Bacterial toxin with healing effect

Date:
October 13, 2020
Source:
Friedrich-Schiller-Universitaet Jena
Summary:
A bacterial toxin promoting tissue healing has been discovered. The
compound, found in Staphylococcus aureus, does not just damage
cells, but also stimulates tissue regeneration.



FULL STORY ==========================================================================
A bacterial toxin promoting tissue healing has been discovered. The
compound, found in Staphylococcus aureus, does not just damage cells,
but also stimulates tissue regeneration.


========================================================================== Normally they are among the many harmless organisms found in and on
the human body: one in four people have millions of Staphylococcus
aureus bacteria on their skin and on the mucous membranes of the
upper respiratory tract, without being aware of it. In some cases,
however, the harmless bacteria can turn into pathogens, which can lead
to skin inflammation and lung infections, or -- in the worst cases --
sepsis. "This happens especially when the bacteria multiply too fast,
for example when a person's immune system is weakened by an infection
or injury," says Prof. Oliver Werz of Friedrich Schiller University Jena
in Germany.

The Professor for Pharmaceutical Chemistry and his team have studied the molecular defence mechanisms of the human immune system in the fight
against such Staphylococcus aureus infections and made a surprising
discovery. As the research team reports in the current issue of
the specialist journal Cell Reports, the toxic cocktail with which Staphylococcus aureus damages cells and tissues also has positive effects: specific immune cells are stimulated by the bacterial toxin to produce specialised messenger substances that help to reduce inflammation and
to promote tissue healing. Prof. Werz expects this hitherto unknown
mechanism to be significant for future treatments of skin inflammation
and chronic wounds.

Immune cells produce anti-inflammatory messenger substances In their
latest study, the researchers from the University of Jena, Jena University Hospital and the Leibniz Institute on Aging -- Fritz Lipmann Institute
(FLI), together with colleagues from Harvard Medical School and the
University of Naples, have studied in particular the bacterial toxin
"?- Hemolysin" and examined its effect on M2 macrophages. M2 macrophages
are immune cells which, in the later stages of an inflammatory reaction,
ensure that bacteria that have been killed, and damaged cell components,
are removed, and that the tissue regenerates. "They are therefore a kind
of cellular waste disposal," says Paul Jordan, doctoral candidate in
Werz's team and lead author of the publication, describing the function
of these cells.

The researchers showed that ?-hemolysin binds to specific receptor
proteins on the surface of M2 macrophages and thus triggers the production
of anti- inflammatory messenger substances in the cells, which then cause
the inflammation to resolve. In the study, the scientists were also able
to show that these transmitters promote tissue regeneration in an animal
model. The anti-inflammatory messenger substances include resolvins,
maresins and protectins that are formed from omega-3 fatty acids.


========================================================================== Story Source: Materials provided by
Friedrich-Schiller-Universitaet_Jena. Original written by Ute
Scho"nfelder. Note: Content may be edited for style and length.


========================================================================== Journal Reference:
1. Paul M. Jordan, Jana Gerstmeier, Simona Pace, Rossella Bilancia,
Zhigang
Rao, Friedemann Bo"rner, Laura Miek, O'scar Gutie'rrez-Gutie'rrez,
Vandana Arakandy, Antonietta Rossi, Armando Ialenti, Cristina
Gonza'lez- Este'vez, Bettina Lo"ffler, Lorena Tuchscherr, Charles
N. Serhan, Oliver Werz. Staphylococcus aureus-Derived a-Hemolysin
Evokes Generation of Specialized Pro-resolving Mediators Promoting
Inflammation Resolution.

Cell Reports, 2020; 33 (2): 108247 DOI: 10.1016/j.celrep.2020.108247 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2020/10/201013134304.htm

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