Please use this identifier to cite or link to this item: https://doi.org/10.1159/000358236
Title: Preferential Silent Survival of Intracellular Bacteria in Hemoglobin-Primed Macrophages
Authors: Subramanian, Karthik
Winarsih, Imelda 
Keerthani, Chandrakumaran
Ho, Bow 
Ding, Jeak Ling 
Keywords: Science & Technology
Life Sciences & Biomedicine
Immunology
Hemoglobin
Macrophages
Intracellular bacteria
Infection
Apoptosis
STAPHYLOCOCCUS-AUREUS
INFECTED ERYTHROCYTES
SCAVENGER RECEPTOR
CELL-DEATH
P38 MAPK
SALMONELLA
HEMOLYSIS
MALARIA
HEME
MECHANISMS
Issue Date: 1-Jan-2014
Publisher: KARGER
Citation: Subramanian, Karthik, Winarsih, Imelda, Keerthani, Chandrakumaran, Ho, Bow, Ding, Jeak Ling (2014-01-01). Preferential Silent Survival of Intracellular Bacteria in Hemoglobin-Primed Macrophages. JOURNAL OF INNATE IMMUNITY 6 (4) : 515-529. ScholarBank@NUS Repository. https://doi.org/10.1159/000358236
Abstract: Hemolysis releases hemoglobin (Hb), a prooxidant, into circulation. While the heme iron is a nutrient for the invading pathogens, it releases ROS, which is both microbicidal and cytotoxic, making it a double-edged sword. Previously, we found a two-pass detoxification mechanism involving the endocytosis of Hb into monocytes in collaboration with vascular endothelial cells to overcome oxidative damage. This prompted us to examine the effect of Hb priming on host cell viability and intracellular bacterial clearance during a hemolytic infection. Here, we demonstrate that Hb-primed macrophages harbor a higher intracellular bacterial load but with suppressed apoptosis. p-ERK and p-p38 MAPK were significantly downregulated, with concomitant impairment of Bax and downstream caspases. The Hb-primed cells harboring intracellular bacteria upregulated anti-inflammatory IL-10 and downregulated proinflammatory TNF-α, which further enhanced the infectivity of the neighboring cells. Our findings suggest that opportunistic intracellular pathogens exploit the Hb-scavenging machinery of the host to silently persist within the circulating phagocytes by suppressing apoptosis while escaping immune surveillance. © 2014 S. Karger AG, Basel.
Source Title: JOURNAL OF INNATE IMMUNITY
URI: https://scholarbank.nus.edu.sg/handle/10635/234933
ISSN: 1662-811X
1662-8128
DOI: 10.1159/000358236
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