How plague attacks us – and how we should defend ourselves
The Black Death was most likely a combination of the bubonic and pneumonic plagues, according to most scientists in the field.
Bacteria control cytokines
Gemini says that researchers at NTNU-CEMIR have discovered how some of these bacterial effector proteins can block new signaling pathways in our innate immune system.
The researchers focused on how bacteria manipulate the cell’s secretion of the signal molecules (called cytokines) IL-1β and IL-18. These excretions can produce anti-bacterial responses in mammals.
“Yersinia is very effective in controlling the secretion of these cytokines. One type of effector molecule called YopM can inhibit the activation of a cell complex called the pyrin inflammasome, which regulates the release of IL-1β and IL-18,” says Lien.
One bacterial strain that lacks YopM and that is weakened in normal mice can cause disease reactions in mice lacking pyrin. This result has proven that this mechanism is important for immune functions in mammals.
New defense mechanisms
Evolution allows humans can develop new defense mechanisms against such attacks. People who survive bacterial attacks and go on to have children will pass on their genes and their ability to resist disease to the next generation.
Eventually, individuals who fight off bacterial attacks can come to predominate in an entire population, especially if the illness is so damaging or deadly that it prevents people from passing on their genes.
This situation can lead to unexpected results – like that it may be an advantage to be exposed to less serious illnesses.
Rare disease can provide greater resistance
“It’s interesting that some people, like those who have the autoinflammatory disease Familial Mediterranean fever (FMF), have mutations in their pyrin molecule. These patients may have an increased level of IL-1β and IL-18,” says Lien.
One hypothesis is that these individuals may have had a different resistance to infections, such as the Black Death, throughout the ages.
Might this population have been more resistant since they have greater amounts of signal substances? Could this have been a positive selection factor that helped them, on average, to have more surviving children than those who did not have increased resistance?
FMF is a rare disease in Norway. It is much more common in Turkey, for example, which was one of the portals for bringing plague from Asia to Europe during the Black Death in the Middle Ages.
“More research may be able to find connections between these pyrin mutations, historic epidemics and pandemics, and modern infections,” Lien says.
He adds that the CEMIR project has already found complex interactions between bacteria and host organisms, and shown new aspects of how the body fights infections.
— Read more in D. Ratner et al., “Bacterial secretion systems and regulation of inflammasome activation,” Journal of Leukocyte Biology Online 10, no. 1 (3 November 2016) (doi: 10.1189/jlb.4MR0716-330R); D. Ratner et al., “Manipulation of IL-1b and IL-18 production by Yersinia pestis effectors YopJ and YopM and redundant impact on virulence,” Journal of Biological Chemistry 291 (16 February 2016): 9894-905 (doi: 10.1074/jbc.M115.697698); and D. Ratner et al., “The Yersinia pestis effector YopM inhibits Pyrin inflammasome activation,” PLOS Pathogens (2 December 2016):e1006035 (doi: org/10.1371/journal.ppat.1006035)
