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tinybabymoose t1_iuhswx8 wrote

This is not going to be a compete answer but there’s several processes involved. First for the WBCs to get to the right area of tissue in the body, the blood vessel wall cells start expressing “selectins” which start to slow the WBCs down, then the WBCs bind and cross through the vessel wall using integrins and Cell adhesion molecules. Also there are macrophages and dendritic cells which when they encounter a pathogen release “chemokines” which create a concentration gradient for the WBCs to follow. Once close enough to the bacteria, neutrophils particularly are able to follow bacteria in the same way, following the concentration gradient of products the bacteria is releasing. (I can’t remember which chemical they follow but I think it may be ammonia?)

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Xambia t1_iuhtjma wrote

Replying to tinybabymoose (#381,517)

Once the neutrophils make it to the bacteria they follow chemoattractants released from the bacteria (and behave as you see in the video) usually in response to oligopeptides released from the bacteria which have a formyl functional group attached to the N-terminus of the peptide (ex: fMLP)

Edit: I should add that these oligopeptides bind to protein receptors (GPCRs) on the surface of the neutrophil and the location of these activated receptors on its surface let the neutrophil "know" where to go.

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fujiko_chan t1_iui8wrx wrote

Replying to tr14l (#383,875)

Not quite. I know this isn't ELI5, but basically if the WBCs are policemen, the selectins (and others) on/near the vessel wall are going, "Hey, my friend is in trouble! This way!" and pulling on their shirt sleeves. Once it exits the vessel, they can follow concentration gradients.

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BeardsandBio t1_iuiazbs wrote

In the simplest terms, when good cells die they breakdown and leave a flare behind. The scout white blood cells immediately go there to investigate and try and quarantine off the area and once they're there they also release a big smoke signal which attracts the calvary. The scout cells CAN fight but they're undertrained and poorly equipped.

Once the calvary and scouts are fighting, they'll often send a messenger back home who contacts the specialist to come join the fight... the specialist are veteran cells who trained to fight in specific conditions and better equipped.

In order to ensure the enemies are defeated the body itself makes the entire battle field cater to their advantages. Fevers, selectins, permeability etc all are auto responses to improve the wbcs shots at winning and being effective

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sharplydressedman t1_iuicqhm wrote

At a very simple level, it's all concentration gradients. Kind of like a dog can sniff and follow a scent trail from a very faint signature, following the trail until it is eventually on top of the target. Immune cells like the one in the video (presumably a monocyte or macrophage) have receptors specifically designed for Pathogen-Associated-Molecular-Patterns (PAMPs). PAMPs are molecules that are found on bacteria, fungi, viruses etc that our immune cells have evolved to recognize with receptors specific to them (antibodies not needed). An example of a PAMP is endotoxin/LPS that is a part of the bacterial cell wall. So for example, the bacteria sheds LPS or other pieces of its cell wall as it floats around, and the immune cell "sniffs" it out with its receptor and starts following the trail.

It gets more complex. There are hierarchical signals for what determines which direction an immune cell will migrate. For example, if local tissue cells realize there is an active ongoing infection, they will secrete "red flag" signals to recruit nearby immune cells to the area. These signals are called chemokines. So the immune cell floating around your blood will first detect the chemokines and realize something is wrong, and will enter the area where they are coming from. From that point on, if it senses PAMPs (the bacterial molecules), it'll switch and start moving toward the bacteria.

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femsci-nerd t1_iuiemb8 wrote

The WBCs know to "follow" the bacteria through the process of chemotaxis. Invaders like bacteria quickly get covered with cytokines and IgM and these are the things that the WBCs are attracted to. It's basically driven by thermodynamics but they are reacting to the blood soluble things that get quickly bound by non-self molecules.

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dabman t1_iuim5ha wrote

Replying to UpsetRabbinator (#390,039)

Seems like this would be difficult. I suppose if a cell released a sudden massive amount of chemical trail, and then was able to taper it off, it could give the illusion that the white cell overshot its target and it should stop or reverse to find it. I imagine the immune system itself has evolved to target a chemical release trail that is more passively released though, and not something the bacterial cell could easily develop an ability to control. Many chemicals released are dissolved gases for example, and may readily diffuse through cell walls without much ability to be concentrated/controlled.

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Paroxysm111 t1_iuiua52 wrote

There are two methods the body uses. First there's just numbers and random chance. In the clip you're mentioning, it could be that the white blood cell just happened to be moving that way. There are likely other WBC in the slide that aren't moving towards bacteria.

The other method is chemical messages. Bacteria produce waste wherever they are. WBC are drawn to the waste and to pieces of bacteria. The cells in your body also make messenger proteins when they're attacked/damaged by bacteria. The WBC follow these messenger proteins from low concentrations to high concentrations.

