Activated MacrophageMacrophages are big and smart white blood cells that chase, capture, engulf, and digest intruders. They trap and phagocytize (literally, “eat”) their enemies. They can multiply rapidly when necessary. However, they’re naturally indolent and need to be activated by Vitamin D.

Here’s how it works. When a macrophage isn’t swimming in the blood stream, a it can slowly “walk” through tissues using self-generated stumpy little (one micron) “legs” (about ten of them sprout at a time). The macrophage ambles over to and snuggles up alongside a pathogen, quickly identifies it as foe, sprays it with membrane-frying free radical-laden beams, grabs, engulfs, smothers, kills, and digests them. If the pathogen is further away, or trying to escape, the macrophage chases after it, extrudes a cluster of long thin sticky spaghetti-like tentacles that wrap around and ensnare the pathogen, clutching it in an unbreakable strangle hold.

It is totally amazing that this complex and truly violent scenario is unfolding in you and me billions of times per minute.

 

Macrophages and oxidative bursts

A powerful weapon possessed by a macrophage weapon is the “GcMAF Macrophage oxidative burst“oxidative burst” (also widely known as the “respiratory burst”). An enzyme (called NADPH oxidase) stationed in the Macrophage’s outer membrane sprays out a beam of highly reactive free electrons, like bullets from a machine gun.

The NADPH gun emits a particle beam that blast tumour cells and microbes to smithereens. The electrons in the beam emerge one at a time, but they really really don’t want to be “free,” so—as fast as they possibly can—they snatch another electron to form a stable pair (we are talking nanoseconds here). A chain reaction of electron-snatchings triggered by the oxidative burst literally vaporizes molecules in the outer wall of a pathogen, ripping holes in it.

 

Now the membrane that held the victim together literally falls apart, spilling out its contents. Without an intact outer membrane, a pathogen can’t survive for very long. Oxidative bursts don’t happen all of the time. That would be a waste of firepower. The “trigger” that turns it on is the perceived proximity of a pathogen. When a macrophage comes into immediate contact with “enemy,” then—and only then—does it turn on the electron death beam.

There are lots of oxygen (O2) molecules everywhere in our bodies. When released, most of the electrons in the death ray beam crash into one of these omnipresent oxygen molecules, from which they quickly grab the electron they need to make a stable pair. The oxygen molecule now is missing one of its electrons, and is thus transformed into the violently corrosive free radical known as “superoxide” (O2-). Now superoxide is the one wanting an electron, and it will destroy anything in its path to get one. That “anything” would be the virus, bacterium, or cancer cell our macrophage has grabbed with its pseudopod. Suddenly the invader finds itself with a huge hole in its outer membrane. It’ll die soon.

Only activated macrophages are going to deliver oxidative bursts that are potent enough to be effective. If the immune system has been compromised by pathogens and put macrophages to sleep, the oxidative burst degenerates into a piddly potato gun that’s not going to hurt anybody. Firepower—or lack thereof—is what we are talking about here.  Activated macrophages fire the atomic equivalent of millions of rounds a second and never have to pause to reload

 Phagocytosis and phagolysosome formation

GcMAF Macrophage PhagocytosisOnce the macrophages have ensnared their victim, the engulfing process ensues. The outer membranes of the macrophage, nearest the microbe or cancer cell, simply merge into one another so that the victim is completely surrounded and encapsulated in what is called a phagolysosome. (“Phago ” means “eat,” “lyso” means “digest,” and “some” means “cell” or “body.”) Amoeba-like, the macrophage has reshaped itself such that the phagolysosome lies deep inside. Then the membrane that makes up the wall surrounding the phagolysosome shoots more death rays at its captured prey (just to make sure it is dead), and proceeds to digest it with an array of corrosive enzymes.

 

Opsonins: Super Glue “binding enhancers” that help macrophages latch onto enemies
To help them grab and hold their victims, macrophages send signals to nearby lymphocytes, instructing them to spray a thin coating of sticky proteins onto potential prey. Then, when the macrophages long thin arms make contact with the pathogen this “super glue” coating hardens, making it impossible for the it to shake loose.

