Effect of n-Butanol on macrophage functions: An in vitro study

Satapathy, Sandeep

doi:10.9790/3008-0431017

Cited by 1 publication

(1 citation statement)

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“…A significant reduction in superoxide ion and nitrite ion release was observed when RAW 264.7 macrophages were exposed to SPD‐MAA. Alcohol has been previously reported to reduce phagocytic function, antimicrobial activity, superoxide ion, and nitric oxide release from macrophages (Andrade et al., ; Castro et al., ; D'Souza et al., ; Libon et al., ; Satapathy and Shrivastava, ; Szabo, ). Our findings may suggest MAA adduct formation could be one of the mechanisms through which alcohol may exert such actions.…”

Section: Discussionmentioning

confidence: 99%

Malondialdehyde–Acetaldehyde‐Adducted Surfactant Protein Alters Macrophage Functions Through Scavenger Receptor A

Sapkota

Kharbanda

Wyatt

2016

Alcoholism Clin & Exp Res

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Background Reactive aldehydes like acetaldehyde and malondialdehyde generated as a result of alcohol metabolism and cigarette smoke exposure lead to the formation of malondialdehyde-acetaldehyde-adducted proteins (MAA adducts). These aldehydes can adduct to different proteins such as bovine serum album (BSA) and surfactant proteins A or D (SPA, SPD). Macrophages play an important role in innate immunity, but the effect of MAA adducts on macrophage function has not yet been examined. Because macrophage scavenger receptor A (SRA; CD204) mediates the uptake of modified proteins, we hypothesized that the effects of MAA modified proteins on macrophage function are primarily mediated through SRA. Methods and Results We tested this hypothesis by exposing SPD-MAA to macrophages and measuring functions. SPD-MAA treatment significantly stimulated pro-inflammatory cytokine TNF-α release in the macrophage cell line, RAW 264.7. A significant reduction in phagocytosis of zymosan particles was also observed. SPD-MAA stimulated a significant dose-dependent increase in TNF-α and IL-6 release from peritoneal macrophages of WT mice. But a significantly less TNF-α and IL-6 were released from peritoneal macrophages of SRA−/− mice. We observed a significant reduction in phagocytosis of zymosan particles in peritoneal macrophages from WT mice treated with SPD-MAA. No further SPD-MAA-induced reduction was seen in peritoneal macrophages form SRA−/− mice. SPD-MAA treatment significantly increased SRA mRNA expression, but had no effect on surface receptor protein expression. Protein kinase C alpha inhibitor and NF-κB inhibitor significantly reduced pro-inflammatory cytokine release in response to SPD-MAA. Conclusion In conclusion, our data demonstrate that SRA is important for MAA-adducted protein-mediated effect on macrophage functions.

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