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SHR Neuro Cancer Cardio Lipid Metab Microb
Rittchen, S; Jandl, K; Lanz, I; Reiter, B; Ferreirós, N; Kratz, D; Lindenmann, J; Brcic, L; Bärnthaler, T; Atallah, R; Olschewski, H; Sturm, EM; Heinemann, A.
Monocytes and Macrophages Serve as Potent Prostaglandin D2 Sources during Acute, Non-Allergic Pulmonary Inflammation.
Int J Mol Sci. 2021; 22(21): 11697
Doi: 10.3390/ijms222111697
[OPEN ACCESS]
Web of Science
PubMed
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- Leading authors Med Uni Graz
- Heinemann Akos
- Rittchen Sonja
- Co-authors Med Uni Graz
- ATALLAH Reham
- Bärnthaler Thomas
- Böhm Eva
- Brcic Luka
- Jandl Katharina
- Lanz Ilse
- Lindenmann Jörg
- Olschewski Horst
- Reiter Bernhard
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- Abstract:
- Acute respiratory inflammation, most commonly resulting from bacterial or viral infection, is one of the leading causes of death and disability worldwide. The inflammatory lipid mediator prostaglandin D2 (PGD2) and its rate-limiting enzyme, hematopoietic PGD synthase (hPGDS), are well-known drivers of allergic pulmonary inflammation. Here, we sought to investigate the source and role of hPGDS-derived PGD2 in acute pulmonary inflammation. Murine bronchoalveolar monocytes/macrophages from LPS- but not OVA-induced lung inflammation released significant amounts of PGD2. Accordingly, human monocyte-derived macrophages expressed high basal levels of hPGDS and released significant levels of PGD2 after LPS/IFN-γ, but not IL-4 stimulation. Human peripheral blood monocytes secreted significantly more PGD2 than monocyte-derived macrophages. Using human precision-cut lung slices (PCLS), we observed that LPS/IFN-γ but not IL-4/IL-13 drive PGD2 production in the lung. HPGDS inhibition prevented LPS-induced PGD2 release by human monocyte-derived macrophages and PCLS. As a result of hPGDS inhibition, less TNF-α, IL-6 and IL-10 could be determined in PCLS-conditioned medium. Collectively, this dataset reflects the time-dependent release of PGD2 by human phagocytes, highlights the importance of monocytes and macrophages as PGD2 sources and suggests that hPGDS inhibition might be a potential therapeutic option for acute, non-allergic lung inflammation.
- Find related publications in this database (Keywords)
- prostaglandin D-2
- hPGDS
- lipopolysaccharide
- acute lung injury
- mononuclear phagocytes
- precision-cut lung slices