Effect of ketorolac on phagocytosis of Candida albicans by peritoneal macrophages

Fraser-Smith, Elizabeth B.; Matthews, Thomas R.

doi:10.1016/0162-3109(88)90003-3

Cited by 4 publications

(2 citation statements)

References 13 publications

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“…Thus, physicians of patients with, for example, respiratory virus infections do not hesitate to prescribe NSAIDs: the removal of opsonized virus is relatively unaffected, if affected at all, and the secondary discomfort and potential tissue damage mediated by cytokines and other soluble inflammatory factors is reduced. By contrast, steroid anti-inflammatory agents can be sufficiently potent to inhibit scavenger cell removal of opsonized targets (Fraser-Smith and Matthews, 1988;Kurihara et al, 1984;Paape et al, 1991), and these agents have, perhaps not surprisingly, proven to be ineffective as an AD treatment (Aisen et al, 2000). Based on our data, and on the data from a wide range of other AD reports (reviewed in Akiyama et al, 2000), we believe that the restricted actions of NSAIDs on soluble inflammatory mediators makes these agents an ideal adjunct to vaccination and other A␤-removal therapies.…”

Section: Discussionmentioning

confidence: 91%

“…Although we agree that microglia may play a role in the clearance of A␤, we also believe that nonsteroidal anti-inflammatory drugs (NSAIDs) could be an important therapeutic adjunct in this process. In particular, secondary production of the inflammatory mediators studied here is typically inhibited by NSAIDs at conventional therapeutic doses (e.g., Du and Li, 1999;Heneka et al, 2000;Henrotin et al, 1999), whereas the process of scavenger cell attack on opsonized targets is so powerful that it is relatively unaffected by these agents at normal doses, particularly in comparison with steroid antiinflammatories (e.g., Fraser-Smith and Matthews, 1988;Kurihara et al, 1984;Paape et al, 1991). Thus, physicians of patients with, for example, respiratory virus infections do not hesitate to prescribe NSAIDs: the removal of opsonized virus is relatively unaffected, if affected at all, and the secondary discomfort and potential tissue damage mediated by cytokines and other soluble inflammatory factors is reduced.…”

Section: Discussionmentioning

confidence: 98%

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Inflammatory repertoire of Alzheimer's disease and nondemented elderly microglia in vitro

Lue

Rydel

Brigham

et al. 2001

Glia

349

232

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We have previously developed and characterized isolated microglia and astrocyte cultures from rapid (<4 h) brain autopsies of Alzheimer's disease (AD) and nondemented elderly control (ND) patients. In the present study, we evaluate the inflammatory repertoire of AD and ND microglia cultured from white matter (corpus callosum) and gray matter (superior frontal gyrus) with respect to three major proinflammatory cytokines, three chemokines, a classical pathway complement component, a scavenger cell growth factor, and a reactive nitrogen intermediate. Significant, dose-dependent increases in the production of pro-interleukin-1beta (pro-IL-1beta), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory peptide-1alpha (MIP-1alpha), IL-8, and macrophage colony-stimulating factor (M-CSF) were observed after exposure to pre-aggregated amyloid beta peptide (1-42) (Abeta1-42). Across constitutive and Abeta-stimulated conditions, secretion of complement component C1q, a reactive nitrogen intermediate, and M-CSF was significantly higher in AD compared with ND microglia. Taken together with previous in situ hybridization findings, these results demonstrate unequivocally that elderly human microglia provide a brain endogenous source for a wide range of inflammatory mediators.

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 98%

Inflammatory repertoire of Alzheimer's disease and nondemented elderly microglia in vitro

Lue

Rydel

Brigham

et al. 2001

Glia

349

232

View full text Add to dashboard Cite

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The Pharmacologic Activity of Ketorolac Tromethamine

Rooks

1990

Pharmacotherapy

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Ketorolac tromethamine is a highly potent member of a class of compounds having both analgesic and antiinflammatory activity. In animal pain models using underlying inflammation, ketorolac markedly inhibited the pain response and increased the pain threshold; it did not exhibit any narcotic or central nervous system depressant effects. It was also active in rat models of acute and chronic inflammation and pyresis. These activities are mediated primarily by potent prostaglandin cyclooxygenase inhibitory activity. Mild central nervous system and cardiovascular effects occurred only at doses far greater than those required for analgesic and antiinflammatory activity. Solutions of ketorolac tromethamine are not irritating. When given intramuscularly to rabbits (0.31‐5% solutions), no drug‐related irritation or changes in serum creatine phosphokinase were seen. The agent was not irritating when applied to the skin or eyes (≤0.5% solutions) of animals.

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Microglial chemotaxis, activation, and phagocytosis of amyloid β-peptide as linked phenomena in Alzheimer's disease

Rogers

Lue

2001

Neurochemistry International

212

131

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Effect of ketorolac on phagocytosis of Candida albicans by peritoneal macrophages

Cited by 4 publications

References 13 publications

Inflammatory repertoire of Alzheimer's disease and nondemented elderly microglia in vitro

Inflammatory repertoire of Alzheimer's disease and nondemented elderly microglia in vitro

The Pharmacologic Activity of Ketorolac Tromethamine

Microglial chemotaxis, activation, and phagocytosis of amyloid β-peptide as linked phenomena in Alzheimer's disease

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