Role of Inflammation

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3D model of antibody

The Role of Inflammation in Rosacea

Pulling information liberally from the following Southern Illinois University School of Medicine abstract:

The triggers of acute inflammation are released by mast cells, sensitive cells which are scattered throughout ordinary connective tissues and which react to tissue damage or other disturbance. The basic components of the inflammatory response are:

  • Vasodilation
  • Increased vascular permeability
  • Emigration of white blood cells

There are a host of reactions involved in this process, but keeping it very simple, vasodilation causes the redness or flushing we see with rosacea. Some rosaceans flush just on their face, which is comparatively vascular and tends to show a flush first, while others show signs of flushing on their neck, chest and arms, and other body parts.

The increased vascular permeability, along with the vasodilation, is then meant to prepare the way for leukocytes or white blood cells (including neutrophils, lymphocytes and monocytes) to leak out of the vessels and enter the inflamed tissue for healing. When the leukocytes leak out into the surrounding tissue, the fluid build-up which follows is called edema and is visible as puffiness or swelling, and the increased metabolic activity associated with leukocyte activity also generates heat, contributing to local warmth.

The Neutrophil Leukocytes seem to play one of the most important roles in rosacea, and they are the reason rosacea has been referred to as 'neutrophilic dermatosis'. These leaking neutrophils end up causing the often resultant papules and pustules (p&p's) associated with rosacea, and are also responsible for stimulating Vascular Endothelial Growth Factor (VEGF) which promotes additional vascular growth, and thus the visible and non-visible excess blood vessels:

Over time, this process builds on itself, more blood vessel growth allows more inflammation, which only creates more blood vessel growth, etc. Something causes the inflammatory response to begin with, but once it starts, the excess blood vessels feed more inflammation, and more inflammation creates more blood vessel growth, etc.

It seems that scientists have a pretty good grip on the above-mentioned process. The real question is what causes the inflammation which leads up to this neutrophilic dermatosis. Backing up to the mast cell, mast cells contain receptors that, when activated, cause the mast cell to release histamine and tnf-a:

Tnf-a stimulates the production of Arachidonic Acid via Phospholipase A2 from our cellular lipid stores. Arachidonic Acid is then responsible for the production of a host of downstream leukotrienes through the 5-lipoxygenase (5-LOX) pathway, and these leukotrienes seem to be responsible for many of the problems associated with the inflammatory response:

Arachidonic Acid is also responsible for the production of downstream prostaglandins and thromboxanes, which play a role in making the blood vessels dilated and leaky:

The unanswered question, though, is what sets off this inflammatory event in the first place? Could it be some bacterial, viral, or fungal pathogen? Is there a genetic role where rosaceans might inherit the potential for more 5-LOX and/or COX production? Could environmental or topical insult damage and/or irritate the tissues and lead to this inflammatory response? Could frequent flushing from allergies, heat, hot flashes, etc cause tissue damage or irritation, which then leads to this response? Finally, once this inflammatory response is initiated, could it become a self-perpetuating cycle whereby inflammation leads to more flushing and tissue damage, which only causes more inflammation?

Many researchers theorize that our current western diet contains too large a percentage of the pro-inflammatory omega-6 fatty acids in comparison to other less-inflammatory omega-6 and omega-3 fatty acids, and this imbalance contributes to most of the modern world's inflammatory problems (arthritis, heart disease, Alzheimers, Crohn's disease, and rosacea, amongst others). Theoretically, decreasing the intake of pro-inflammatory omega-6 fatty acids and increasing the intake of the less-inflammatory omega-6 and omega-3 fatty acids will help to reduce the inflammatory reaction.

Research suggests that this will not stop the inflammatory reaction altogether, and interestingly, some studies seem to suggest that some pathogens, in addition to being capable of initiating an inflammatory response, are themselves capable of Arachidonic Acid production:

It also appears that some of the downstream products of Arachidonic Acid - prostaglandin E2 and thromboxane B2, both produced under the COX pathway - can actually up-regulate infections by some pathogens, i.e. C. albicans:

This is particularly interesting, since the prior-referenced study suggests that once they take hold, C. albicans can then produce additional Arachidonic Acid. Studies have also identified other pathogens that either thrive off of or help to promote the prostaglandin, thromboxane and leukotriene rich environment found in TH2 type diseases such as rosacea (see Role of Parasites & Fungi).

Finally, studies also suggest that blood sugar levels, exercise and women's hormonal fluctuations can all influence the inflammatory response through the Arachidonic Acid pathway as well.

Useful links:

  • INFLAMMATION AND REPAIR Note: Do a find on "LEARN FIRST" for start of a great explanation of the inflammatory process