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ROSACEA and ARTHRITIS - a conspiracy between bacteria

Updated: Jun 28


In cooking, instinct often guides us in choosing condiments. We seek out aromas and flavors that stimulate the palate and enhance the taste of our food. This intuition also serves as a means to address health issues and has significantly aided me in overcoming various health challenges. Frequently, I have managed to prevent inflammations from developing into more serious conditions. To understand the efficacy of herbs, I turn to science for answers.

The ancient practice of using aromatic herbs in cooking to enhance flavor or for therapeutic purposes has been studied by scientists aiming to understand how the chemical components of these plants interact with our immune system.

Aromatic herbs and spices, when used as condiments, can influence the enzymes of the digestive system and the intestinal bacteria. Some promote the absorption of nutrients that our bodies may lack, while others reduce the absorption of sugars and carbohydrates, helping to prevent diabetes and fat accumulation. Many aromatic herbs and spices also alter the intestinal flora, encouraging the growth of beneficial bacteria that ensure proper digestive function and reduce disease risk. Therefore, choosing the right condiments is an effective way to prevent nutritional deficiencies and strengthen the immune system.

The intestine - our second brain

Our body, and by extension, our immune system, is the result of countless chemical reactions occurring simultaneously. These reactions serve various purposes, such as producing energy, repairing tissues, and combating diseases. We can influence these reactions through changes in diet, medication, and other means. However, just as we can manipulate our body chemistry, other organisms can do the same. This is the story of our body's invisible alchemists.

An imbalance in the intestinal flora can lead to the excessive growth of bacteria that become virulent, escaping their usual habitat—the intestines—and invading other parts of the body. In their virulent state, these bacteria communicate and coordinate through a system called quorum sensing, enabling them to develop strategies to combat rival bacteria and evade the immune system with impunity.


To move easily through the body's cells, these bacteria cause inflammation in muscles and joints to provoke an immune response. During the tissue repair process, the production of filopodia—fiber systems that accumulate in muscles—is stimulated. Filopodia facilitate communication between cells and promote the transport of nutrients necessary for healing. However, the presence of filopodia also enables bacteria to spread throughout the body, leading to widespread infections. Concurrently, the immune system responds by activating cytokines and interleukins, inflammatory substances needed to combat pathogens. In this case, however, these substances do not act against the invading bacteria; instead, they eliminate bacteria that compete with the invaders.


Symptoms of inflammation


Throughout my adult life, I have experienced inflammation that caused pain and stiffness in my muscles and spine. In recent years, these inflammations have rapidly worsened, leading to calcifications that affected many other muscles in my body. If the situation weren't so serious, I could compare the discomfort to a game of 'Twister,' as my muscles felt twisted and contorted. As a result of this inflammation, I also experienced blurred vision, loss of balance, dizziness, ear infections, and rosacea—a chronic inflammation of my face. The calcification of muscles near my chest made breathing difficult, sometimes to the point of panic, though I learned to manage this. Overall, I lost significant muscle strength, particularly in my right arm and legs, making it impossible to walk without assistance. However, the most frightening symptom was the intense pressure I felt on the right side of my brain. Socializing with friends became increasingly difficult, and I avoided leaving the house.

In an attempt to alleviate the symptoms, I turned to physiotherapy, which I soon realized was the key to feeling better. After a few years, my muscles gradually regained flexibility. One by one, the symptoms of imbalance, dizziness, digestive issues, muscle stiffness, blurred vision, and finally the pressure on the right side of my brain, disappeared. To achieve this result, I dedicated myself entirely to understanding and addressing the root cause of these symptoms. Since it all began with digestive problems, I focused my attention on the bacteria that colonize the digestive system

By sharing my experience I hope that, in the future, other people who find themselves in a similar situation can have a starting point to face this problem.


Bacteria that cause muscle damage


Tests on my stomach revealed that the frequent inflammation I experienced was caused by the presence of the bacterium Helicobacter pylori. This bacterium thrives on hydrogen, which is abundantly supplied by other intestinal bacteria such as Klebsiella pneumoniae. By consuming hydrogen, H. pylori reduces the production of gastric acid and digestive enzymes, compromising the digestion of food, especially starches. These unmetabolized starches then reach the intestines, where they serve as food for Klebsiella pneumoniae. This interaction between bacteria perpetuates the infection and contributes to gastrointestinal problems.


Klebsiella pneumonia


Klebsiella pneumonia

Klebsiella p. manages to bypass the immune system by disguising itself. Through the biofilm (protective layer), which it produces using hyaluronic acid from muscles and joints, it goes unnoticed without triggering any reaction from the immune system. As a result, little by little, muscles and joints lose flexibility. Inflammation generally starts in the lower back and spreads to other parts of the body, with a very specific characteristic: it affects one side of the body more than the other. This is the characteristic that defines the problem of muscle calcification Ankylosing spondylitis which, according to scientific studies, is linked to the presence of this bacteria. (1)


Hyaluronic acid is a substance necessary to protect joints and is part of the cartilage production process. In some people, genetic factors stimulate the action of the BMP-7 protein, which promotes the production of excessive hyaluronic acid, favoring the virulent growth of Klebsiella pneumonia. (2) (3)

To reduce the growth of bacteria, in addition to avoiding the consumption of foods rich in starch such as potatoes, pasta, bread and beans, care must be taken to consume these foods on the day they are prepared as, a few hours later, starches become resistant to digestion, that is, they are not digested by the intestines and only serve as food for intestinal bacteria.

