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Depletion of Spleen Macrophages Delays AA Amyloid Development: A Study Performed in the Rapid Mouse Model of AA Amyloidosis
Linköping University, Department of Clinical and Experimental Medicine, Division of Inflammation Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Diagnostics, Department of Clinical Pathology and Clinical Genetics.
Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
Uppsala University, Sweden .
2013 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 8, no 11, e79104- p.Article in journal (Refereed) Published
Abstract [en]

AA amyloidosis is a systemic disease that develops secondary to chronic inflammatory diseases Macrophages are often found in the vicinity of amyloid deposits and considered to play a role in both formation and degradation of amyloid fibrils. In spleen reside at least three types of macrophages, red pulp macrophages (RPM), marginal zone macrophages (MZM), metallophilic marginal zone macrophages (MMZM). MMZM and MZM are located in the marginal zone and express a unique collection of scavenger receptors that are involved in the uptake of blood-born particles. The murine AA amyloid model that resembles the human form of the disease has been used to study amyloid effects on different macrophage populations. Amyloid was induced by intravenous injection of amyloid enhancing factor and subcutaneous injections of silver nitrate and macrophages were identified with specific antibodies. We show that MZMs are highly sensitive to amyloid and decrease in number progressively with increasing amyloid load. Total area of MMZMs is unaffected by amyloid but cells are activated and migrate into the white pulp. In a group of mice spleen macrophages were depleted by an intravenous injection of clodronate filled liposomes. Subsequent injections of AEF and silver nitrate showed a sustained amyloid development. RPMs that constitute the majority of macrophages in spleen, appear insensitive to amyloid and do not participate in amyloid formation.

Place, publisher, year, edition, pages
Public Library of Science , 2013. Vol. 8, no 11, e79104- p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-102982DOI: 10.1371/journal.pone.0079104ISI: 000327254700092OAI: oai:DiVA.org:liu-102982DiVA: diva2:685448
Note

Funding Agencies|Swedish Research Council|GTW5343|County Council of Ostergotland Magnus Bergvalls research foundation||Ingrid Svenssons research foundation||Broderna Karlssons research foundation||Hildur Pettersons research foundation||

Available from: 2014-01-09 Created: 2014-01-09 Last updated: 2017-12-06

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Lundmark, KatarzynaVahdat Shariatpanahi, Aida

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