Acetylsalicylic acid has no effects on various isolated immune cells in vitro

Uhlenbruck, G.; Lötzerich, H.; Bernhardt, J.; Rogalla, K

doi:10.1007/bf00634294

Cited by 4 publications

(4 citation statements)

References 18 publications

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“…This is also worthy of note that ASA can induce IFN-γ production typical of T cell phenotypes [115][116][117], which suggests that ASA may enhance T cell effector responses. On the other hand, some evidences from prior research also indicate that ASA could not affect lymphocyte proliferation or viability [118][119][120][121].…”

Section: Asa and T Effector Cellsmentioning

confidence: 92%

Aspirin and immune system

Hussain

Javeed

Ashraf

et al. 2012

International Immunopharmacology

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Section: Asa and T Effector Cellsmentioning

confidence: 92%

Aspirin and immune system

Hussain

Javeed

Ashraf

et al. 2012

International Immunopharmacology

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“…With respect to high-dose aspirinrecommended previously as a potential adjuvant to multifocal angiostatic therapy-its inhibitory impact on NF-κB activity may act as a countervailing factor. Aspirin does not appear to have a direct influence on NK activity, 100,101 and its ability to inhibit both isoforms of cox should exert a favorable influence in that regard. On the other hand, activation of NF-κB in macrophages plays an important role in macrophage activation; in particular, NF-κB activity promotes transcription of both IL-12 and IL-15, key factors in the maturation and activation of NK cells.…”

Section: Boosting Immune Defenses: Focus On Natural Killer Cellsmentioning

confidence: 99%

Toward a Core Nutraceutical Program for Cancer Management

McCarty

Block

2006

Integr Cancer Ther

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As previously suggested, it may be feasible to impede tumorevoked angiogenesis with a nutraceutical program composed of glycine, fish oil, epigallocatechin-3-gallate, selenium, and silymarin, complemented by a low-fat vegan diet, exercise training, and, if feasible, a salicylate and the drug tetrathiomolybdate. It is now proposed that the scope of this program be expanded to address additional common needs of cancer patients: blocking the process of metastasis; boosting the cytotoxic capacity of innate immune defenses (natural killer [NK] cells); preventing cachexia, thromboembolism, and tumor-induced osteolysis; and maintaining optimal micronutrient status. Modified citrus pectin, a galectin-3 antagonist, has impressive antimetastatic potential. Mushroom β-glucans and probiotic lactobacilli can amplify NK activity via stimulatory effects on macrophages. Selenium, β-carotene, and glutamine can also increase the number and/or cytotoxic activity of NK cells. Cachectic loss of muscle mass can be opposed by fish oil, glutamine, and β-hydroxy-β-methylbutyrate. Fish oil, policosanol, and vitamin D may have potential for control of osteolysis. High-dose aspirin or salicylates, by preventing NF-κB activation, can be expected to aid prevention of metastasis and cachexia while down-regulating osteolysis, but their impacts on innate immune defenses will not be entirely favorable. A nutritional insurance formula crafted for the special needs of cancer patients can be included in this regimen. To minimize patient inconvenience, this complex core nutraceutical program could be configured as an oil product, a powder, and a capsule product, with the nutritional insurance formula provided in tablets. It would be of interest to test this program in nude mouse xenograft models.

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“…Some NSAIDs do inhibit others from enhancing the proliferation, but this was not seen consistently [81–85]. …”

Section: In Vitro Diagnosis Of Aerdmentioning

confidence: 99%

Pathogenic Mechanisms andIn VitroDiagnosis of AERD

Schäfer

Maune

2012

Journal of Allergy

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Aspirin-exacerbated respiratory disease (AERD) refers to chronic rhinosinusitis, nasal polyposis, bronchoconstriction, and/or eosinophilic inflammation in asthmatics following the exposure to nonsteroidal anti-inflammatory drugs (NSAIDs). A key pathogenic mechanism associated with AERD is the imbalance of eicosanoid metabolism focusing on prostanoid and leukotriene pathways in airway mucosa as well as blood cells. Genetic and functional metabolic studies on vital and non-vital cells pointed to the variability and the crucial role of lipid mediators in disease susceptibility and their response to medication. Eicosanoids, exemplified by prostaglandin E2 (PGE2) and peptidoleukotrienes (pLT), are potential metabolic biomarkers contributing to the AERD phenotype. Also other mediators are implicated in the progress of AERD. Considering the various pathogenic mechanisms of AERD, a multitude of metabolic and genetic markers is suggested to be implicated and were introduced as potential biomarkers for in vitro diagnosis during the past decades. Deduced from an eicosanoid-related pathogenic mechanism, functional tests balancing PGE2 and pLT as well as other eicosanoids from preferentially vital leukocytes demonstrated their applicability for in vitro diagnosis of AERD.

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Acetylsalicylic acid has no effects on various isolated immune cells in vitro

Cited by 4 publications

References 18 publications

Aspirin and immune system

Aspirin and immune system

Toward a Core Nutraceutical Program for Cancer Management

Pathogenic Mechanisms andIn VitroDiagnosis of AERD

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