Development of pro-inflammatory phenotype in monocytes after engulfing Hb-activated platelets in hemolytic disorders

Copyright © 2016 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 175(2017) vom: 07. Feb., Seite 133-142
1. Verfasser: Singhal, Rashi (VerfasserIn)
Weitere Verfasser: Chawla, Sheetal, Rathore, Deepak K, Bhasym, Angika, Annarapu, Gowtham K, Sharma, Vandana, Seth, Tulika, Guchhait, Prasenjit
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2017
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Coagulation and hemolytic disorders Hemoglobin Inflammation Monocytes Platelets Hemoglobins Interleukin-1beta Lipopolysaccharide Receptors mehr... Platelet Glycoprotein GPIb-IX Complex Receptors, IgG Tumor Necrosis Factor-alpha Interleukin-10 130068-27-8
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245 1 0 |a Development of pro-inflammatory phenotype in monocytes after engulfing Hb-activated platelets in hemolytic disorders 
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520 |a Monocytes and macrophage combat infections and maintain homeostatic balance by engulfing microbes and apoptotic cells, and releasing inflammatory cytokines. Studies have described that these cells develop anti-inflammatory properties upon recycling the free-hemoglobin (Hb) in hemolytic conditions. While investigating the phenotype of monocytes in two hemolytic disorders-paroxysmal nocturnal hemoglobinuria (PNH) and sickle cell disease (SCD), we observed a high number of pro-inflammatory (CD14+CD16hi) monocytes in these patients. We further investigated in vitro the phenotype of these monocytes and found an estimated 55% of CD14+ cells were transformed into the CD14+CD16hi subset after engulfing Hb-activated platelets. The CD14+CD16hi monocytes, which were positive for both intracellular Hb and CD42b (platelet marker), secreted significant amounts of TNF-α and IL-1β, unlike monocytes treated with only free Hb, which secreted more IL-10. We have shown recently the presence of a high number of Hb-bound hyperactive platelets in patients with both diseases, and further investigated if the monocytes engulfed these activated platelets in vivo. As expected, we found 95% of CD14+CD16hi monocytes with both intracellular Hb and CD42b in both diseases, and they expressed high TNF-α. Furthermore our data showed that these monocytes whether from patients or developed in vitro after treatment with Hb-activated platelets, secreted significant amounts of tissue factor. Besides, these CD14+CD16hi monocytes displayed significantly decreased phagocytosis of E. coli. Our study therefore suggests that this alteration of monocyte phenotype may play a role in the increased propensity to pro-inflammatory/coagulant complications observed in these hemolytic disorders-PNH and SCD 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 4 |a Coagulation and hemolytic disorders 
650 4 |a Hemoglobin 
650 4 |a Inflammation 
650 4 |a Monocytes 
650 4 |a Platelets 
650 7 |a Hemoglobins  |2 NLM 
650 7 |a Interleukin-1beta  |2 NLM 
650 7 |a Lipopolysaccharide Receptors  |2 NLM 
650 7 |a Platelet Glycoprotein GPIb-IX Complex  |2 NLM 
650 7 |a Receptors, IgG  |2 NLM 
650 7 |a Tumor Necrosis Factor-alpha  |2 NLM 
650 7 |a Interleukin-10  |2 NLM 
650 7 |a 130068-27-8  |2 NLM 
700 1 |a Chawla, Sheetal  |e verfasserin  |4 aut 
700 1 |a Rathore, Deepak K  |e verfasserin  |4 aut 
700 1 |a Bhasym, Angika  |e verfasserin  |4 aut 
700 1 |a Annarapu, Gowtham K  |e verfasserin  |4 aut 
700 1 |a Sharma, Vandana  |e verfasserin  |4 aut 
700 1 |a Seth, Tulika  |e verfasserin  |4 aut 
700 1 |a Guchhait, Prasenjit  |e verfasserin  |4 aut 
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