Sidenote: There are no pictures, and I describe famous paintings as “it has a building, and the sky is blue,” so I’ll do my best to give a fair description. I hope you enjoy it.
I was recently rereading Sun Tzu’s The Art of War, and I realized that the most significant campaigns are not the ones described throughout history as countless geographical battlefields but the ones that go on every second, minute, hour, and every day inside our body. Our immune system has mastered the art of war.
Our immune system has two components: the innate immune system and the adaptive immune system. The innate immune system, which exists before exposure, is the quickest to respond and is short-term. Our adaptive immune system has a slower response and provides us with long-term protection against invaders (microbes). Keep in mind that the innate immune pathway is required to activate the adaptive immune system, so they are not mutually exclusive. For this lesson, let’s focus on the innate immune system.
In preparing this lesson, I described the processes I plan to convey to my wife. I tried countless ways to explain it, and in her own “light bulb” moment, my wife paraphrased it in a way that made a lot of sense.
“So, soldiers with ladders are storming a castle, and on the outside of the castle, there are ten soldiers who have never seen invaders like this, naturally acting to defend the castle,” she said. “All the people inside have no idea what is going on yet. After learning of this threat and realizing that ten soldiers are not enough to protect the future against these invaders, they teach the people inside the castle what invaders with ladders look like. In the future, when these invaders try their trickery again, the 100 people inside can defend the castle along with the ten soldiers outside, allowing the ten soldiers outside to carry on with their normal duties. The soldiers on the outside are the innate immune system, and the people on the inside are the adaptive immune system”.
All I could do was sit in amazement at her story, and I secretly wished that I had come up with it! Did I tell you I think she is amazing? Okay, so let’s get into the innate immune system.
When you think about the immune system, it’s often easy to overlook the first line of defense against invading microbes: our skin. Skin gets a bad wrap (no pun intended). It’s our largest organ, yet it gets overlooked. Our skin provides the first barrier to microbes. If they can’t get into our tissues, we don’t need to wage a defense against them. So yes, washing your hands is a big deal. Long ago, the importance of our skin was the topic of great discussion in preventing surgical site infections. A total game changer in disease prevention! Our skin is our force field. But every defense has its weaknesses. Our skin is no different. Our skin is not impenetrable and can be damaged, allowing microbes to enter.
IMPORTANT NOTE: The vast world of microbes is a fascinating universe of adaptive forms that, with an almost obsessive compulsion, continually strive to outwit our immune system, including penetrating that first barrier, our skin. Once inside, they adapt to evade “capture,” which would almost certainly lead to their death (lysis). I don’t want to make you paranoid, but there are billions and billions (thank you, Carl) of microbes that want to check into our amazing hotel.
The good thing is, though, we are ready! Our immune system is prepared, willing, and able.
If the microbe does penetrate the skin and enter our tissue, now what? Prepare to be awed.
Our blood is circulating white blood cells called neutrophils and monocytes. The tissues have sentinel cells called dendritic cells, macrophages, and mast cells. They combine forces to attack the foreign microbe and return the body to health (homeostasis). If all you wanted to know is the innate immune system, there you have it. If you want to know the specifics, carry on.
Once the foreign microbe is in the tissue, it tries to do its thing and divide and conquer. Left unchecked, this leads to illness. Our immune system, however, has other plans. The invader has “antigens” that help our immune system recognize it as foreign. Many times, I hear people describe antigens as proteins. They can be, but they can also be peptides, lipids, polysaccharides, and nucleic acids. For the purpose of this lesson, let’s just stick with the fact that our immune system can recognize them and wage a response. The sentinel cells (dendritic, macrophages, and mast cells) all produce cytokines, which help initiate the inflammatory response, allowing white blood cells to go from the circulatory system into the tissue by crossing the epithelial barrier between them. One of these cytokines is probably something you are familiar with: histamine! When you take an antihistamine, you prevent the action of this cytokine.
This is a thought-provoking question: How do antihistamines impact your immune system? I won’t answer this for you. Go down the rabbit hole!
When the sentinel cells recognize the microbe, they release cytokines. These cytokines bind to specific luminal receptors on the endothelial cells, activating adhesion molecules whose sole purpose is to slow and stop the circulating neutrophils and monocytes.
A cool thought: If you could look at the blood flowing through our body, it moves incredibly fast. Our immune system recognizes that you can’t go from fast to stop without some assistance. That is where adhesion molecules come into play.
These adhesion molecules produce a low-affinity effect, slowing down the white blood cells. On a micoscope, you can see them start to slow down. Then, a reaction between intercellular adhesion molecule 1 (ICAM1) on the endothelial cells and lymphocyte function-associated antigen-1 (LFA-1) on the leukocyte causes “stable arrest,” stopping the white blood cell in its tracks. Think of these reactions as causing the lining of the epithelium to get sticky like Velcro and catching the speeding blood cell. Once the white blood cell is stopped, the neutrophil flattens and squeezes between two epithelium cells, entering the tissue. Now the party begins!
Once inside the tissue, the neutrophil detects the invader, ingests, and kills it (phagocytosis). In doing so, it makes the ultimate sacrifice, giving its life in the process (apoptosis). These dead cells produce quite a mess, leading to pus formation (in case you were curious). While this is happening, the same action that caused the neutrophils to slow down, stop, migrate through the epithelium, and enter the battle in the tissue, also happens to the circulating monocytes. An interesting name change occurs during this process. In the circulatory system, they are called monocytes. Once they enter the tissue, they become macrophages, which means big eaters, and they are big. They are the largest type of leukocyte (white blood cell) in the blood. They can also become monocytic-derived dendritic cells (but that’s too technical for right now). The point is that they are big, love to eat, and are there to help the neutrophils. They also phagocytose dead neutrophils, thereby cleaning up the place, so to speak.
Now that the neutrophils and monocytes have done their job, the body hopefully returns to a state of health or homeostasis. The inflammatory response from the cytokines is stopped, the adhesion action is stopped, the leukocytes (neutrophils and monocytes) are now free-flowing through the area without slowing down or stopping, and all is good! Or is it? The next stop is the adaptive immune system.
I hope you enjoyed this and found it helpful.
Peace,
Jeff
About the Author:
Jeffrey Gemignani has been a nurse for 17 years, having started with his ADN at Gateway Technical College in Kenosha, Wisconsin, and then obtaining a BSN from Concordia University. He currently works as an Oncology Nurse Navigator and enjoys every minute of it.
Jeffrey is an independent contributor to CEUfast’s Nursing Blog Program.
Please note that the views, thoughts, and opinions expressed in this blog post are solely of the independent contributor and do not necessarily represent those of CEUfast. This blog post is not medical advice. Always consult with your personal healthcare provider for any health-related questions or concerns.
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