Fungal Infections, Histamine Intolerance, and Mast Cells
Fungal infections, histamine intolerance, and mast cells have a crucial connection which is often overlooked as one source of histamine intolerance.
It is common to talk about mast cells as part of an allergic (even anaphylactic) reaction. But their role in allergic reactions is only a small part of the job of the mast cell. Another crucial role mast cells play is in identifying and treating pathogen; such as bacteria, viruses, parasites and fungi.
Mast cells reside strategically through-out the body in tissues that are commonly exposed to the external environment, such as the skin, airways and the gut. There they are one of the first cells to make contact with pathogens.
For this life-saving task, the mast cells are perfectly equipped. They are heavily armed with mediators (molecules such as histamine, TNF and interleukins), that can be released upon contact with pathogens.
The mast cell is designed to identify pathogens. When they identify pathogens they trigger the acute inflammatory mediators which call more cells into the infected site. Histamine, for instance, increases blood flow to the damaged site and make the vessels “leakier”. This leakiness allows the other inflammatory mediators access. There they combine forces with free radicals to “eat” the infection.
Mast cells are able to identify molecules on the surface of bacteria. These molecules bind to receptors on the surface of mast cells and trigger the release of inflammatory mediators including histamine. Also, mast cells release molecules (proteases and cathelicidins) that can directly kill bacteria.
When it comes to viral infections, the process is very similar. Mast cells can be activated by viruses via a specific cell surface receptor, which triggers the release of mediators (mainly interferon) that elicit an antiviral immune response. However, there is evidence that mast cells can also be harmful in viral infections. One study showed that in response to respiratory virus, mast cells could exacerbate or lead to the development of asthma.
The same principles apply to parasitic infections. Mast cells are preferentially located in tissues targeted by parasites, e.g., the skin and gut. These mast cells express receptors that identify specific parasitic components. Upon activation, mast cells release several inflammatory mediators that trigger the immune response, necessary to get rid of the parasites.
The role of mast cells in fungal infections is a lot less clear. Similarly to parasites, fungi enter the body via mast cell rich organs (skin, gut and airways), and it is also known that mast cells have receptors that can recognise fungi and trigger anti-fungal responses. Mast cells produce several molecules (interleukins, interferon and more) that have been shown to be involved in protective host responses to fungal pathogens. Although there is a lack of scientific studies on fungal infections it’s highly likely that mast cells are also important players in the fight against fungal infections.
The gastrointestinal tract, as well as the skin, have the highest amount of mast cells (in a normal state). During an infection the number of mast cells will rapidly increase in the gut. As the mast cells increase, and interact with the pathogens, they release more inflammatory mediators (including histamine). If the histamine load exceeds the ability to degrade it then the result will be histamine intolerance.
Candida and Food Allergies
Studies show that if your gut is colonised with the fungus Candida you are likely to become sensitive against food antigens (food allergy), because of the increased number of mast cells, and the hyper permeability of the gastrointestinal mucosa (which is caused by histamine release).
If you have histamine intolerances and food allergies it is very important to test for pathogens. As a minimum they can be contributing to the histamine load if you have a histamine related disease. They could also just be the cause.