In a new study, Dr. Adrienne Mottis at EPFL and her colleagues have shown that a biological phenomenon known as "mitohormesis" can be exploited to address acute respiratory distress syndrome (ARDS). Mitohormesis describes the fact that mild stress to a cells mitochondria can induce a series of responses that increase the cells health and viability. Many respiratory infections, including influenza or COVID-19, cause severe stress to cells and organs, leading to acute respiratory distress syndrome, which in turn, eventually leads to mortality in elderly or vulnerable people. Dr. Mottis explained that mitochondria are the cells main energy-harvesting organelles and are therefore constantly monitored by the cells "surveillance" systems. If the mitochondria malfunction or are subjected to stress, this continuous quality control can activate adaptive compensatory responses known as "mitochondrial stress responses".

He further explained that a mild level of mitochondrial stress can be beneficial for the cell and the organism since the positive effects of these stress responses can overcome the negative effects of the initial stressor. Also, mitochondria have evolved from bacteria; therefore, they are susceptible to antibiotics. Therefore, the researchers looked at various antibiotics that could stress mitochondria and identified novel molecules in the family of the tetracyclines, a class of antibiotics that block the synthesis of mitochondrial proteins and are used to counter several infections, such as acne, cholera, plague, malaria, and syphilis, in the study.

The study showed that 9-TB-triggered mitochondrial responses activate the ATF4 signaling pathway, a well-described response to multiple cellular stressors, and also mobilize signaling pathways of innate immunity, the so-called type I interferon response. As a result, 9-TB improved the survival of mice subjected to a lethal influenza infection while it did not impact the viral load. Resistant hosts fight infection by eliciting an immune response that reduces pathogen load, whereas tolerance refers to the mechanisms that limit the extent of organ dysfunction and tissue damage caused by infection, not necessarily impacting pathogen load. 

(Source: https://www.hindustantimes.com/lifestyle/health/stressed-mitochondria-help-cells-to-withstand-lung-infections-study-101662009914761.html )