Planta Med 2019; 85(18): 1528
DOI: 10.1055/s-0039-3400033
Main Congress Poster
Poster Session 2
© Georg Thieme Verlag KG Stuttgart · New York

Eupatoriopicrin enhance the phagocytosis through modulation of S.aureus uptake and killing by THP-1 cells

B Gierlikowska
1   Medical University of Warsaw,, Banacha 1, Warsaw, Poland
2   Cambridge Institute for Medical Research, University of Cambridge,, Cambridge, United Kingdom
,
C Klapholz
2   Cambridge Institute for Medical Research, University of Cambridge,, Cambridge, United Kingdom
,
K Brown
2   Cambridge Institute for Medical Research, University of Cambridge,, Cambridge, United Kingdom
3   Cambridge Centre for Lung Infection, Papworth Hospital,, Cambridge, United Kingdom
,
AK Kiss
1   Medical University of Warsaw,, Banacha 1, Warsaw, Poland
,
A Floto
2   Cambridge Institute for Medical Research, University of Cambridge,, Cambridge, United Kingdom
3   Cambridge Centre for Lung Infection, Papworth Hospital,, Cambridge, United Kingdom
› Author Affiliations
Further Information

Publication History

Publication Date:
20 December 2019 (online)

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Phagocytes play an essential role in the host defense against pathogens. The recognition of S.aureus can be promoted either by opsonins (opsonic phagocytosis), or by binding to surface receptors (nonopsonic phagocytosis). The ability of macrophages to directly interact with nonopsonized bacteria depends on the recognition by Toll-like receptors (TLRs) [1]. Following uptake, the killing of S.aureus is closely related with MAP kinases promoting of trafficking the bacteria into mature phagolysosomes [2].

The treatment of S.aureus infections is still poorly ensured and searching new drugs is highly needed. We tested the hypothesis that eupatoriopicrin through enhancement of phagocytosis suppress growth of S.aureus in phagocytes (THP-1 cells). To verify this hypothesis we evaluated influence of eupatoriopicrin tested at concentration range 2.5–0.5 µM on (I) uptake of S.aureus by THP-1 cells performed by flow cytometry; (II) killing ability of THP-1 performed by CFU analysis; (III) MAP kinases modulation analyzed by westernblotting; (IV) cytokines release performed by ELISA tests and (V) morphology of THP-1 analyzed by confocal microscopy.

Our observations showed that eupatoriopicrin-treatment enhanced the phagocytosis through significant increase of the number of phagocyted bacteria. We noticed correlation between modulation of MAP kinases signaling and suppression of S.aureus growth which may be relate with promotion of phagolysosomal acidification. The modulation of MAP kinases also resulted in inhibition of IL-1β, TNFα and IL-8 release.

Our observations indicate the promising benefits for enhancing the canonical killing of pathogens through phagocytosis using plant-derived compounds.

 

  • References

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