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. 2020 Jul 3;10:10976. doi: 10.1038/s41598-020-67345-3

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Suggestion of mechanism of activation of the cyclooxygenase pathway stimulated by Cr-LAAO. The representative scheme shows Cr-LAAO action on neutrophils. Firstly, Cr-LAAO interacts with the cellular membrane by an unknown mechanism (01), leading to PKC activation (02), which stimulates the p38 MAPK phosphorylation (03), and cPLA₂ phosphorylation and activation (04). Activated cPLA₂ cleaves membrane phospholipids to form arachidonic acid (AA) (05). AA can be catalyzed by COX-1 or COX-2 (06), forming PGH2, metabolized by PTGES (07) to form PGE₂ (08) for release (09). Activation of cPLA₂ (10) and DGAT (11) may lead to increased numbers of LBs in neutrophils because LB is rich in arachidonic acid (AA) for PGE₂ synthesis. Cr-LAAO can utilize LBs content to release PGE₂ (12). Thus, in the presence of cPLA₂-α (CAY10650) (13) and DGAT (A922500) (14) inhibitors, there is a decrease in the PGE₂ level released (15). This figure was created using images from Servier Medical Art Commons Attribution 3.0 Unported License (https://smart.servier.com). Servier Medical Art by Servier is licensed under a Creative Commons Attribution 3.0 Unported License.