A recent study featured in PLOS Pathogens revealed that sepsis could increase the risk of life-threatening secondary infection in mice by averting recruitment of cell that expert to fight against infection.
Sepsis is a life-threatening condition caused by an immune response triggered by an infection. It causes 5.3 million deaths each year. A maximum number of the mortality was due to the disruption of immune response that opens the door for life-threatening secondary infections.
The team led by the Derek Danahy already expound that sepsis interrupts the immune system by reducing the amount and activity of memory T cells that circulate throughout the body, recognizing and attacking specific bacteria, viruses, or cancer cells. Hence they investigated the effect of sepsis on tissue-resident memory T cells (TRM) that stick to the skin, lungs, and gut – through which the infection enters the body.
The mice were infected with viruses that induce production of TRM in the skin. Later the researchers punctured the gut to release bacteria-containing fecal material into the body that results in infection and sepsis and induced activation of the TRM. The impact of sepsis on TRM was assessed by using molecular techniques.
The researchers found that the amount and function of TRM in the skin was not affected by the sepsis and the cells succeeded themselves in maintaining the functions. Generally, TRM cells recognize invaders required for the recruitment of other immune cells (bystander T and B cells) to fight infection, but this process in mice was get blocked by the sepsis.
Usually, sepsis interrupts the activity of specific interferons, but in the mice, it disturbed the production of specific interferons that recruit the bystander T and B cells and increased the risk of secondary infection.
In conclusion, further studies are required for the better insight of sepsis impact. The researchers have to look at the duration of the effect and impact on the TRM present in other parts of the body. The application of study outcomes in human could help to develop the treatment strategy for secondary infection in patients with sepsis.