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goldblumspowerbook t1_iuj476z wrote

I refer you to the lyrics of the great scientific work/rap song “Ridin’ Dirty” by Chamillionaire*. “They see me rollin’”—selectins are weaker adhesion molecules that are expressed on blood vessel walls due to local inflammation caused by bacteria. These cause white blood cells to roll along the walls of the blood vessels (rather than floating) in the area of an infection. “They hatin’”—cytokines and chemokines, floating protein mediators of inflammation, cause white blood cells to be activated and get primed to eat and destroy bacteria “Patrollin’”—when they reach the area of the injury, where the maximum amount of chemokines are, the white cells use integrins, deep proteins under the endothelial cells, to pull their way out of the blood vessels. In the tissues they eat foreign material, continue to express inflammatory mediators, and many of them die, forming the gross white substance of puss. “Tryin’a catch me ridin’ dirty”—bacteria express foreign molecules on their cell surfaces such as lipopolysaccharide. These pathogen-associated molecular patterns identify them as foreign or dirty and tag them for endocytosis by neutrophils and macrophages. “Tryin’a catch me ridin’ dirty”—complement is a protein in the blood which can be activated through multiple inflammatory means and tags infectious organisms for destruction as well as kills infected cells. This is a second way for foreign material to be recognized.

Source: PhD in microbiology. Fan of rap.

Edit: Chamillionaire did Ridin' Dirty. I hereby rescind my claim to having a PhD.

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bawki t1_iuj4nho wrote

Replying to tinybabymoose (#381,517)

Also the majority of WBC kind of "roll" along the blood vessel walls, which is a process corticosteroid therapy can disrupt. This will manifest as initial pseudo leukocytosis as it frees leukocytes from the blood vessel walls and therefore increase blood concentration for leukocytes.

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InnkaFriz t1_iujchnc wrote

Replying to sharplydressedman (#387,419)

Thanks for the info! Follow up - is there a “red list” of bacteria patterns? Because afaik we do have a lot of bacteria we basically rely on for our health, and I’d assume that there is some mechanism to ignore them

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CynicalDarkFox t1_iujieo7 wrote

Replying to InnkaFriz (#399,033)

From what I know, that helpful bacteria is more situated in the GI tract rather than floating around the body.

However, it wouldn’t be a long shot to assume that helpful/neutral bacteria wouldn’t give off these chemicals that a pathogen would either since they aren’t exactly there to propagate selfishly.

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Limmert t1_iujwe7i wrote

Replying to CTH2004 (#399,034)

They don’t «smell» it like we think of the word «smell». It’s more like: pieces (chemoattractants) fall of the bacteria and attaches to receptor on phagocyte (because high consentration of a substance = higher chance of said substance to «collide» with the receptor on the phagocyte).

And when a «piece» binds to the receptor it causes an intracellular signal in said phagocyte -> phagocyte shoots out lamellipodium (which basically is a grappler that binds to the ecm in the direction of the receptor binding, and contracts pulling the phagocyte in that direction) -> repeat until catching your target.

I don’t know if that made any sense? Or if it was an answer to your question? The evolution is rather uncertain i believe.

Edit: Fagocyte -> phagocyte

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Oubastet t1_iujy1g0 wrote

Replying to BeardsandBio (#386,911)

>In order to ensure the enemies are defeated the body itself makes the entire battle field cater to their advantages. Fevers, selectins, permeability etc all are auto responses to improve the wbcs shots at winning and being effective

That's the best explanation of why symptoms, such as fever, happen that I've ever read.

It's to disadvantage the invader and provides an advantage to the defense.

Sometimes the defense can cause more harm than good, but that's a different topic.

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Jimmy_Smith t1_iujz6c0 wrote

Replying to WasabiSteak (#402,766)

These are called opportunistic pathogens. They may normal gut bacteria like e. coli, but when it enters the bloodstream or travels up your urethra to your kidneys they will kill you.

Now some of these bacteria may stay put either because they are inhibited by competing bacteria which is why some research focuses on transplating gut microbiome, but sometimes bacteria wait until they have enough around for a massive attack through quorum sensing.

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sharplydressedman t1_iujzkmj wrote

Replying to InnkaFriz (#399,033)

Well, yes and no - this will require a bit of a deeper dive into immunology. Our immune system has two general branches, the adaptive (slower but can "learn") and innate (quick but limited to pre-determined common patterns). There isn't a "red list" per se for the innate immune system since it is evolutionarily more efficient for our innate immune cells to have the receptors for the definitely dangerous patterns, and let the adaptive immune system "learn" which patterns are safe.

As a metaphor for the innate immune system, the TSA displays a list of things that are definitely banned on planes. They may not need to have a list of things that are "definitely safe", they can figure that out along the way.

Anyway to return to your question, the adaptive immune system DOES have the ability to identify molecules that are safe. "Mucosal tolerance" refers to the ability of the body to suppress immune responses against antigens that are encountered in the gastrointestinal tract. This is not only to protect the commensal bacteria that live in our intestines, but also prevents our immune system from flaring up against the molecules in our food.

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keloidoscope t1_iuk7rx5 wrote

Replying to lupadim (#410,912)

if you think it's overly complex, how does that argue for intelligent design?

Natural selection only rewards economy and elegance when it confers a selective advantage, and inherited traits don't get magically optimised even when they start to get baroque or unwieldy in descendant species.

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