Innate immunity includes the cells and processes that protect us, in a non-specific way, from infection by foreign invaders.
It recognizes and responds to pathogens in a generic way, but unlike the adaptive immune system, it does not confer long-lasting or protective immunity to the host.
The innate immune system is a real multi-tasker and does three main things. Some of them happen concurrently, others follow a serial pattern.
The things that this aspect of our immunity does for us includes:
Anyone having an irresistible urge to be a microbiologist should check out the scientific work below that dives very deep into the innate immune system. Click on the link or book cover for more information.
First on the scene are the leukocytes, or white blood cells. This should be easy to remember since leuko is Greek for "white" and cyte is "cell", ergo, white cell.
Since innate immunity has many different threats to fight, white blood cells had to learn different ways of fighting; like karate, judo and jujitsu. The three white-cell street fighters are the Phils; eosinophil, basophil and neutrophil.
Again, easy to remember. "Phil" is Greek for affinity or liking or loving something.
Neutrophil means "loving neither" since "neutro" is Latin for "neutral". The neither in this case is acids and bases. They are neutral which makes it easy to stain them with a non-acidic or basic dye.
Neutrophils fight bacteria and die to form pus. Yep, that nasty yellow-green stuff is dead neutrophils.
Basophil means loving foundation. "Baso" is Greek for foundation. The term is used to describe any cell that has grain-like particles in its cytoplasm, the foundation or the gel inside of cells, and stains a certain way when exposed to certain dyes.
Basophils fight allergic reactions by releasing histamine and leukotrienes which both mediate allergic responses. They also fight mechanical trauma by releasing chemical messengers, called cytokines, which direct white blood cells to the site where they are needed.
Eosinophil is loving dawn. "Eos" is Greek for dawn. Eosinophils become stained when exposed to a dye known as eosin; thus the term eosinophil. They fight parasitic infection and have a role in allergic reactions.
These three players in the innate immunity process were differentiated by how they react to staining dye to enable us to view them. Without the dye, these cells would be virtually invisible under magnification. Read on to see what else they do.
Innate immunity requires specialized hand-to-hand fighters for the inflammatory response.
These are the white blood cells (leukocytes) made up of neutrophils and monocytes. Both are phagocytes meaning that they ingest or eat foreign particles.
Photo: Single neutrophil consuming anthrax bacteria (orange)
Another phagocyte in the innate immunity arena is the macrophage, or big eater. He eats dead leukoscytes as well as invaders, all of which are removed from the battlefield and out of the body.
Phagocytes eat until they die and the formation of pus is the manifestation of all those dead phagocytes. If you see pus, just take comfort in knowing that a lot of invaders bit the dust.
Neutrophils, mentioned above, release chemicals that cause the lining of the blood vessels to retract and separate leaving holes in the vessel walls.
The holes allow other leukocytes (phagocytes and macrophages) to move in and out of the vessels to assess damage and eat debris and invaders.
Innate immunity calls on another key fighter in the battle against foreign invaders; the Mast cell.
Mast cells contain granules rich in histamine, the release of which causes dilation of blood vessels and increases permeability (holes) and exudation (leakage of fluids through the holes in the vessel walls and into the injured cell tissue). Basophils can also release histamine.
Mast cells also make and release eosinophils which eat harmful invaders as well as regulate the inflammatory response so it does not go on too long or become too severe.
Platelets are cell fragments that help stem bleeding and are the first responders to hemorrhaging.
Killer T-cells are not the same as Natural killer (NK) cells. NK cells don't have surface antigen receptors and innate immunity doesn't require any mission priority from them at all.
They are programmed to recognize virus infected cells, tumor cells and damaged, mutated host cells. The NK cells kick in first since they can recognize non-antigen chemical changes in virus infected cells.
When a virus gets in a cell, it changes things in the cell and the NK cells can recognizes those changes.
In order to do their job, they have to touch the infected cell (how's that for a kiss of death) and release perforin and licen, chemicals that dissolve the cellular structure, thus preventing further replication.
