TAILIEUCHUNG - Báo cáo khoa học: Phagocytosis of bacteria is enhanced in macrophages undergoing nutrient deprivation

Phagocytosis represents a mechanism used by macrophages to remove pathogens and cellular debris. Recent evidence suggests that phagocytosis is stimulated under specific conditions of stress, such as extracellular pres-sure and hypoxia. | ỊFEBS Journal Phagocytosis of bacteria is enhanced in macrophages undergoing nutrient deprivation Wim Martinet1 Dorien M. Schriivers1 Jean-Pierre Timmermans2 Arnold G. Herman1 and Guido R. Y. De Meyer1 1 Division of Pharmacology University of Antwerp Belgium 2 Laboratory of CellBiology and Histology University of Antwerp Belgium Keywords autophagy heterophagy p38 MAP kinase scavenger receptor A starvation Correspondence W. Martinet Division of Pharmacology University of Antwerp Universiteitsplein 1 B-2610 Antwerp Wilrijk Belgium Fax 32 3 820 25 67 Tel 32 3 820 26 79 E-mail These authors contributed equally to this work Received 28 November 2008 revised 28 January 2009 accepted 5 February 2009 doi Phagocytosis represents a mechanism used by macrophages to remove pathogens and cellular debris. Recent evidence suggests that phagocytosis is stimulated under specific conditions of stress such as extracellular pressure and hypoxia. In the present study we show that amino acid or glucose deprivation caused an increase in the phagocytosis of heat-inactivated Escherichia coli and Staphylococcus aureus by macrophages but not the uptake of platelets apoptotic cells or beads. Increased phagocytosis of bacteria could be blocked by phagocytosis inhibitors and was found to be dependent on p38 mitogen-activated protein kinase activity and scavenger receptor A. Although nutrient deprivation is a strong stimulus of autophagy autophagosome formation was not critical for the uptake of bacteria because phagocytic clearance was not inhibited after down-regulation of the autophagy essential gene Atg7. Moreover enhanced uptake of bacteria should not be considered as a general stress response because phagocytosis of bacteria was not stimulated after exposure of macrophages to the genotoxic agent camptothecin heat 40 C or thapsigargin-induced endoplasmic reticulum stress. Overall the results obtained in the present study indicate that .

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