Typically, a macrophage sends out a cluster of (say twenty or so) sticky pseudopods that surround the pathogen, encasing it in a mesh like affair, not unlike a large fish net, in which the pathogen becomes ensnared. Like a fly in flypaper, the pathogen is both stuck in it and to it, so there is no way to get loose. Then it is gradually surrounded and engulfed, ending up snugly inside the macrophage as a phagolysosome, in which it spends its last few moments as a life form before being digested down into its component parts by various free radicals and enzymes.The sticky proteins are called “binding enhancers” or “opsonins.” The gluing process is called “opsonization.”

Interestingly, when a macrophage grabs an pathogen this way, it wants its fellow immune cells to know prey is nearby, so—like an isolated soldier who has stumbled upon a group of enemy troops and is calling for backup— it sends out protein signals telling nearby macrophages to make more of the receptors that specialize in grabbing specifically that kind of enemy. There’s safety in numbers.

Technically this is called “up regulating expression of complement receptors on neighboring phagocytes.”

Macrophages phagolysosome execution (and dismantling) chamber

GcMAF Macrophage CytoplasmIf, somehow, a pathogen has survived the oxidative burst and phagocytosis, it will not survive the death chamber. Once eaten, internalized, and embedded in the macrophage’s cytoplasm, the enemy is imprisoned in a round cyst-like bubble inside the macrophage (called a phagolysosome) into which are squirted all sorts of digestive enzymes and many more rounds of oxidative burst, just for good measure. Pretty things do not happen inside of phagolysosomes. If the cancer cell or microbe is not already dead, the phagolysosome “death chamber” will certainly polish it off. (“Phago” means “to eat.” “Lyso” means “to dissolve.” “Some” means “sack” or “bag.”)

Once the dismembering process is complete, the phagolysosome slides over and makes contact with the outer cell membrane, merges with it, then disgorges the now harmless breakdown products (nucleic acids, fatty acids, amino acids, etc.) out into the extracellular fluid. They are then taken up by nearby cells and recycled into new body parts.
The ecologically-minded among us should find the efficiency of this process commendable. Nothing is wasted.

Scary toxic bad guys are killed, dismantled, and transformed into spare parts for the good guys: us.

Macrophages – Communicating with the immune system

Immune Cell CommunicationImmune cells—macrophages and lymphocytes— carry on a constant blather, like a huge town hall meeting room where everybody is talking at once. However, since the talking is a release of “messenger molecules” and the listening is done by protein receptors, immune cells can actually listen while they are talking!! This simultaneous talking and listening makes for a far faster exchange of messages.

There is so much activity, what with the constant molecular chatter coupled with a madhouse of cellular scrambling to grab and kill enemy cells as rapidly as possible, that the casual observer might get the impression of chaos. But there are no wasted efforts here, like a Beethoven symphony, everything is extremely well-organized and perfectly coordinated.

The chemical chatter among macrophages and other immune cells is extremely rapid and efficient. Macrophages release clouds of messenger molecules (cytokines, interferons, leukotrienes, and other small molecules)—at rates of up to thousands of molecules per second per cell. Each molecule carries a specific request or command. Like “Bring me this,” or “We need some of that over there,” or “Kill everything that looks like this.” “We need an inflammatory response over here.” Or “We don’t need to do that anymore.” They discuss what the enemy looks like and how aggressive he is. They tell each other how hard to work. They label targets for other cells to identify and kill. They talk about where the enemy is hiding. They discuss current enemy strategy and how best to outmaneuver it.

Exponential self-cloning: the ultimate weapon.

Activated Macrophage Self CloningLast, but definitely not least, macrophage — if outgunned — play the population card: they multiply rapidly. When they find themselves in an area of high pathogen density, they don’t have to call up the draft to get more troops; they simply clone themselves, which they can do on very short notice.

More macrophages automatically translates into more of all the other weapons enumerated above. But, again, this multiplication process occurs only in activated macrophages.

Without Vitamin D, macrophages languish but in the presence of Vitamin D, their activity level increases exponentially.

Once activated, macrophages multiply rapidly and attack ferociously.

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