How do pathogens learn to be pathogens? Partnerships between microbes
leading to human disease

Date:
February 7, 2022
Source:
University of Exeter
Summary:
New research discovered that the fungus Rhizopus fights back
against soil predators and human immune cells by partnering with
a bacteria called Ralstonia in a two-way partnership.



FULL STORY ==========================================================================
New research discovered that the fungus Rhizopusfights back against soil predators and human immune cells by partnering with a bacteria called Ralstoniain a two way partnership.


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The microscopic world resembles our world in some surprising ways. The environment around us is inhabited by microbes living in complex
communities - - some friendly and some not so friendly. Microbes
compete with each other for resources and must also hide from or fight predators. One example of this is the fungus Rhizopus, which grows
in the soil and on spoiled food and is the cause of "black fungus"
outbreaks in covid patients.

In the soil, its predator is the amoeba Dictyostelium,a single celled
microbe that can move through the soil and engulf Rhizopus, devouring
it for nutrients.

Scientists from the universities of Exeter and Birmingham found
Rhizopusfights back against this predator by partnering with a bacteria
called Ralstoniain a two way partnership. By living inside Rhizopus, Ralstoniahides from the predator. In return, Ralstoniamakes a toxin that Rhizopuscan use to neutralize the predator, preventing it from feeding
on the pair.

Why does this matter to human disease? Our immune cells are very much like
the predator Dictyostelium: They seek out, engulf, and destroy foreign
microbes that enter our bodies, protecting us from infection. This means
that Rhizopusand Ralstoniacan use the same strategy to avoid predators
in the soil to evade our own immune systems. By learning to fight off
predators in the soil, Rhizopushas also learned how to cause disease
in humans.

This work showed that when its partnership with Ralstonia is disrupted,
animals infected with Rhizopus are able to survive this devastating
disease. The hope is that by better understanding the ecology and
strategies for survival that Rhizopus and other pathogens use in their
normal environments, we will be better prepared to combat these microbes
when they cause human disease.

"This work is really important because while its been known that fungal- bacterial partnerships in the soil impact plant disease for many years,
this is the first example of a bacterial-fungal partnership contributing
to mucormycosis in humans. We hope this will help us develop better
strategies for treating this devastating disease," says Dr Elizabeth
Ballou, one of the Principal Investigators for this project.

This work was led by Dr. Herbert Itabangi, who was a joint student
between Dr.

Elizabeth Ballou (Exeter) and Dr. Kerstin Voelz (Birmingham). Dr. Itabangi
was funded by a Wellcome Trust Strategic Award (led by Prof Neil Gow
while at Aberdeen). Dr. Itabangi's discovery is a key step forward
in our understanding of the "black fungus" that causes mucormycosis
and was responsible for nearly 40,000 deaths in 2021 as part of the
COVID-19 pandemic.

========================================================================== Story Source: Materials provided by University_of_Exeter. Note: Content
may be edited for style and length.


========================================================================== Journal Reference:
1. Herbert Itabangi, Poppy C.S. Sephton-Clark, Diana P. Tamayo,
Xin Zhou,
Georgina P. Starling, Zamzam Mahamoud, Ignacio Insua, Mark Probert,
Joao Correia, Patrick J. Moynihan, Teclegiorgis Gebremariam, Yiyou
Gu, Ashraf S. Ibrahim, Gordon D. Brown, Jason S. King, Elizabeth
R. Ballou, Kerstin Voelz. A bacterial endosymbiont of the fungus
Rhizopus microsporus drives phagocyte evasion and opportunistic
virulence. Current Biology, 2022; DOI: 10.1016/j.cub.2022.01.028 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2022/02/220207135837.htm

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