How does your immune system attack bacteria, viruses, parasites, etc.?

Osmosis Jones - that's it! Thanks.

/goes off to download a new Linux distro...
 
Still like this stuff :D

[video=youtube;7AWfzy7wdv4]http://www.youtube.com/watch?v=7AWfzy7wdv4[/video]
 
[video=youtube;LIyvrcHnriE]http://www.youtube.com/watch?v=LIyvrcHnriE[/video]
 
There are a variety of cells involved in immune responses. The major important ones are:

1) phagocytes (such as macrophages and neutrophils); these cells ingest other harmful cells and break them down sort of like how you ingest and break down food. They are usually present on site to react immediately to infection but they have their limits and once they have consumed a certain number of invaders they die. Some of them can also be directed to consume particular entities using antibodies.

2) helper T cells; these cells do exactly what their name implies, they help. They don't diretly do any killing, what they do is they release chemicals that act like chum for real killing immune cells, attracting them and intensifying the immune response when the helper's detect the presence of an invader. Think of them as immune response cheerleaders.

3) killer T cells; these cells are really mean buggers, they possess some very potent chemicals within them that disintegrate other cells along with a set of protein complexes that function a lot like a hypodermic needle able to penetrate through the outer coatings of harmful pathogens. Killer T cells will bind to a pathogen and drill through the outer coating in order to release the potent chemicals into that pathogen and destroy it. One of the interesting things about Killer T's is that they are the cells in your immune system best equipped to deal with some of the more difficult pathogens to combat such as viruses and cancers.

4) B cells; these cells are responsible for the production of antibodies once they are activated as (they then become known as plasma cells). For pretty much each pathogen there is a specific antibody produced that responds to that pathogen and only that pathogen. Antibodies bind to that pathogen and in doing so cover up its active sites (the areas on the pathogen that allow it to bind to, and interact with, your body through which it performs its harmful effects) thereby neutralising the pathogen. The antibodies also act as big "eat me" flags for phagocytes, attracting them and encouraging them to consume the antibody-coated invader.

5_ Memory cells; whe you encounter a pathogen for the first time not all immune cells engage in the fight, some become dormant and sit in places like your lymph nodes (read up on Wikipedia about what the lymph system is but it is sort of an overflow system for the liquid component of your blood among other things). Memory cells are these dormant cells. They live a very long time and, having been created in response to a specific pathogen, carry the knowledge of how to make specific antibodies dealing with that particular pathogen. When the memory cells again detects the pathogen later it allows your body to respond far more quickly to that pathogen through the production of new B cells already tailored specifically to fight that pathogen.

Depending on the type of pathogen present your response will be different. Antibodies for example are not effective against cancers while killer T's are somewhat effective in some circumstances (though often killer T's) aren't enough and you require medical intervention such as chemo and radiotherapy). Antibodies are great against bacterial infections for example. There are also many different types of antibodies and your body cycles through each type in turn as longa s the infection endures in an attempt to find an effective type.

Note I have simplified this a little so some of what I have said is not strictly true but will do for the purposes of a basic explanation.

This was very interesting, thank you.

I have a few questions please.

  1. Why does your immune system attack cancer cells, when these are cells created by your own body?
  2. Are B cells related to beta cells in the pancreas?
  3. How do immune cells manage to recognise invading organisms?
  4. Why don't some foreign bodies, like metal and silicone implants, cause an immune response?

I think it's fascinating how memory cells remember pathogens.
 
This was very interesting, thank you.

I have a few questions please.

  1. Why does your immune system attack cancer cells, when these are cells created by your own body?
  2. Are B cells related to beta cells in the pancreas?
  3. How do immune cells manage to recognise invading organisms?
  4. Why don't some foreign bodies, like metal and silicone implants, cause an immune response?
Now those are some awesome questions.

  1. Unfortunately we don't know too much about that yet but we are making progress. Somehting to keep in mind is that the immune system responds not to a whole pathogen but to specific tiny molecular portions of the pathogen termed "antigens". Now even though cancer was originally a part of you and has now gone rogue, and hence it looks a lot like you on a molecular level, a lot of cancers do still have cancer-specific antigens that the immune system can, in some occasions, pick up on.

