikel der Ausgabe 5/2017

Inflammation 5/2017 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.