Language
Country/Area
No result found
The secret weapon of pathogenic bacteria: Why losing their secretion system makes them harmless?
In the biological world, the competition for survival of pathogens is extremely fierce. In order to survive within the host, pathogenic bacteria have evolved various secretion systems to inject effector proteins into host cells. These effector proteins facilitate their invasion. , immune suppression and other functions. The mechanism behind this process, especially why the loss of the secretion system renders pathogenic bacteria harmless, has become the focus of the latest research.
Effector proteins have a wide range of functions, covering a variety of internal processes in cells.
These effector proteins mainly enter host cells through three major secretion systems (T3SS, T4SS and T6SS). Take the type 3 secretion system (TTSS) as an example. When pathogenic bacteria such as Yersinia pestis lose this system, it is enough to completely lose their pathogenicity, even when introduced directly into the blood. Cannot cause any disease.
In addition to the traditional secretion system, some bacteria have also been found to use outer membrane vesicles to transport effector proteins. This approach allows bacteria to more flexibly adjust their environment or invade target cells. Although we can predict the presence of some effector proteins through genome sequencing, the number of effector proteins in many bacteria remains unclear. For example, studies of pathogenic E. coli showed that although more than 60 effector proteins were predicted, only 39 were actually shown to be secreted into human Caco-2 cells.
There are also significant differences in effector proteins between different strains. Taking the plant pathogenic bacterium Pseudomonas syringae as an example, the number of effector proteins ranges from 14 to more than 150 types among different strains.
Once these bacteria are engulfed by host cells, they use effector proteins to evade the host's immune response.
The operating mechanism of these effector proteins is special. They control the endocytic pathway of the host cell or interfere with the host's apoptosis process. For example, the effector proteins of certain pathogenic bacteria can prevent the host from initiating the apoptotic program, thus maintaining its survival environment. Effector proteins in some bacteria, such as enteropathogenic Escherichia coli (EPEC), not only inhibit apoptosis, but also promote inflammatory responses and accelerate the spread of infection.
This complex interaction between microorganisms and their hosts often triggers us to rethink the operation of the human immune system. When the host's immune response is effectively suppressed, pathogenic bacteria can easily invade and reproduce. However, if this effective secretion system is interrupted, the bacteria will lose the ability to fight the host and become harmless.
The seemingly invisible confrontation between microorganisms is actually one of the most profound laws of survival in the biological world. This not only involves how bacteria defend themselves, but also enlightens us in exploring anti-infection strategies. As our understanding of the behavior of these microorganisms increases, discovering the potential to reverse these pathogens may lead to the creation of new treatments.
The attention of various cases makes us re-examine the impact of bacterial secretion system on its pathogenicity.
In summary, understanding how pathogenic bacteria use effector proteins to interact with host cells is an important part of studying pathogenicity. This is not limited to prevention and treatment methods in the medical field, but can also inspire the future development of biotechnology. We can’t help but ask, can these anti-host technologies also become a breakthrough in future advanced medical treatment to combat various chronic and acute diseases?
