Google AI overview says "Mitochondria: Mtb targets mitochondria to alter their function and morphology. This manipulation of mitochondria is central to the success of a Mtb infection."
Ogre 发表于 2024-12-03 08:43 Google AI overview says "Mitochondria: Mtb targets mitochondria to alter their function and morphology. This manipulation of mitochondria is central to the success of a Mtb infection."
by ChatGpt-- Tuberculosis (TB), caused by Mycobacterium tuberculosis, primarily affects lung tissue but can impact multiple organs throughout the body. The primary cell organelles affected by TB infection are those involved in the immune response and cellular defense mechanisms, as well as organelles associated with intracellular trafficking and autophagy. Here are the key organelles that are most directly impacted by tuberculosis infection: 1. Lysosomes Mycobacterium tuberculosis is known to invade and survive within macrophages, a type of immune cell. Upon phagocytosis, the bacterium is engulfed by the macrophage and transported into a phagosome. Normally, phagosomes fuse with lysosomes to form phagolysosomes, where pathogens are degraded. However, M. tuberculosis can block this fusion, allowing it to survive and replicate within the phagosome. This interference with lysosomal fusion prevents the destruction of the bacteria, and M. tuberculosis uses the lysosomal machinery to avoid degradation. 2. Mitochondria Mitochondria are crucial for cellular energy production and apoptosis regulation. TB infection can lead to mitochondrial dysfunction in host cells, particularly in immune cells like macrophages. The bacteria may disrupt mitochondrial dynamics, including mitochondrial membrane potential and ATP production, thereby impairing the immune cell's ability to respond effectively. Mitochondria are also involved in the regulation of autophagy, a process through which cells degrade and recycle damaged components. M. tuberculosis can manipulate mitochondrial signaling to suppress autophagy and inhibit the host cell’s ability to clear the bacteria. 3. Endoplasmic Reticulum (ER) The ER plays a key role in protein synthesis and lipid metabolism. During TB infection, the bacteria can manipulate the ER to create a "safe haven" within the host cell. M. tuberculosis interacts with the ER membrane and can induce the formation of specialized vacuoles (often called ER-associated vacuoles) to establish a niche for replication. The ER stress response, also known as the unfolded protein response (UPR), is activated during TB infection as a result of increased cellular stress, affecting protein folding and secretion. This can influence the ability of the host cell to mount an effective immune response. 4. Autophagosomes Autophagy is an essential cellular process for degrading and recycling cellular components, and it plays a role in the immune response to infection. In macrophages, autophagosomes are critical for the degradation of engulfed bacteria. M. tuberculosis can subvert the autophagic pathway, preventing the fusion of autophagosomes with lysosomes, thereby avoiding degradation. Some forms of TB, particularly latent TB, are associated with changes in the autophagic process, potentially contributing to the persistence of the bacteria within host cells. 5. Golgi Apparatus The Golgi apparatus is involved in the trafficking and processing of proteins and lipids within the cell. M. tuberculosis can alter Golgi apparatus function and cellular trafficking to help the bacteria evade immune detection. The bacterium may exploit host cell machinery to alter vesicular trafficking pathways, aiding in its survival and replication inside macrophages. 6. Nucleus Infected cells may undergo changes in nuclear signaling during TB infection, especially as part of the inflammatory response. Macrophages can release inflammatory cytokines (e.g., TNF-α, IL-6) to initiate immune responses, and TB can induce a transcriptional shift within the host cell nucleus to promote chronic inflammation. The host cell nucleus may also be impacted in terms of DNA damage response and repair mechanisms, which can be altered during chronic infection, potentially leading to host cell survival and immune evasion. In summary, TB infection predominantly affects the lysosomes, mitochondria, endoplasmic reticulum, and autophagosomes, as these organelles are key in the host's immune response, intracellular trafficking, and defense against pathogens. The manipulation of these organelles by M. tuberculosis contributes to the bacterium’s ability to evade the immune system and persist within the host.
The lysosome is the organelle most directly affected by tuberculosis (TB) infection. Mycobacterium tuberculosis, the bacterium that causes TB, infects macrophages (a type of immune cell) and survives inside them by interfering with the normal function of lysosomes. Specifically, the bacterium prevents the fusion of the phagosome (the vesicle that engulfs the bacterium) with the lysosome. This allows the bacteria to evade degradation by the lysosome’s hydrolytic enzymes, enabling it to persist and replicate within the host cells.
