Mycobacterium tuberculosis virulence factors
سؤال جديد:السلام عليكم ...
ازيك يا دكتور احمد ..
ممكن حضرتك تقولي ازاي بكتريا ال T.B بتستفيد من ال lipid componant of cellwall ؟؟؟؟؟؟؟؟؟
حاجة كمان ....واضح ان بكتريا ال T.B بكتريا هايفة معندهاش اي virulence factors >>>هل كان ممكن الجسم يكبر دماغة وميعملش
ضدها اي حاجة بما انها معندهاش toxins وكمان لانها مشلولة ويتجنب التدمير الناتج من type IV hypersensitivity ؟؟؟؟؟؟؟؟؟
الاجابة:
بص يا استاذ ...
Regarding lipid component of cell wall of Mycobacterium tuberculosis:
The high concentration of lipids in the cell wall of Mycobacterium tuberculosis have been associated with these properties of the bacterium:
- Impermeability to stains and dyes.
- Resistance to many antibiotics.
- Resistance to killing by acidic and alkaline compounds.
- Resistance to osmotic lysis via complement deposition.
- Resistance to lethal oxidations and survival inside of macrophages.
يعني ببساطه كده الدهون دي ليها دور قوي في اها تهرب من خلايا المناعة وتضللها, ده غير حماتها من عوامل المناعه المختلفه التانية
اما بالنسبة ان البكتريا دي هايفة ومعندهاش أي virulence factors
فده مش واقع
لأن الدهون اللي كانت في الجزء الاول من السؤال واحد من ال virulence factors دي
ياتري ازاي؟؟
غير اللي انا ذكرته فوق
فصاحبنا ده بيعمل الاتي:
Peripheral cell wall lipids of Mycobacterium tuberculosis are inhibitory to surfactant function in the lung
انا مش حابب ادخل في تفاصيل يمكن ماتهمش طالب سنه تالته طب بس انا هاذكرهملك باختصار شديد كالاتي:
Mycobacterium tuberculosis does not possess the classic bacterial virulence factors such as toxins, capsules and fimbriae. However, a number of structural and physiological properties of the bacterium are beginning to be recognized for their contribution to bacterial virulence and the pathology of tuberculosis.
MTB has special mechanisms for cell entry: The tubercle bacillus can bind directly to mannose receptors on macrophages via the cell wall-associated mannosylated glycolipid, LAM, or indirectly via certain complement receptors or Fc receptors.
MTB can grow intracellularly: This is an effective means of evading the immune system. In particular, antibodies and complement are ineffective. Once MTB is phagocytosed, it can inhibit phagosome-lysosome fusion. The exact mechanism used by MTB to accomplish this is not known but it is thought to be the result of a protein secreted by bacterium that modifies the phagosome membrane. The bacterium may remain in the phagosome or escape from the phagosome, in either case finding a protected environment for growth in the macrophage.
MTB interferes with the toxic effects of reactive oxygen intermediates produced in the process of phagocytosis by two mechanisms:
1. Compounds including glycolipids, sulfatides and LAM down regulate the oxidative cytotoxic mechanism.
2. Macrophage uptake via complement receptors may bypass the activation of a respiratory burst.
Antigen 85 complex: This complex is composed of a group of proteins secreted by MTB that are known to bind fibronectin. These proteins may aid in walling off the bacteria from the immune system and may facilitate tubercle formation although evidence of this is lacking.
Slow generation time: Because of MTB's slow generation time, the immune system may not readily recognize the bacteria or may not be triggered sufficiently to eliminate them. Many other chronic disease are caused by bacteria with slow generation times, for example, slow-growing M. leprae causes leprosy, Treponema pallidum causes syphilis, and Borrelia burgdorferi causes Lyme disease.
High lipid concentration in cell wall: as mentioned previously, accounts for impermeability and resistance to antimicrobial agents, resistance to killing by acidic and alkaline compounds in both the intracellular and extracellular environment, and resistance to osmotic lysis via complement deposition and attack by lysozyme.
Cord factor: The cord factor is primarily associated with virulent strains of MTB. It is known to be toxic to mammalian cells and to be an inhibitor of PMN migration. However, its exact role in MTB virulence is unclear.
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