What happens in the immune system when macrophages are deprived of oxygen?

An image to illustrate macrophae=ges
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What happens in the immune system when macrophages are deprived of oxygen?

According to the University of Erlangen-Nuremberg, Germany, “infected tissue has a low concentration of oxygen. The body’s standard immune mechanisms, which rely on oxygen, can then only function to a limited extent.” They asked the question of how the immune system nevertheless manages to control bacteria under such conditions. The research gave an insight into macrophages, which are part of the congenital immune system.

What are macrophages?

Phagocytes are cells in the body which work to protect it against dying cells, bacteria and other foreign cells. Macrophages are a type of phagocyte in the congenital immune system. Macrophages play a key role in defending against the intracellular pathogens which cause infection. Intracellular pathogens can cause tuberculosis, Legionnaires’ disease or Q fever, for example.

The processes in the immune system

The researchers found that: “fewer metabolites are produced in the citric acid cycle under hypoxic conditions, leading to a reduced rate of reproduction among bacteria in macrophages.”

The team also observed that:

  • Changes in the mitochondrial metabolism of the macrophages were caused by signalling pathways due to the lack of oxygen;
  • This leads to a reduction in various metabolites in the citric acid cycle, especially citrate; which
  • Prevents bacteria reproduction, due to the fact that citrate is an essential growth factor for certain bacteria.

Prof. Jantsch from Universität Regensburg, said: “Our results describe a method of pathogen control which does not depend on oxygen and which we were not aware of until now.”

Fighting infectious diseases

FAU scientist PD Dr. Lührmann said: “The pharmacological influence of these signalling pathways opens up new opportunities for fighting infectious diseases.”

The report adds: “This knowledge will open future research avenues on the pathogenesis of chronic Q fever. In addition, the regulation of TCA cycle metabolites by HIF1α represents a previously unappreciated mechanism of host defense against intracellular pathogens.”

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