Jiama20242025 发表于 2024-12-03 22:33 The lysosome is the organelle most directly affected by tuberculosis (TB) infection. Mycobacterium tuberculosis, the bacterium that causes TB, infects macrophages (a type of immune cell) and survives inside them by interfering with the normal function of lysosomes. Specifically, the bacterium prevents the fusion of the phagosome (the vesicle that engulfs the bacterium) with the lysosome. This allows the bacteria to evade degradation by the lysosome’s hydrolytic enzymes, enabling it to persist and replicate within the host cells.
谢谢
老师给的一个文件，200多页，说让读其中的5页。我读了，没说这个事。没有课本
请问是在哪里查到的？
作业学校规定家长不可以帮忙的
这道题问的是免疫细胞如何杀病原体
这道题我学了几十年生物都不知道答案。
出题老师的初衷是让学生阅读指定论文，然后从中间找答案。
美国各科强调大量阅读，而阅读科学文献并做批判性报告在一些好高中比如Potomac School, TJHSST是必修课，叫research seminar，我以前只在研究生阶段才有research seminar课。
Tuberculosis (TB), caused by Mycobacterium tuberculosis, primarily affects lung tissue but can impact multiple organs throughout the body. The primary cell organelles affected by TB infection are those involved in the immune response and cellular defense mechanisms, as well as organelles associated with intracellular trafficking and autophagy. Here are the key organelles that are most directly impacted by tuberculosis infection: 1. Lysosomes Mycobacterium tuberculosis is known to invade and survive within macrophages, a type of immune cell. Upon phagocytosis, the bacterium is engulfed by the macrophage and transported into a phagosome. Normally, phagosomes fuse with lysosomes to form phagolysosomes, where pathogens are degraded. However, M. tuberculosis can block this fusion, allowing it to survive and replicate within the phagosome. This interference with lysosomal fusion prevents the destruction of the bacteria, and M. tuberculosis uses the lysosomal machinery to avoid degradation. 2. Mitochondria Mitochondria are crucial for cellular energy production and apoptosis regulation. TB infection can lead to mitochondrial dysfunction in host cells, particularly in immune cells like macrophages. The bacteria may disrupt mitochondrial dynamics, including mitochondrial membrane potential and ATP production, thereby impairing the immune cell's ability to respond effectively. Mitochondria are also involved in the regulation of autophagy, a process through which cells degrade and recycle damaged components. M. tuberculosis can manipulate mitochondrial signaling to suppress autophagy and inhibit the host cell’s ability to clear the bacteria. 3. Endoplasmic Reticulum (ER) The ER plays a key role in protein synthesis and lipid metabolism. During TB infection, the bacteria can manipulate the ER to create a "safe haven" within the host cell. M. tuberculosis interacts with the ER membrane and can induce the formation of specialized vacuoles (often called ER-associated vacuoles) to establish a niche for replication. The ER stress response, also known as the unfolded protein response (UPR), is activated during TB infection as a result of increased cellular stress, affecting protein folding and secretion. This can influence the ability of the host cell to mount an effective immune response. 4. Autophagosomes Autophagy is an essential cellular process for degrading and recycling cellular components, and it plays a role in the immune response to infection. In macrophages, autophagosomes are critical for the degradation of engulfed bacteria. M. tuberculosis can subvert the autophagic pathway, preventing the fusion of autophagosomes with lysosomes, thereby avoiding degradation. Some forms of TB, particularly latent TB, are associated with changes in the autophagic process, potentially contributing to the persistence of the bacteria within host cells. 5. Golgi Apparatus The Golgi apparatus is involved in the trafficking and processing of proteins and lipids within the cell. M. tuberculosis can alter Golgi apparatus function and cellular trafficking to help the bacteria evade immune detection. The bacterium may exploit host cell machinery to alter vesicular trafficking pathways, aiding in its survival and replication inside macrophages. 6. Nucleus Infected cells may undergo changes in nuclear signaling during TB infection, especially as part of the inflammatory response. Macrophages can release inflammatory cytokines (e.g., TNF-α, IL-6) to initiate immune responses, and TB can induce a transcriptional shift within the host cell nucleus to promote chronic inflammation. The host cell nucleus may also be impacted in terms of DNA damage response and repair mechanisms, which can be altered during chronic infection, potentially leading to host cell survival and immune evasion.
In summary, TB infection predominantly affects the lysosomes, mitochondria, endoplasmic reticulum, and autophagosomes, as these organelles are key in the host's immune response, intracellular trafficking, and defense against pathogens. The manipulation of these organelles by M. tuberculosis contributes to the bacterium’s ability to evade the immune system and persist within the host.
老师自己给的一个文件，200页。我没给
我也是医学背景，但还是学渣，所以，不会
谢谢理解
这个我还真不知道。不可以讨论的吗？
搜了，没搜到
谢谢