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Histamine
Histamines
Our relationship with histamine is complicated. This chemical messenger helps our brains stay alert, lets our stomachs dissolve food, and powers our immune systems to root out and kill infectious parasites. However, anyone who suffers from minor to severe allergies knows histamine can have a dark side, too. Learn more.
Histamines released in response to and Infected eye
Image by Hızır Erdem Uygun/Wikimedia
Injured site and tissue repair
Image by CNX OpenStax/Wikimedia
We should all be thankful to have some histamine in our bodies. This chemical messenger helps our brains stay alert, lets our stomachs dissolve food and powers our immune systems to root out and kill infectious parasites. However, anyone who suffers from minor to severe allergies knows histamine can have a dark side, too.
Source: National Institute of Allergy and Infectious Diseases (NIAID)
Histamine Testing
Also called: Histamine Determination, Histamine Intolerance, Histapenia Test, Histemia Test
This test measures the amount of histamine in a sample of your blood or urine. Histamine is a compound released when the immune system recognizes certain substances as potentially harmful to the body. Too much or too little histamine in the body can cause severe health conditions.
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Cooperation between Innate and Adaptive Immune Responses
Image by CNX Openstax
Inflammation is the standard, initial response of the body to injury. Whether biological, chemical, physical, or radiation burns, all injuries lead to the same sequence of physiological events. Inflammation limits the extent of injury, partially or fully eliminates the cause of injury, and initiates repair and regeneration of damaged tissue. Necrosis, or accidental cell death, causes inflammation. Apoptosis is programmed cell death, a normal step-by-step process that destroys cells no longer needed by the body. By mechanisms still under investigation, apoptosis does not initiate the inflammatory response. Acute inflammation resolves over time by the healing of tissue. If inflammation persists, it becomes chronic and leads to diseased conditions. Arthritis and tuberculosis are examples of chronic inflammation. The suffix “-itis” denotes inflammation of a specific organ or type, for example, peritonitis is the inflammation of the peritoneum, and meningitis refers to the inflammation of the meninges, the tough membranes that surround the central nervous system
The four cardinal signs of inflammation—redness, swelling, pain, and local heat—were first recorded in antiquity. Cornelius Celsus is credited with documenting these signs during the days of the Roman Empire, as early as the first century AD. A fifth sign, loss of function, may also accompany inflammation.
Upon tissue injury, damaged cells release inflammatory chemical signals that evoke local vasodilation, the widening of the blood vessels. Increased blood flow results in apparent redness and heat. In response to injury, mast cells present in tissue degranulate, releasing the potent vasodilator histamine. Increased blood flow and inflammatory mediators recruit white blood cells to the site of inflammation. The endothelium lining the local blood vessel becomes “leaky” under the influence of histamine and other inflammatory mediators allowing neutrophils, macrophages, and fluid to move from the blood into the interstitial tissue spaces. The excess liquid in tissue causes swelling, more properly called edema. The swollen tissues squeezing pain receptors cause the sensation of pain. Prostaglandins released from injured cells also activate pain neurons. Non-steroidal anti-inflammatory drugs (NSAIDs) reduce pain because they inhibit the synthesis of prostaglandins. High levels of NSAIDs reduce inflammation. Antihistamines decrease allergies by blocking histamine receptors and as a result the histamine response.
After containment of an injury, the tissue repair phase starts with removal of toxins and waste products. Clotting (coagulation) reduces blood loss from damaged blood vessels and forms a network of fibrin proteins that trap blood cells and bind the edges of the wound together. A scab forms when the clot dries, reducing the risk of infection. Sometimes a mixture of dead leukocytes and fluid called pus accumulates in the wound. As healing progresses, fibroblasts from the surrounding connective tissues replace the collagen and extracellular material lost by the injury. Angiogenesis, the growth of new blood vessels, results in vascularization of the new tissue known as granulation tissue. The clot retracts pulling the edges of the wound together, and it slowly dissolves as the tissue is repaired. When a large amount of granulation tissue forms and capillaries disappear, a pale scar is often visible in the healed area. A primary union describes the healing of a wound where the edges are close together. When there is a gaping wound, it takes longer to refill the area with cells and collagen. The process called secondary union occurs as the edges of the wound are pulled together by what is called wound contraction. When a wound is more than one quarter of an inch deep, sutures (stitches) are recommended to promote a primary union and avoid the formation of a disfiguring scar. Regeneration is the addition of new cells of the same type as the ones that were injured (Figure).
Source: CNX OpenStax
Name a disease, and likely, inflammation is involved
Image by StoryMD
Many of the chemical mediators discussed in this section contribute in some way to inflammation and fever, which are nonspecific immune responses discussed in more detail in Inflammation and Fever. Cytokines stimulate the production of acute-phase proteinssuch as C-reactive protein and mannose-binding lectin in the liver. These acute-phase proteins act as opsonins, activating complement cascades through the lectin pathway.
Some cytokines also bind mast cells and basophils, inducing them to release histamine, a proinflammatory compound. Histamine receptors are found on a variety of cells and mediate proinflammatory events, such as bronchoconstriction (tightening of the airways) and smooth muscle contraction.
