Insights into Alkaline Phosphatase Anti-Inflammatory Mechanisms
Larissa Balabanova,
Georgii Bondarev,
Aleksandra Seitkalieva,
Oksana Son,
Liudmila Tekutyeva
Affiliations
Larissa Balabanova
G.B. Elyakov Pacific Institute of Bioorganic Chemistry, Far Eastern Branch, Russian Academy of Sciences, Prospect 100-Letya Vladivostoka 152, 690022 Vladivostok, Russia
Georgii Bondarev
Youth Research Laboratory of Recombinant DNA Technologies, Advanced Engineering School, Institute of Biotechnology, Bioengineering and Food Systems, Far Eastern Federal University, 10 Ajax Bay, Russky Island, 690922 Vladivostok, Russia
Aleksandra Seitkalieva
G.B. Elyakov Pacific Institute of Bioorganic Chemistry, Far Eastern Branch, Russian Academy of Sciences, Prospect 100-Letya Vladivostoka 152, 690022 Vladivostok, Russia
Oksana Son
Youth Research Laboratory of Recombinant DNA Technologies, Advanced Engineering School, Institute of Biotechnology, Bioengineering and Food Systems, Far Eastern Federal University, 10 Ajax Bay, Russky Island, 690922 Vladivostok, Russia
Liudmila Tekutyeva
Youth Research Laboratory of Recombinant DNA Technologies, Advanced Engineering School, Institute of Biotechnology, Bioengineering and Food Systems, Far Eastern Federal University, 10 Ajax Bay, Russky Island, 690922 Vladivostok, Russia
Background: The endogenous ecto-enzyme and exogenously administered alkaline phosphatase (ALP) have been evidenced to significantly attenuate inflammatory conditions, including Toll-like receptor 4 (TLR4)-related signaling and cytokine overexpression, barrier tissue dysfunction and oxidative stress, and metabolic syndrome and insulin resistance, in experimental models of colitis, liver failure, and renal and cardiac ischemia-reperfusion injury. This suggests multiple mechanisms of ALP anti-inflammatory action that remain to be fully elucidated. Methods: Recent studies have contributed to a deeper comprehension of the role played by ALP in immune metabolism. This review outlines the established effects of ALP on lipopolysaccharide (LPS)-induced inflammation, including the neutralization of LPS and the modulation of purinergic signaling. Results: The additional mechanisms of anti-inflammatory activity of ALP observed in different pathologies are proposed. Conclusions: The anti-inflammatory pathways of ALP may include a scavenger receptor (CD36)-mediated activation of β-oxidation and oxidative phosphorylation, caveolin-dependent endocytosis, and selective autophagy-dependent degradation.