    There was recently an article here in the CA section that discussed a new approach to cancer treatment. The treatment involved extracting killer T cells from a cancer patient and inserting new genes into those killer T cells that gave them the ability to recognise antigens specific to the cells that were cancerous. Basically teaching the killer T cells to kill cancer. Then the killer T cells were put back into the patients and they killed all the cancer in a matter of days because finally the patient's immune system was able to effectively recognise and hence effectively kill, the cancer.
  2. No B cells are not related to Beta cells in the pancreas. Beta cells occur in the Islets of Langerhans and are responsible for the release of insulin. They don't take part in immune responses. (though they can be the target of autoimmune responses when your immune system recognises your own beta cells as foreign and destroys them leading to type I Diabetes)
  3. As I mentioned above the immune system recognises the pathogen by recognising specific antigens present on the pathogen. These antigens are usually small portions of proteins or carbohydrates on the surface of the pathogen, something sticking out and easy to bind to.

    My memory is a little foggy here but in the case of your immune cells they possess proteins on the cell membrane that are shaped to bind to a particular range of antigens present on pathogens or they bind indirectly through an antibody.

    In the case of antibodies it is even more dynamic. Antibodies act as kind of an antigen-to-immune cell converter plug. On one end of the antibody is a molecular structure that is specifically organised to bind to proteins on immune your immune cells. That part never changes. Then on the other end of the antibody is a head portion that is swapped out as needed for a new head piece specific to whichever antigen happens to be detected at that time. So the swappable head portion binds to the antigen on the pathogen and then the other end binds to an immune cell. That immune cell then performs its function to eliminate that pathogen (even if it doesn't have a specific binding site for the antigens on the actual pathogen - neat huh?). So for example if that immune cell is a phagocyte (e.g. a neutrophil) then it will bind to the antibody and consume the pathogen bound to the other end and digest it.

    When students are first taught about how these binding pairs work they are told to visualise a lock and a key. The analogy is a good one as the antigen is like the key and the antibody and cellular proteins that bind to those antigens are like the lock.
  4. Our immune system isn't usually keyed to launching a coordinated offensive against things like silicone. We specifically use materials in implants in the body that won't illicit an immune response in the average human being. Note that in the example of silicon breast implants they usually have a protective membrane surrounding them to keep the silicone implant separated from the body tissues. Even then some silicone is probably still going to find its way out at some point and when it does it will be picked up by the garbage collectors of the immune system, the macrophages. These massive cells lumber about in your tissues devouring cellular debri and waste products. It will have no qualms about grabbing some silicone. So in a manner of speaking the silicone of breast implants does in fact become a victim of your immune system.

    Ironically I have read before that silicone gels can act as adjuvants (substances that enhance the immune response to an antigen).

Again I have simplified this somewhat so some of it may not be strictly accurate but it serves the purposes for a first stop explanation. I'm also working from memory so some info might need some updating too. If anybody with knowledge of immunology spots anything they feel is an omission or an error please feel free to weigh in. :p

I think it's fascinating how memory cells remember pathogens.
Indeed. They use this memory response as the basis for treatment with vaccines. Without that memory function our immune systems would be very inefficient. We would be like babies, getting very ill when exposed to things that, as adults, we shrug off.
 
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s/very much/at all

Antibiotics have zero effect on viruses. Which is why there's still no cure for the common cold. Or Herpes.
No. We have antivirals to kill viruses. It's simply a case of not understanding them very well. They are after all not technically alive so there's less ways of killing them.

Doesn't stop some moron doctors from prescribing antibiotics for a common cold, nor the insistence by some people on receiving them...:(
This is actually justified. Some symptoms are not what's expected with a cold. When there's an infection the immune system is compromised so there's a chance of developing bacterial infections. But people shouldn't ask for the antibiotic and rather let the doctor make that decision.


Sorry for not answering the OP question but it IS very complicated. On a basic level all cells have on their surface receptors and proteins. Immune cells pick up on these from foreign cells but ignore those on the surface of our own cells. When they do there is a kind of directed mutation that enables the mutated immune cells called antibodies to recognise specific invaders and attack them. This happens the first time they encounter a pathogen. If they encounter it a second time the antibodies are already present and the immune response is quicker and stronger. This is how it can be detected if you've ever been exposed to a particular disease. Occasionally the immune cells go rogue and mutate against normal body cells. Celiac for example is where antibodies are made to attack the gluten in wheat but they also cause a reaction with the intestinal wall. Though not a true autoimmune disease it is responding to something it should not respond to.