In addition to histamine, mast cells may release other chemical mediators, such as leukotrienes. Leukotrienes are lipid-based proinflammatory mediators that are produced from the metabolism of arachidonic acid in the cell membrane of leukocytes and tissue cells. Compared with the proinflammatory effects of histamine, those of leukotrienes are more potent and longer lasting. Together, these chemical mediators can induce coughing, vomiting, and diarrhea, which serve to expel pathogens from the body.
Certain cytokines also stimulate the production of prostaglandins, chemical mediators that promote the inflammatory effects of kinins and histamines. Prostaglandins can also help to set the body temperature higher, leading to fever, which promotes the activities of white blood cells and slightly inhibits the growth of pathogenic microbes (see Inflammation and Fever).
Another inflammatory mediator, bradykinin, contributes to edema, which occurs when fluids and leukocytes leak out of the bloodstream and into tissues. It binds to receptors on cells in the capillary walls, causing the capillaries to dilate and become more permeable to fluids.
| Chemical Defenses of Nonspecific Innate Immunity | ||
|---|---|---|
| Defense | Examples | Function |
| Chemicals and enzymes in body fluids | Sebum from sebaceous glands | Provides oil barrier protecting hair follicle pores from pathogens |
| Oleic acid from sebum and skin microbiota | Lowers pH to inhibit pathogens | |
| Lysozyme in secretions | Kills bacteria by attacking cell wall | |
| Acid in stomach, urine, and vagina | Inhibits or kills bacteria | |
| Digestive enzymes and bile | Kill bacteria | |
| Lactoferrin and transferrin | Bind and sequester iron, inhibiting bacterial growth | |
| Surfactant in lungs | Kills bacteria | |
| Antimicrobial peptides | Defensins, bacteriocins, dermicidin, cathelicidin, histatins, | Kill bacteria by attacking membranes or interfering with cell functions |
| Plasma protein mediators | Acute-phase proteins (C-reactive protein, serum amyloid A, ferritin, fibrinogen, transferrin, and mannose-binding lectin) | Inhibit the growth of bacteria and assist in the trapping and killing of bacteria |
| Complements C3b and C4b | Opsonization of pathogens to aid phagocytosis | |
| Complement C5a | Chemoattractant for phagocytes | |
| Complements C3a and C5a | Proinflammatory anaphylatoxins | |
| Cytokines | Interleukins | Stimulate and modulate most functions of immune system |
| Chemokines | Recruit white blood cells to infected area | |
| Interferons | Alert cells to viral infection, induce apoptosis of virus-infected cells, induce antiviral defenses in infected and nearby uninfected cells, stimulate immune cells to attack virus-infected cells | |
| Inflammation-eliciting mediators | Histamine | Promotes vasodilation, bronchoconstriction, smooth muscle contraction, increased secretion and mucus production |
| Leukotrienes | Promote inflammation; stronger and longer lasting than histamine | |
| Prostaglandins | Promote inflammation and fever | |
| Bradykinin | Increases vasodilation and vascular permeability, leading to edema |
Source: CNX OpenStax
How Does an Allergic Response Work?
Image by NIAID
Histamine is a signaling molecule, sending messages between cells. It tells stomach cells to make stomach acid. And it helps our brain stay awake. You may have seen these effects illustrated by medicines that block histamine. Some antihistamines can make us sleepy and other antihistamines are used to treat acid reflux.
Histamine also works with our immune system.
It helps protect us from foreign invaders. When the immune system discovers an invader, immune cells called B-cells make IgE antibodies. The IgE’s are like “WANTED” signs that spread throughout the body, telling other immune cells about specific invaders to look for.
Eventually mast cells and basophils pick up the IgE’s and become sensitized. When they come in contact with a target invader…They spew histamine and other inflammatory chemicals.
Blood vessels become leakier, so that white blood cells and other protective substances can sneak through and fight the invader.
Histamine’s actions are great for protecting the body against parasites.
But with allergies, the immune system overreacts to harmless substances, not parasites. This is when histamine becomes our foe. Common allergens include peanuts, pollen, and animal dander.
Leaky vessels cause tearing in eyes, congestion in the nose, and swelling...basically anywhere. Histamine works with nerves to produce itching. In food allergies it can cause vomiting and diarrhea. And it constricts muscles in the lungs, making it harder to breathe.
Most worrisome is when histamine causes anaphylaxis, a severe reaction that is potentially fatal. Swollen airways can prevent breathing, and a rapid drop in blood pressure could starve organs of vital blood.
So what can be done about histamine?
Antihistamines block cells from seeing histamine and can treat common allergies. Medicines like steroids can calm the inflammatory effects of allergies. And anaphylaxis needs to be treated with a shot of epinephrine, which opens up airways, and increases blood pressure.
So our relationship with histamine is…complicated. We can do better.
Source: MedlinePlus
Antihistamines
Image by Phn003 at English Wikibooks
Source: National Cancer Institute (NCI)
AllegraFX - an antihistamine pharmaceutical drug used in the treatment of hay fever, allergy symptoms, and urticaria,whose name is allegra
Image by Hanabishi/Wikimedia
Antihistamines. These medications counter the effects of histamine, the substance that makes eyes water and noses itch and causes sneezing during allergic reactions. Sleepiness was a problem with the oldest antihistamines, but the newest drugs do not cause such a problem. Antihistamines come as pills or nose sprays.
Source: National Library of Medicine (NLM)
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