Pathogenesis of Mycobacterium Tuberculosis and Its Interaction with the Host
Mycobacterium tuberculosis (M. tuberculosis) is a Gram-positive, acid-fast bacterium that is the causative agent of tuberculosis (TB),a chronic infectious disease that primarily affects the lungs. TB is one of the leading causes of death from infectious diseases worldwide, with an estimated 10 million new cases and 1.5 million deaths in 2020.
The pathogenesis of M. tuberculosis is complex and involves a delicate interplay between the bacterium and the host immune system. The bacterium has evolved a number of strategies to evade the host immune response and establish a chronic infection. These strategies include:
- The ability to survive within macrophages: Macrophages are immune cells that engulf and destroy foreign particles. However, M. tuberculosis has the ability to survive within macrophages, where it can replicate and spread to other cells.
- The ability to suppress the host immune response: M. tuberculosis produces a number of factors that can suppress the host immune response, including lipoarabinomannan (LAM),which inhibits the production of cytokines that are essential for the immune response.
- The ability to form biofilms: Biofilms are communities of bacteria that are surrounded by a protective matrix of extracellular material. Biofilms can protect M. tuberculosis from the host immune response and from antibiotics.
The host immune response to M. tuberculosis is complex and involves both innate and adaptive immune mechanisms. The innate immune response is the first line of defense against infection and involves a number of mechanisms, including:
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Language | : | English |
File size | : | 2925 KB |
Text-to-Speech | : | Enabled |
Screen Reader | : | Supported |
Enhanced typesetting | : | Enabled |
Print length | : | 405 pages |
- Phagocytosis: Macrophages and neutrophils are phagocytic cells that can engulf and destroy M. tuberculosis.
- Natural killer (NK) cells: NK cells are cytotoxic lymphocytes that can kill M. tuberculosis-infected cells.
- Cytokines: Cytokines are proteins that are produced by immune cells in response to infection. Cytokines can activate other immune cells and help to coordinate the immune response.
The adaptive immune response is a more specific response to infection that is mediated by T lymphocytes and B lymphocytes. T lymphocytes are activated by antigens, which are pieces of M. tuberculosis that are recognized by the immune system. Activated T lymphocytes can kill M. tuberculosis-infected cells or produce cytokines that help to activate other immune cells. B lymphocytes produce antibodies, which are proteins that can bind to M. tuberculosis and help to neutralize it.
The pathogenesis of M. tuberculosis is determined by the balance between the host immune response and the bacterium's ability to evade the immune response and establish a chronic infection. In healthy individuals, the immune response is able to control the infection and prevent the development of disease. However, in individuals with weakened immune systems, such as those with HIV/AIDS or diabetes, M. tuberculosis can establish a chronic infection and cause disease.
The pathogenesis of M. tuberculosis is a complex and dynamic process that involves a delicate interplay between the bacterium and the host immune system. The bacterium has evolved a number of strategies to evade the host immune response and establish a chronic infection. However, the host immune response is able to control the infection and prevent the development of disease in healthy individuals. In individuals with weakened immune systems, M. tuberculosis can establish a chronic infection and cause disease.
Understanding the pathogenesis of M. tuberculosis is essential for the development of new and more effective treatments for TB.
5 out of 5
Language | : | English |
File size | : | 2925 KB |
Text-to-Speech | : | Enabled |
Screen Reader | : | Supported |
Enhanced typesetting | : | Enabled |
Print length | : | 405 pages |
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5 out of 5
Language | : | English |
File size | : | 2925 KB |
Text-to-Speech | : | Enabled |
Screen Reader | : | Supported |
Enhanced typesetting | : | Enabled |
Print length | : | 405 pages |