How your body is structured is also important. Lymph nodes are glands that keep the parts of your body isolated to an extent. They make it harder for pathogens to enter other parts of the body undetected. Lymph nodes act as filters or traps. They contain a high concentration of immune cells making it almost impossible for pathogens to go around without being detected.
 
How do antibiotics kill bacteria? Why don't they kill healthy cells too?
 
Antibiotics are substances that interfere with the working of bacteria. They either attach to receptors on or in the bacterial cell that elicit some sort of response or to other substances they need to survive. Sort of like throwing a spanner in a machine. These receptors and substances have to be unique to the pathogen or they will kill healthy cells. Many broad spectrum antibiotics act on elements found not only in pathogenic bacteria but the harmless ones too.
 
How do antibiotics kill bacteria? Why don't they kill healthy cells too?

depends on the type of antibiotic. You get bactericidal and static antibiotics, cidal ones physically kill the bacteria (like beta lactams) static antibiotics prevent the bacteria from replicating allowing the immune system to kill them and not be overwhelmed by numbers

Cidal antibiotics (ABs) kill bacteria by many modalities. Beta lactams ABs, like penicillin, kill the bacteria by steric hindrance they stop the synthesis of the bacterial cell wall. Then the bacterium has autolysins that aid with destroying the old cell wall however with synthesis inhibited the bacterium destroys the cell wall without any new wall being produced (cell wall inhibitors) hence it dies.

Now there are too many antibiotics to explain but see in the case of penicillin it doesnt kill healthy human cells because human cells do not possess a cell wall. This is known as selective toxicity
 
What's the difference between Gram-positive and Gram-negative bacteria? Some antibiotics state they only work on one or the other. Why is this?
 
Humberto reminds me of this :D

[video=youtube;BJlV49RDlLE]http://www.youtube.com/watch?v=BJlV49RDlLE[/video]
 
What's the difference between Gram-positive and Gram-negative bacteria? Some antibiotics state they only work on one or the other. Why is this?
To put it most simply gram positive bacteria take up a stain/dye used to prepare cells for looking at under a microscope and so are stained. The dye is known as crystal violet. Gram negative bacteria don't take up crystal violet well and so are stained a far lighter colour.

The stain works by finding a molecular component in bacterial cell walls called peptidoglycan. Gram positive bacteria show up purple or a dark blueish colour while the gram negative bacteria show up a much lighter pinky colour. It is a way of differentiating between them.

Unfortunately I don't know much about how antibiotics work so I will leave that more complicated part up to RiaX. :p
 
What's the difference between Gram-positive and Gram-negative bacteria? Some antibiotics state they only work on one or the other. Why is this?

Its just simply the spectrum of activity of the antibiotic. As pointed out previously gram positive and gram negative is classified on how much dye is taken up by the peptidoglycan (component of the cell wall).

Gram positive bacteria hence generally have a thicker cell wall and higher numbers of cross links. This is where antibiotics gets very complex and to spare your sanity just know that larger molecules have difficulty penetrating the wall or binding to peptidoglycan like the cephalosporins, which decrease in gram positive spectrum with an increase in generation.

Obviously its more complex than this
 
For how long can bacteria and viruses live outside their host? What constitutes a hospitable environment for them? What simples measures can one take to make things less hospitable for them?

To my knowledge, viruses don't survive well outside the human body, but some bacteria can survive up to a few days on things like door handles.

Putting food in fridges and freezers won't necessarily kill bacteria on the food either.

Some bacteria (e.g. Helicobacter pylori) can survive stomach acid.
 
Without biological fluids they dont live very long. Technically a virus is non living anyways.

WRT to being "clean" with a single sneeze can contain over 10 000 000 000 bacteria. Now you have your sanitizers that claim to kill 99.9% of germs. so 0.1% of 10 000 000 000 is 100000000 but it only takes 15 or so to infect you :p

be glad you have that immune system and that its uber complex :p

generally most bacteria are killed in the stomach and even if they survive that, the radical pH change from the stomach to the small intestine kills the rest, if they survive that the normal flora of the colon will kill them and if they survive that your body will flush them out in some very violent diarrhea (hence when you have diarrhea its always best to let it run and do fluid replacement therapy)

Thats the purpose of the normal flora it prevents random bacteria from colonizing parts of your body. The skin for example has staph as the flora
 
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