12 Questions
Which component of lipopolysaccharide (LPS) triggers the production of antibodies?
O antigen
What is the role of nitric oxide produced due to endotoxin activation?
Causing hypotension
Which proteins are depleted due to activation of tissue factor by endotoxins, increasing the risk of bleeding?
Coagulation proteins
How do complement system activation by endotoxins contribute to inflammation?
Forming membrane attack complexes
Which type of exotoxin enters the host cell and alters protein synthesis or enzyme activity?
Type 3
Which bacterium produces a type 1 exotoxin named toxic shock syndrome toxin (TSST-1) that stimulates an extreme immune response?
Staphylococcus aureus
Which bacterial exotoxin damages cell membranes directly, causing alterations in electrolyte and water movement within the cell?
Type 2
Which exotoxin acts as a superantigen, enhancing interaction between antigen-presenting cells and T cells?
Toxic shock syndrome toxin (TSST-1)
Which exotoxin inhibits protein synthesis by cleaving 35S rRNA at position 1712?
Exotoxin A
Which exotoxin blocks inhibitory neurotransmission at the spinal cord level, leading to muscle rigidity and spasms?
Tetanospasmin
'Heat-labile enterotoxin (LT)' is an exotoxin produced by which bacterium?
Escherichia coli
'Leukocytin' is an exotoxin produced by which bacterium, causing neutrophil destruction?
Staphylococcus aureus
Study Notes
- Bacterial endotoxins and exotoxins are the two types of toxins produced by bacteria.
- Endotoxins are located in the outer membrane of gram-negative bacteria, specifically in the lipopolysaccharides (LPS).
- LPS has three main parts: lipid A, core polysaccharide, and O antigen.
- Lipid A is the immunogenic component of LPS, causing a reaction in the immune system.
- O antigen is antigenic, triggering the production of antibodies.
- Endotoxins are produced from the bacterial chromosome.
- Endotoxins trigger negative effects in the host by activating macrophages, complement system, and tissue factor within the coagulation cascade.
- Macrophages are activated by lipid A, releasing cytokines such as interleukin-1, interleukin-6, TNF-alpha, and nitric oxide.
- Interleukin-1, interleukin-6, and TNF-alpha act on the hypothalamus, stimulating the release of prostaglandin E2, causing a fever.
- Nitric oxide induces vasodilation and increased capillary permeability, leading to hypotension and multisystem organ failure.
- Complement system activation results in the formation of membrane attack complexes, damaging the bacteria.
- C3a and C5a, byproducts of complement system activity, cause histamine release and neutrophil chemotaxis, increasing inflammation.
- Tissue factor (factor III) is activated by endotoxins, initiating the coagulation cascade and forming clots, but depleting coagulation proteins and increasing the risk of bleeding (disseminated intravascular coagulation).
- Exotoxins are proteins produced inside gram-positive and gram-negative bacteria and excreted from the cell.
- Exotoxins can affect host cells in three ways: type 1 (damaging the cell membrane), type 2 (inhibiting specific enzymes or metabolic pathways), and type 3 (injecting toxins into the host's cells).
- Examples of bacteria producing exotoxins include Staphylococcus aureus, Clostridium tetani, and Clostridium botulinum.- Type 1 exotoxins act as super antigens and enhance the interaction between antigen presenting cells and T cells, resulting in increased inflammatory response.
- They bind to the connection between MHC2 molecules and t cell receptors, modulating the activity of the immune response.
- Type 2 exotoxins damage the cell membrane directly, creating pores or damaging phospholipid bilayers.
- This type of toxin has cytotoxic effects, altering electrolyte and water movement in the cell.
- Type 3 exotoxins enter the cell by binding to a specific protein on the target cell, then inhibiting protein synthesis or modulating enzyme or protein activity.
- Some bacteria use an injectosome to inject the toxin directly into the host cell.
- Staphylococcus aureus produces a type 1 exotoxin that enhances the immune response, making it a significant example.- Staphylococcus aureus produces a type 1 exotoxin called toxic shock syndrome toxin (TSST-1) that acts as a super antigen, stimulating an extreme immune response and causing fever, rash, and hypotension.
- Clostridium perfringens releases the type 2 exotoxin alpha toxin, which damages cell membranes by activating phospholipase C and producing reactive oxygen species, leading to inflammation, neutrophil activation, and vasoconstriction.
- Vibrio cholerae produces the neurotoxin cholera toxin, a type 1-3 exotoxin, which enters cells through the AB5 receptor and activates adenylate cyclase, increasing intracellular cyclic AMP and causing severe diarrhea and fluid loss.
- Streptolysin O and leukocytin are type 2 exotoxins produced by Staphylococcus aureus, damaging cell membranes and causing hemolysis and neutrophil destruction, respectively.
- Diphtheria toxin, produced by Cory Caebacterium diphtheriae, is a type 3 exotoxin that inhibits protein synthesis by inactivating the eukaryotic protein elongation factor 2 (EF-2).
- Pseudomonas aeruginosa produces exotoxin A, a type 2 exotoxin that inhibits protein synthesis by cleaving the 35S rRNA at position 1712.
- Shigella dysenteriae produces Shiga toxin, a type 2 AB5 exotoxin that inhibits protein synthesis by cleaving the 28S rRNA at position 4311.
- Escherichia coli produces a type 1-like exotoxin called heat-labile enterotoxin (LT), which activates adenylate cyclase and increases intracellular cyclic AMP, leading to diarrhea and fluid loss.
- Bordetella pertussis produces pertussis toxin, a type 2 AB5 exotoxin that inactivates adenylate cyclase and decreases intracellular cyclic AMP, leading to apnea and paroxysmal coughing.
- Clostridium tetani produces tetanospasmin, a type 2 exotoxin that blocks inhibitory neurotransmission at the spinal cord level, causing muscle rigidity and spasms.
- Clostridium botulinum produces botulinum toxin, a type 1-3 exotoxin that blocks the release of acetylcholine at the neuromuscular junction, causing muscle paralysis.
- Exotoxins are typically proteinaceous substances produced by bacteria, while endotoxins are lipopolysaccharide (LPS) components of the bacterial cell wall. Exotoxins can be released into the environment, while endotoxins remain within the bacterial cell.
- Exotoxins can act by various mechanisms, including super antigen effects, damaging cell membranes, inhibiting protein synthesis, altering cell signaling, and altering the activity of specific proteins and enzymes.
- Some exotoxins are named after the bacteria that produce them, such as tetanospasmin (Clostridium tetani) and botulinum toxin (Clostridium botulinum).
- Exotoxins are generally considered more toxic than endotoxins, as they require much lower concentrations to cause harm. Additionally, exotoxins can act at a distance from the bacterial cell, allowing for systemic effects, while endotoxins primarily cause local inflammatory responses.
Test your knowledge on the differences between bacterial endotoxins and exotoxins, their structures, mechanisms of action, and examples of bacteria producing them. Learn about endotoxins' effects on host defense systems and inflammatory responses, as well as exotoxins' impact on cell membranes, protein synthesis, and immune modulation.
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