February 14, 2006, Hurricane Katrina landed six months later, Louisiana, New Orleans, a flooded residential wall covered with dangerous mold Sina Technology News Beijing time September 20, according to foreign media reports, the average daily inhalation of human fungal spores in the number of 1000 to 10 billion between. Especially in the rainstorm and floods after a few days, a large number of fungi breeding, the air seems to be filled with moldy smell. Every tiny mold spores are likely to be attached to our warm, damp lungs, where they stretch the tenders, grow like vines, invade our internal organs, and slowly consume our lives.
Fortunately, the human immune system leaves most people free from such a painful way of death. However, our immune system is not every day in the fierce fungal campaign. A new study said that in the face of fungal spores invasion, the immune system of the means of defense in fact much clever.
In a paper published in the journal Science, researchers point out that immune cells in the lungs begin to provide a comfortable environment for fungal spores and then induce them to turn on self-destruction programs. When the researchers use genetic engineering methods to inhibit the self-destruction system of spores, the immune cells in mice can not prevent the penetration of mold. Tobias Hohl, an infectious disease expert from the Memorial Sloan Kettering Cancer Center, said the findings suggest that our immune system is used by the United States. A very clever way to “keep the lungs sterilized and immune”.
However, not everyone is so lucky. Some people’s immune system due to drug effects, other infections or autoimmune disorders and other reasons, in the fight against fungal infection greatly reduced. Researchers hope that further research on defensive fungi may be able to provide new treatment and intervention strategies for vulnerable groups of patients.
In order to defeat the fungal infection, the researchers observed the interaction between the immune cells of mammals and the spores of Aspergillus fumigatus. Aspergillus fumigatus is the most common cause of fungal pneumonia around the world. Researchers have noted that there seems to be an important interaction between Aspergillus fumigatus spores and neutrophils. Neutrophils are a kind of blood leukocytes and a highly mobile immune cell. When pathogens are invaded or damaged, they will rush to the scene. At the same time as phagocytosis, the release can promote the inflammatory response Of the chemical signal.
When Aspergillus fumigatus spores into mammals, they are engulfed by neutrophils – a process that is known to be phagocytically – but itself will not be killed. In contrast, these spores appear to have died of programmed cell death, the so-called “apoptosis”.
programmed cell death (PCD) is a common mechanism in animals, plants and fungal cells, during which the cells commit suicide in accordance with a predetermined procedure to allow the organism to obtain greater benefit. In some cases, such as irresistible stress conditions, or deoxyribonucleic acid (DNA) occurs irreparable damage, the cells will start self-destruction procedures. If a cell loses its ability to perform procedural death, it can be considered “immortal”. The lack of procedural death is an important indicator of cancer cells and tumor development. In order to confirm that neutrophils triggered a programmed death mechanism of spore cells, the researchers turned to genetic engineering methods. They selected a gene in the spore DNA. In humans, similar genes have the function of encoding Survivin protein (a member of the family of apoptosis suppressors). In human cells, Survivin protein can block the programmed death process. As a result, the researchers have genetically modified Aspergillus fumigatus spores to produce proteins that are similar to Survivin proteins, making them more difficult to self-destruct. <Genus
In mice, fusarium oxysporum spores with a large number of Survivin proteins do not die like normal spores, and they become more deadly – in an experiment killed nearly three times the normal number of animals. Researchers further analyzed the discovery that Survivin protein-producing spores have resulted in “severe tissue damage”. However, when the researchers add a drug that blocks the Survivin protein, these spores begin to die in neutrophils and do not cause serious illnesses as before.
So how does neutrophils cause spores to commit suicide? In the laboratory, the researchers noted that those with a large number of Survivin protein spores than the normal spores can survive the oxidative pressure. The researchers thought that immune cells may be using NADPH oxidase to deceive the fescue spores, making them mistaken for their own into a dangerous environment. This inference is consistent with the occurrence of defects in some NADPH oxidase genes, who face a higher risk of fungal infection in their lives than usual.
Surely, mice lacking NADPH oxidase were almost unable to resist the infection of Aspergillus fumigatus spores, regardless of the high levels of Survivin protein in these spores. In other words, if there is no “tension” of the enzyme, neutrophils can not “fool” fungal spores to commit suicide. In summary, the researchers’ findings suggest that our immune system has a cunning skill that protects us from fungi. The researchers hope that if we can find the same clever way, applied to the fungal self-destruction system, perhaps one day will be able to better protect those vulnerable patients. (Any day)