October 28, 2017 9:00 pm


The role of bacteria and mast cells is an emerging area of medical research.

Mast cells are best recognized for their role in inflammation, allergies, and lectins.

Yet mast cells play a critical role in the defense against and clearance of pathogens, bacteria, and viral infections.

A significant body of research demonstrates that pathogenic bacteria or bacteria cell wall products activate mast cells to produce an anti-bacterial response.

This natural role of mast cells seems to have slipped off the radar.

A recent discussion paper co-authored by Theoharides highlights the impact on bacteria and mast cells. I also updated this post in November 2017 following a highly detailed Swedish review of the role of mast cells in bacterial infections.

This paper so mirrors my observations that I wanted to highlight these views while waiting for the research to catch up.


histamine intolerance, mast cell activation, autoimmunity, Alison Vickery, Health, Australia


Bacteria and Mast Cells

Mast cells are part of our immune system.

They act as sentries, stationed predominantly in the skin, the airways, the intestines, or, more importantly, where our body meets the environment.

When stimulated, for example, by bacteria, mast cells produce a range of mediators as a helpful protective measure and simultaneously cause wide-ranging symptoms.

Mast cells were perfectly designed to act in this way.

From a functional perspective, the question is not only “how do we suppress the mast cell in acting in this way” but, more importantly, “what is the mast cell trying to respond to?”


Mast Cell Activation Syndrome

Mast cell activation syndrome is an acquired condition and is very common.

Syndromes are not really “diseases” in which the body’s cells have stopped working, which need to be managed with surgery or drugs. Instead, they are a pattern of symptoms as the body adapts to stressors. Removing the stressor often resolves the syndrome.

Rather than one heterogeneous disease, mast cell activation syndrome can be seen as an umbrella term, with a significant variance in mast cell response depending on the trigger.

Any adverse stimulus, such as inflammation, infections, or mold, not just bacteria, can cause the mast cell to release or even dump immune mediators, including histamine.


The Life of Mast Cells

Mast cells have a limited life before being replenished. In the same way, we shed skin; we shed mast cells, which are constantly being renewed.

Removal of the trigger stimulating the mast cell is hypothesized to diminish mast cell activation over time. Speaking personally, this was a two-year process for me.

Furthermore, the increasing severity of the trigger is likely to inhibit the ability of the mast cell to turn over.


Protective Mast Cells and Bacteria

A landmark 1996 study established that mast cells play a crucial role in protection from pathogenic bacteria.

While many of these can be present, helicobacter pylori are present in around 50% of the world’s population and highly prevalent in my client base. It is easily treated with herbal substances in even the most sensitive client.

In addition to activating the mast cell, helicobacter pylori deplete vitamin B12, vitamin C, and core minerals and cause significant mucosal damage. It is also one of the leading causes of autoimmune thyroid diseases.

There is also considerable evidence that when endotoxins engage with mast cells, they activate them.

Endotoxins are part of the bacteria’s cell wall or biofilm released upon the bacteria’s death. Another term for endotoxins is lipopolysaccharides.

Dysbiosis, such as Small Intestinal Bacterial Overgrowth (SIBO), and bacterial biofilms produce endotoxins.

SIBO, in particular, is highly prevalent, in my experience, with mast-cell activation, and addressing dysbiosis can significantly reduce mast cell activation even in the most sensitive of people.


Dysfunctional Mast Cells and Bacteria

While there is strong evidence that mast cells protect against bacterial infections, some studies show that mast cells can also worsen bacterial assault.

A landmark 2010 study demonstrated that whether mast cells played a protective or harmful role depended on the severity of the bacterial infection.

As the severity of the infection increases, the body switches to other mediators to attend to the bacterial infection, including interleukin-4. Simplistically, the function of the mast cell is sacrificed in favor of other higher-powered meditators.

There is also strong evidence that some bacteria interfere with the function of the mast cell in an attempt to suppress its effectiveness and optimize its virulence.

From my point of view, this is another compelling reason why trying to eradicate the pathogenic bacteria or root cause is more pressing than trying to control the release of mediators by the mast cell.


Invasion of Mast Cells by Bacteria

Many pathogenic bacteria have also been shown to invade mast cells, increase their chance of survival, and replicate intracellularly.

