Upregulation of the macrophage scavenger receptor in response to different forms of injury in the CNS

Bell, M. D.; López-González, Rodrigo; Lawson, L.J.; Hughes, Derralynn; Fraser, Iain P.; Gordon, Siamon; Perry, V.H.

doi:10.1007/bf01191555

Cited by 111 publications

(67 citation statements)

References 29 publications

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“…In addition, thioglycolate-elicited cells, which are enriched in infiltrating monocyte/macrophages, also up-regulate SR-A in response to LPS. The fact that these cells only up-regulated SR-A expression 2-fold in response to LPS is consistent with the observation that a variety of inflammatory stimuli, such as thioglycolate broth, elicit SR-A expression in mice (23). Thus, for resident mouse macrophages, mouse macrophages rich in infiltrating monocyte/macrophages, and three mouse macrophage cell lines, LPS induces a different pattern of SR-A expression relative to that reported for human monocyte/macrophages.…”

Section: Discussionsupporting

confidence: 69%

“…Injection of LPS into the hippocampus of wild-type BALB/c mice was correlated with increased SR-A expression on infiltrating macrophages and microglia (23). Furthermore, macrophages from wild-type mice primed with Calmette-Guérin bacillus expressed scavenger receptor activity, and when SR-A knockout mice were challenged with a systemic dose of LPS, they were more susceptible to endotoxic shock (8).…”

Section: Discussionmentioning

confidence: 93%

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Lipopolysaccharide Induces Scavenger Receptor A Expression in Mouse Macrophages: A Divergent Response Relative to Human THP-1 Monocyte/Macrophages

Fitzgerald

Moore

Freeman

et al. 2000

The Journal of Immunology

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Gene deletion studies indicate that the macrophage scavenger receptor A (SR-A) protects mice from LPS-induced endotoxemia. Paradoxically, cultured human monocyte-derived macrophages down-regulate SR-A expression when exposed to LPS. We found that human THP-1 monocyte/macrophages decrease SR-A expression in response to LPS independent of their differentiation status. In contrast, primary and elicited mouse peritoneal macrophages as well as the J774A.1 and RAW264.7 mouse macrophage lines increase SR-A expression in response to LPS. Exposure to LPS caused J774A.1 and RAW264.7 cells to increase SR-A transcripts by 3- and 5-fold, respectively. LPS caused a concomitant 3-fold increase in SR-A protein levels and increased cell membrane expression of the receptor. RAW264.7 cells increased SR-A transcript levels in response to LPS at concentrations as low as 1 ng/ml, and the response was saturated at 10 ng/ml. The LPS induction of SR-A transcripts required continual protein synthesis and began at 8 h, peaked by 16 h, and persisted for at least 48 h. LPS induction did not increase SR-A gene transcription or affect alternative transcript splicing, but mildly increased mature transcript stability and proceeded in the presence of actinomycin D. Finally, treatment of RAW264.7 cells with TNF-α did not induce SR-A transcript levels, indicating that a TNF-α autocrine/paracrine signaling mechanism alone is not sufficient to recapitulate the LPS induction of SR-A transcripts. The induction of SR-A expression by LPS-stimulated mouse macrophages is the opposite of the down-regulation of SR-A reported in human monocyte-derived macrophages and may have implications for the observed resistance mice show toward endotoxemia.

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Section: Discussionsupporting

confidence: 69%

Section: Discussionmentioning

confidence: 93%

Lipopolysaccharide Induces Scavenger Receptor A Expression in Mouse Macrophages: A Divergent Response Relative to Human THP-1 Monocyte/Macrophages

Fitzgerald

Moore

Freeman

et al. 2000

The Journal of Immunology

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“…19 It too is absent from the normal central nervous system and induction is evidence of macrophage activation. 20 There was widespread induction of both antigens on perivascular macrophages in the Malawian cases, even in vessels containing no sequestered parasites. This strongly suggests that these cells have been activated by contact with leaked plasma proteins.…”

Section: Discussionmentioning

confidence: 99%

Blood-brain barrier function in cerebral malaria in Malawian children.

Brown¹,

Rogerson²,

Taylor³

et al. 2001

The American Journal of Tropical Medicine and Hygiene

146

111

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Abstract. Cerebral malaria (CM) is a serious complication of Plasmodium falciparum infection. Binding of parasitized erythrocytes to cerebral endothelium plays a key role in disease pathogenesis. Central nervous system signs and symptoms (coma, seizures, raised intracranial pressure) predominate in African children, whereas in adults, multiorgan system failure is more common. In this study we investigated whether changes in blood-brain barrier (BBB) structure and function are compatible with the signs and symptoms observed in Malawian children with CM. Immunohistochemistry on autopsy brain tissues from eight cases of CM showed activation of endothelial cells and macrophages, and disruption of endothelial intercellular junctions in vessels containing sequestered parasitized erythrocytes, but no gross leakage of plasma proteins. Examination of the partition of albumin between circulating plasma and the cerebrospinal fluid from 72 cases of CM showed subtle but measurable changes compatible with impaired BBB function in malaria. These findings suggest that BBB breakdown occurs in areas of parasite sequestration in CM in African children.

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“…After axonal injury in the CNS, activated microglia upregulate the expression of both receptors but degenerating myelin is still not cleared effectively by these cells (Bell et al, 1994;Reichert and Rotshenker, 1996). It was therefore suggested that Mac-1 and SRAI/II-mediated myelin phagocytosis may be subject to regulation between efficient and inefficient states (Rotshenker, 2003).…”

Section: Phagocytosis Of Myelin and Axonal Debrismentioning

confidence: 99%

Interactions between Schwann cells and macrophages in injury and inherited demyelinating disease

Martini

Fischer

López-Vales

et al. 2008

Glia

270

237

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In this article we first discuss the factors that regulate macrophage recruitment, activation, and myelin phagocytosis during Wallerian degeneration and some of the factors involved in the termination of inflammation at the end of the period of Wallerian degeneration after peripheral nerve injuries. In particular, we deal with the early events that trigger chemokine and cytokine expression; the role of phospholipase A 2 in initiating the breakdown of compact myelin, and chemokine, cytokine expression; and the role of MCP-1, MIP-1a, and IL-1b in macrophage recruitment and myelin phagocytosis. We also discuss how inflammation may be switched off and the recently identified role of the Nogo receptor on activated macrophages in the clearance of these cells from the injured nerve. In the second half of the article we focus on the role of certain Schwann cell borne cytokines and chemokines, such as M-CSF and MCP-1 as well as intracellular signaling that regulate their expression in animal models of inherited demyelinating disease. Additionally, we present the preservation of sensory nerves fibers from macrophage attack in these animal models as a challenging paradigm for the development of putative treatment approaches. Finally, we also discuss the similarities and differences in these Schwann cell-macrophage responses in injury-induced Wallerian degeneration and inherited demyelinating diseases. Knowledge of the molecular mechanisms underlying Schwann cell-macrophage interaction under pathological conditions is an important prerequisite to develop effective treatment strategies for various peripheral nerve disorders. V V C

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Upregulation of the macrophage scavenger receptor in response to different forms of injury in the CNS

Cited by 111 publications

References 29 publications

Lipopolysaccharide Induces Scavenger Receptor A Expression in Mouse Macrophages: A Divergent Response Relative to Human THP-1 Monocyte/Macrophages

Lipopolysaccharide Induces Scavenger Receptor A Expression in Mouse Macrophages: A Divergent Response Relative to Human THP-1 Monocyte/Macrophages

Blood-brain barrier function in cerebral malaria in Malawian children.

Interactions between Schwann cells and macrophages in injury and inherited demyelinating disease

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