It is truly amazing to see and understand how a seemingly benign thing as an imbalance in a couple of essential fatty acids can contribute or even trigger a whole host of inflammatory and autoimmune diseases.
An imbalance in omega fatty acids can transform our innate immunity from a friend to a foe.
The culprit is inflammation, bad choices in foods are a major cause and numerous authors have attempted to show how to correct the issue through food choices and omega-3 based recipes. One such book is shown below and can be acquired via the link to Amazon.com.
It is important to understand the inflammation causing mechanism so read on.
There are several messengers, made up of fatty acids, in our immune system whose role is to call out the troops when invaders breach the body's defenses.
These are the leukotrienes and prostaglandins, both of which are made up of a fatty acid called Arachidonic Acid (AA). These messengers work hand in hand.
Prostaglandins cause blood vessels to dilate so the white-cell army can get to the injury site. This is the swelling (tumor) and redness (rubor) common to inflammation.
Photo below: skin abscess showing typical swelling and redness of inflammation
Prostaglandins also stimulate nerves that trigger pain (dolor) signals. Without the pain we wouldn't know we were hurt and would likely cause further damage.
Leukotrienes help direct the white-cell army; calling out the troops and telling them where to go when they arrive.
The numbers of leukotrienes present control the magnitude of the attack, the idea being to keep it strong enough to win the battle but not so strong that it causes undue collateral damage to the surrounding site.
One other thing that leukotrienes do is keep the white-cell fighters alive considerably longer than would be able to survive on their own. That is how innate immunity is supposed to work.
Inflammation can move from being part of the cure to being a disease when there is an excess of the two chemical messengers.
In such cases, the inflammation response gets too strong and goes on too long because the excess leukotrienes keep calling for more troops when there is no longer an enemy to fight.
In this case, the inflammatory response causes innate immunity to turn on its own host body. Now we have a hyperinflammatory response or, worse, an autoimmune disease.
Common diseases known to be caused by inflammation are asthma, allergies, rheumatoid arthritis, gout, lupus, inflammatory bowel disease which encompasses Crohn's disease, colitis, and celiac disease.
A number of diseases that are thought to be caused by, or at least promoted by, inflammation are atherosclerosis, diabetes, osteoarthritis, kidney failure, chronic pancreatitis and numerous others.
It is known that leukotrienes and protaglandins, the chemical messengers in the inflammatory response, are made up
of a fatty acid called Arachadonic Acid (AA). So the question is, "where does the over abundance of AA come from"?
Mostly it comes from what we eat. Too many foods we consume today are very high in the fatty acid omega-6 and deficient in omega-3.
Ideally we need a one-to-one ratio of the two omegas. An excess of omega-6 causes a chain reaction of fatty acids that culminate in arachadonic acid which in turn causes a huge excess in the
aforementioned inflammatory messengers.
The excess of these cytokines (prostaglandins and leukotrienes) are going to start screaming "fire" when there is no fire but the agents of inflammation will come and will attack something. With no invader to attack, they will turn on the host body. Thus we end up with inflammation and autoimmune diseases and disorders.
The solution would seem to lie in supplementing with Omega-3, decreasing the consumption of foods high in omega-6
and arachadonic acid, eating low glycemic foods and supplementing with bio-active sugars to ensure the body has all building blocks it needs to construct the glycoforms required in intercellular communication.
Eggs are good for us on one hand but also contribute heavily to the inflammation load. They are full of arachadonic acid and lack the balancing fatty acids to keep the ratio near even.
Certain wild fish are excellent when it comes to getting omega-3 but now we have to be concerned with the mercury load. Farm fish is not the answer since they are usually fed a mix of stuff that increases their AA content.
To get the full story on Arachadonic Acid and how it contributes to the inflammatory disease epidemic in our country, pick up a copy of Floyd Chilton and Laura Tucker's book, "Inflammation Nation"; just click on the link above to Amazon.com.
It is more than anyone would ever need to know about inflammation and is replete with lists of foods and their inflammatory index and suggested recipes for the control of inflammation causing agents.