Dark Banquet - Bill Schutt [42]
Upon encountering an invader (recognized by foreign proteins embedded in its cell wall, or by the specific chemicals it gives off ), the phagocyte wraps its pseudopods around the microbe, drawing it inward. Inside the phagocyte, ingestion soon gives way to digestion as the foreign microbe is imprisoned within a membranous sac containing a nasty stew of lethal enzymes, bactericides, and strong oxidants. In most cases, the result of this chemical onslaught is a breakdown of the invader’s cell wall, followed by a toxic bath and, eventually, death. Any debris that remains is ejected from the phagocyte through a process called exocytosis.
Unfortunately, things aren’t always so easy for the phagocyte, and as we all know, the good guys don’t always win. Pathogenic (disease-causing) microbes have evolved some tricks of their own and many of these organisms have been at it far longer than our immune system has been around to evolve countermeasures. Pathogens like staphylococci bacteria produce their own toxins, which can kill phagocytes. Other invaders, like the AIDS-causing human immunodeficiency virus (HIV), evolve so rapidly that their constantly changing surface proteins are difficult for our immune systems to recognize. Alternately, some invaders, like the tubercle bacillus, are resistant to the phagocyte’s usually deadly chemical bath. These pathogens, responsible for the respiratory disease tuberculosis, are taken into the phagocyte. There they multiply within the bag of toxins they’ve been enclosed in, only to burst forth like Ridley Scott’s Alien, to kill the phagocyte (and traumatize any phagocytes that might be standing around nearby). Similarly, HIV can hide in these long-lived white blood cells, sometimes emerging after years of dormancy, as if from microscopic Trojan horses.
Some types of white blood cells go about defending the body in a very different way. Leukocytes (like basophils and other connective tissue cells called mast cells) function in the body’s inflammatory response. Inflammation is actually a bodily reaction to foreign invaders or tissue damage. During this process, the infecting agent or damaged tissue is partitioned, diluted, and destroyed.
So how does this work?
After getting the call, inflammation-initiating cells release chemicals (like histamine and prostaglandins) that cause blood vessels in the affected area to dilate (increase in diameter) as well as become more permeable. Dilation allows increased blood flow to the site, blood containing oxygen, nutrients, temperature-rising compounds called pyrogens, and an abundance of phagocytic cells. This influx causes the affected area to appear red and even hot to the touch. The increased blood vessel permeability allows plasma (and the phagocyte cavalry) to leak out of the vessels and into the surrounding damaged tissue. The regional swelling that characterizes inflammation is the result.
Macrophages at the site of an inflammatory response to pathogens hunt down and engulf infectious invaders that they encounter. As the battle rages on, millions of them make the ultimate sacrifice and they are posthumously awarded the title of Laudable Pus. Other macrophages get enlisted in the less-popular Cleanup Crew (in which case they get to clean up the laudable pus).*61 Adding to all this excitement, sensory nerve endings, stimulated by the weird chemicals and the swelling, produce the sensation of pain.
Unfortunately, leukocytes and other protective cells are also responsible for some types of allergic reactions. Most commonly, this “hypersensitivity” results from