Once inside the mast cell, they are less likely to clear, more likely to result in chronic infections, and more likely to alter mast cell behavior, including mast cell turnover.

Intra-cellular bacteria can be difficult to pick up on standard testing panels as it is not easily found in urine, blood, or stool tests.

An ultrasound is typically used to pick up intra-cellular bacteria, although Dr. Klinghardt uses ART (an advanced form of kinesiology) testing, which I find highly accurate.



Testing for Mast Cell Activating Bacteria

Several bacteria have been shown to activate mast cells.

The Gi-Map tests for the following mast cell activating bacteria:

Helicobacter Pylori

Enterococcus faecalis

Pseudomonas aeruginosa

Staphylococcus aureus

Streptococcus species

Candida species

Candida albicans, and

Lipopolysaccharide producers (gram-negative bacteria)



Much of the focus within medicine has been on mast cells and their relationship to the mediators they release.

This has led to much discussion about anti-inflammatory and mast cell stabilizing substances which, while helpful, are little more than a band-aid.

From a functional health perspective, the issue is not whether the mast cell is causing a chemical cascade but what is causing that cascade. This blog post outlines the link between pathogenic bacteria and mast cells.

In my observation, even in the most sensitive people, progress can be made by addressing bacterial infections.

Much is still to be learned, and it is encouraging to see mainstream medicine’s increasing interest in the link between bacteria and mast cells.


Additional Reading

Johnzon, Carl-Fredrik, Elin Rönnberg, and Gunnar Pejler. “The role of mast cells in bacterial infection.” The American journal of pathology 186.1 (2016): 4-14.

Conti, Pio, et al. “Link Between Mast Cells and Bacteria: Antimicrobial Defense, Function, and Regulation by Cytokines.” Medical Hypotheses (2017).

Galli, Stephen J., Susumu Nakae, and Mindy Tsai. “Mast cells in the development of adaptive immune responses.” Nature immunology 6.2 (2005): 135-142.

Marshall, Jean S. “Mast-cell responses to pathogens.” Nature reviews. Immunology 4.10 (2004): 787.

Kulka, Marianna, et al. “Mast cells, which interact with Escherichia coli, up-regulate genes associated with innate immunity and become less responsive to Fc?RI-mediated activation.” Journal of leukocyte biology 79.2 (2006): 339-350.

Rönnberg, Elin, Bengt Guss, and Gunnar Pejler. “Infection of mast cells with live streptococci causes a toll-like receptor 2-and cell-cell contact-dependent cytokine and chemokine response.” Infection and Immunity 78.2 (2010): 854-864.

Echtenacher, Bernd, Daniela N. Männel, and Lothar Hültner. “Critical protective role of mast cells in a model of acute septic peritonitis.” Nature 381.6577 (1996): 75-77.

Piliponsky, Adrian M., et al. “Mast cell-derived TNF can exacerbate mortality during severe bacterial infections in C57BL/6-Kit W-sh/W-sh mice.” The American journal of pathology 176.2 (2010): 926-938.

Dahdah, Albert, et al. “Mast cells aggravate sepsis by inhibiting peritoneal macrophage phagocytosis.” The Journal of clinical investigation 124.10 (2014): 4577.

Zhang, Hanying, et al. “Butyrate suppresses murine mast cell proliferation and cytokine production through inhibiting histone deacetylase.” The Journal of nutritional biochemistry 27 (2016): 299-306.

Matsuguchi, T. “Mast cells as critical effectors of host immune defense against Gram-negative bacteria.” Current medicinal chemistry 19.10 (2012): 1432-1442.

Sandig, Hilary, and Silvia Bulfone-Paus. “TLR signaling in mast cells: common and unique features.” Frontiers in Immunology 3 (2012).

Gutiérrez Venegas, Gloria, et al. “Histamine promotes the expression of receptors TLR2 and TLR4 and amplifies sensitivity to lipopolysaccharide and lipoteichoic acid treatment in human gingival fibroblasts.” Cell biology international 35.10 (2011): 1009-1017.

Talreja, Jaya, et al. “Histamine induces Toll-like receptor 2 and 4 expressions in endothelial cells and enhances sensitivity to Gram positive and Gram negative bacterial cell wall components.” Immunology 113.2 (2004): 224-233.

Liu, Z Q., et al. “Vitamin D contributes to mast cell stabilization.” Allergy(2017).