What inflammation looks like up close and personal, part III

February 9, 2011  |  General

Here’s another snippet from the first chapter of my new book, How Your Child Heals. It’s from the chapter about inflammation, and follows from here. You’re finally arrived at the battlefield of inflammation, a sore finger, and are starting to observe what is happening there.

But why did those capillary walls open up and allow all those gaps to form? What could possibly be the usefulness of having all the contents of the blood vessel leak out into the surrounding tissue? You drive on, hoping to find the answer.

There are still many red blood cells passing by your window, but by now there is a vast number of neutrophils, too. There are so many of these and they are all moving along with you toward the end of the finger that it is clear that these amoeba-like creatures are traveling along in response to a signal, a sort of bugle call, which is summoning them to the battleground that is the inflamed fingertip. The summons takes several forms: one comes in the form of substances given off by the germs invading your son’s fingertip; another consists of substances that act as distress calls that are released by the cells living at the point of the enemy invasion; yet another comes from normal blood substances that are activated by all the cellular commotion.

The neutrophils are the foot soldiers in the inflammation wars. Most of the time they are called to fight outside invaders, like bacteria. They pick up the call for help, those released message substances, from the inflamed tissue and follow them exactly as a bloodhound follows a scent; like a bloodhound, the neutrophils can detect the concentration of these substances and keep going in the direction in which the concentration gets higher and higher, until at last they reach their target—the invading bacteria.

You are now moving toward the front lines of the battle, and as you get closer you pass many dead combatants. Bloated neutrophils are stuffed to overflowing with germs, bacteria which look like tiny round clusters of grapes. The neutrophils have engulfed them, eaten them. When they do that they are called phagocytes, a word that even derives from the Greek word “to eat.” There are other cells besides neutrophils that can be phagocytes, but neutrophils are the principal ones. Many of these cells are so full after their bacterial meal that they have broken apart and are merely drifting, dead after sacrificing themselves to destroy the invaders. The liquid around you is a murky soup made up of bits and pieces of cells and bacteria.

Those granular pellets you noticed earlier in the neutrophils are the bullets they use to kill the bacteria when they function as phagocytes. But as they fire off these bullets, the phagocytes themselves are injured beyond repair. Thus, a phagocyte is a sort of suicide cell that sacrifices itself for the good of our bodies. Fortunately, when needed, our bodies can pump out billions upon billions of these cellular soldiers in a very short time. This is why one of the most useful signs of an infection anywhere in our bodies is a increase in the number of neutrophils in our circulation. It is a test physicians use frequently.

Moving on, you explore the war zone a bit further. You suspect this is not a random fight, because there appears to be a method to the phagocytes’ operations. Although as far as you can tell there is no overall, guiding hand—no single commanding general—this army clearly has a coordinated plan. The effect is very much like watching an anthill: at first glance, the ants seem to be scurrying around to no purpose, but if you observe them long enough, you can discern an organized pattern. By converging from all directions on the zone where the bacteria managed to get through your son’s skin, the phagocyte soldiers surround and cordon off the danger area. A glance around the perimeter shows you how that happens. It is a marvel to see.

This battle, like any battle, has its front lines and its rear echelons. As the fight has been raging up front, you see that at the rear of the battle zone other participants have been busy. Behind the phagocytes there is a developing palisade—a stout wall—composed of tough, interlocking ropes. This material is called fibrin. It is also the stuff from which blood clots and scabs are made.

Fibrin is a solid material, but its building blocks are always circulating in the bloodstream, ready for use when needed. Several things can initiate the cascade of events that make the building blocks come together when needed to weave fibrin strands into a barrier. One of these is the debris of the fight, the bits of broken cells. Another is an impressive array of auxiliary cells—support troops—which answer the same call along with the phagocytes and join the scene of action. As the phagocyte soldiers battle the invading bacteria, these supporting cells in the rear erect a defensive barrier to wall off and contain the battle.

You can read about the battle’s conclusion and its aftermath in a later post.


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