Histamine Effect

sports2245 said:

what is confusing to me is when are histamines released & do they attack antigens or visa versa?

This information is coming from Pathophysiology: The Biologic Basis for Disease in Adults and Children, third edition, by Kathryn L. McCance and Sue E. Heuther as well as another book I've referenced below. You may need to read this stuff over a couple of times to really get an understanding of it. It can be a bit difficult to understand on just one read through.

Mast cells are cells that are located in connective tissues near the blood vessels. They contain numerous cellular bags of granules. These bags of granules contain histamine, neutrophil chemotactic factor, eosinophil chemotactic factor, leukotrienes and prostaglandins. I cannot find where histamine, neutrophil chemotactic factor, or eosinophil chemotactic factor are actually synthesized in the body. The mast cell is merely designated as the storage place for them. Leukotrienes and prostaglandins, however, are synthesized as well as stored in the mast cells. The way the mast cell ruptures to release their contents is through a process called degranulation. Degranulation, or rupture, occurs when there has been traumatic injury to a cell or in response to certain allergens.

The effect of histamine depends upon the presence of either an H1 or H2 receptor in the cells. Since you are talking about the skin, the cells of the skin would have to have at least the H1 receptor in order for the inflammation response to take place. The H1 and H2 receptors work in opposition to each other:

• H1 receptors are responsible for promoting inflammation
• H2 receptors suppress the action of leukocytes

This is a safety mechanism so that the inflammatory response can be turned off once the job of dispensing with the invading antigen has been accomplished.

The tricky thing about H1 and H2 receptors is that they are present in varied amounts in the different cell types throughout the body and often both receptors are present together in the cells so they may act in an antagonistic fashion setting up a condition where whichever is present in the most numbers wins out. In chronic inflammatory diseases the H2 receptors are prevalent or the mechanism to turn off the H1 receptors is faulty.

The effect of histamine on H1 is:

• neutophils--is to increase chemotaxis (the movement of white blood cells into the area of inflammation)

The effect of histamine on H2 is:

• neutrophil--is to decrease their activity
• lymphocytes--is to decrease their activity
• eosinophils--is to decrease their activity

So, the answer to part of your question is that histamine does NOT attack antigens. It would be the neutrophils that actually do that. Think of the histamine as being the manager/agent of the little dudes in the WBC bank. The histamine is like the dispatcher that sends the little dudes out to go and get the actual dirty work done.

The Inflammatory Response

I've written about this before. It is actually posted on post #4 of this thread: https://allnurses.com/pathophysiology-t115487/ but I've copied and edited it a bit for you.

The acute inflammatory response starts with mast cells in the involved tissues releasing their contents. I like to think of mast cells as little hand grenades being dropped. When they open they spew out histamine, neutrophil chemotactic factor and eosinophil chemotactic factor. (This is war, baby!) They also bring prostaglandins and leukotrienes to the party.

The histamine, wonderful stuff that it is, causes the blood vessels in the affected area to dilate and increases their permeability (opens the doors). The neutrophil chemotactic factor attracts neutrophils to the site. They are the first group of soldiers in the leukocyte orificenal to get into the fracas. They are primarily involved in phagocytosis. They are followed later by the eosinophils drawn to the area by the eosinophil chemotactic factor to help clean up the mess the neutrophils leave behind. Exudate (pus) results. The lymph nodes are just doing their part of the process, clean up detail—removing and storing the garbage until it can be disposed of. As the infection drags on the prostaglandins and leukotrienes play more of a role in attracting more WBC's to the area of infection. As neutrophils are expended, more reinforcements are needed, so this is why the white count goes up. Review the anatomy and function of the lymphatic system.

The cardinal signs of inflammation are: (1) redness due to the dilation of the blood vessels, (2) heat also due to the vasodilation and increased blood flow, (3) edema due to intravascular fluids leaking into the surrounding tissues from the increased permeability of the blood vessels, and (4) pain due to the pain receptors being stimulated by the swollen tissue and pH changes from all these chemicals excreted during the inflammatory response.

The inflammatory response is a generalized reaction to tissues affected by any invading organisms. The basic purpose is to meet and enemy and destroy them. The actual steps of the Inflammatory response are (page 191, Human Body: An Illustrated Guide to Every Part of the Human Body and How It Works, edited by Ann Baggaley, Dorling Kindersley Publishing, Inc., 2001):

1. An organism invades causing tissue damage. This results in the release of prostaglandins, leukotrienes and histamine (the degranulation of the bags in the mast cells). Result: pain, swelling and movement of WBCs called neutrophils to the site.
2. Neutrophils arrive, called to action by the neutrophil chemotactic factor, again from the degranulation of the bags in the mast cells. The action of the histamine helps the neutrophils to pass through spaces in the blood vessel walls (opens the doors for them) so they can reach the damaged tissues. The neutrophils are drawn to the leukotrienes as well as the toxins produced by the invading organisms.
3. Antibodies, specifically created proteins by the body, arrive and attach themselves to the invading organisms which then are attracted to and attach to the H1 receptors on the neutrophils.
4. Chow time. The neutrophils surround and begin to ingest the invader organism. It cocoons the invader in a structure called a phagosome. This process is called phagocytosis.
5. The invading organism is destroyed in the phagosome. The remains of the organism may be excreted outside the neutrophil or remain within the body of the neutrophil. Either way, the invading organism is dispatched.

The Allergic Response

An allergic response is an overreaction of the immune system to a harmless substance or allergen. Cells of the skin, airway, lungs and stomach can respond to these allergens. What happens is mast cells in these areas release histamine that sets off an allergic response that results in an asthma attack or skin rash. The actual steps of an allergic response are (page 372, Human Body: An Illustrated Guide to Every Part of the Human Body and How It Works, edited by Ann Baggaley, Dorling Kindersley Publishing, Inc., 2001):

1. IgE (Immunoglobulin E), an antibody, is produced when an allergen is inhaled, swallowed or touched and comes into contact with a cell of the skin, airway, lungs or stomach. IgE is a substance that exists as a coating on the surface of most mast cells.
2. In a person who is sensitive to a specific invading allergen, a immediate bond to the IgE molecules on the surface of the mast cells takes place. This is called cross-linking.
3. This cross-linking action is like an "On" switch that causes the granular bags containing histamine within mast cells in the area to rupture and spew their store of histamine which triggers the allergic response. Note: mast cell stabilizers, are drugs given during asthma attacks to inhibit histamine action in an attempt to treat the underlying cause of the asthma attack.