Helicobacter pylori

Helicobacter pylori

H. pylori has developed another strategy to infect the stomach - through the enzyme urease it produces ammonia and carbon dioxide which inhibits gastric acid, facilitating the spread of the bacteria, and also blocks the immune system's attempt to combat the bacteria. (4)

Carbon dioxide is important for activating the AMPKa-FOXO3a-MuRF1 an emergence process that is normally activated when energy production levels are reduced, such as in situations of hunger or fasting. As an alternative to a lack of food, muscles are sacrificed and lose some of their amino acids which are essential for other vital functions. (5)

If this situation persists for a long time, muscles become weak and atrophied and, in addition, the excess carbon dioxide dilates the blood vessels, lowers blood pressure, causes dizziness, headaches, fatigue and can even cause fainting. This was a situation I had to face a few times when I had frequent stomach inflammation.

To reduce muscle damage caused by this bacteria, it is advisable to consume foods rich in aspartic acid (asparagus, dairy products, eggs, peanuts), which promote the production of muscle mass and also increase the circulation of oxygen to the muscles.  Additionally, aspartic acid helps remove excess ammonia from circulation. (6)

The inflammation caused by these two bacteria reduces the production of cartilage and collagen, which are important for the proper functioning of joints and maintaining healthy skin. This explains why I, intuitively, preferred foods rich in collagen and amino acids (such as proline and glycine) which are found in abundance in chicken skin and cartilage. Other foods that I felt the need to consume were eggs, milk, meat, vegetables from the cabbage family (cruciferas), garlic, onion - foods rich in sulfur, an important element for maintaining joint flexibility and helping to eliminate toxins produced by bacteria.

As if all the damage it causes is not enough, this bacteria, through the virulent factor called CagA, stimulates the excessive production of FILOPODIA which, together with an alkaline pH due to the ammonia produced by the bacteria, facilitates the virulent growth of other bacteria.

Complicity between bacteria

S. aureus and Pseudomonas aerogenes are two other bacteria from our body's flora that benefit from these favorable conditions. In their virulent form, these two bacteria use each other's resources to more easily penetrate the tissues to be infected. They damage muscles but they are also linked to many other health problems.

Pseudomonas aerogenes

Pseudomonas aerogenes

When the inflammation of this bacteria predominates, the most evident symptom is frequent respiratory allergies due to an excessive reaction of the immune system. Pseudomonas a. stimulates the production of neutrophils, which are part of white blood cells, the body's main defense against bacteria and other pathogens. Neutrophils, in turn, trigger a process that involves the production of F-Actin filaments to which the bacteria attaches in order to produce its protective biofilm. Due to the biofilm, neutrophils are unable to fight the bacteria and accumulate in the form of NETs (neutrophil extracellular traps) around the infection to prevent the bacteria from spreading to other tissues in the body. But the accumulation of NETs, ​​in turn, also causes inflammation that gives rise to autoimmune diseases. Rheumatoid arthritis, inflammation in the intestines, IBS, Crohn's disease and metabolic diseases are associated with this condition. (7)



In addition to all this, Pseudomonas has an auxotrophic action, that is, it 'steals' the amino acids it needs as energy sources from the organs it is infecting. It mainly consumes tryptophan and a set of amino acids called BCAAS (branched chain amino acids), valine, leucine and isoleucine. BCAAS are important for the production of muscle mass and when they are lacking, muscles weaken and atrophy. Tryptophan is the amino acid that our body metabolizes into serotonin, the neurotransmitter that acts in the brain and regulates mood, sleep and appetite.


S. aureus

Staphylococcus aureus

This is a bacteria that has many features that allow it not only to escape the action of the immune system, but also to easily penetrate the body's tissues. Its most powerful 'weapon' is the enzyme hyaluronidase (8) which destroys hyaluronic acid in areas such as the skin, muscles and joints, areas that this bacteria damages heavily. Hyaluronic acid, in addition to being part of the cartilage production process, works as a lubricant and moisturizer, maintaining tissue flexibility and protecting against muscle wear.

In the presence of this bacteria, the reduction in hyaluronic acid disrupts the normal process of cartilage production and instead stimulates a different pathway called FOXC2-Wnt4-BMP-4 that promotes calcification of muscles and joints. As a result of this inflammation, muscles become stiff and damaged. In the inflammation MYOSITIS OSSIFICANS, which was the cause of the worsening of the muscle problems I experienced, this process is chronically active and worsens over time. (9) (10)

Skin inflammations

Keratosis pilaris (keratosis pilaris) and Rosacea are two skin problems that I inherited from my mother and passed on to my children. In both cases, excess keratin production is noticeable. In the condition Keratosis pilaris, keratin clogs the hair follicles leaving the skin with a rough ‘chicken skin’ texture. It appears mainly on the upper part of the arms and legs but can also appear on the face.

Rosacea manifests itself with redness and the appearance of pustules on the face. In the eyes (ocular rosacea) it causes inflammation, blurred vision, burning and foreign body sensation.

Excessive production of keratin is a normal process that occurs in people with fair skin, to protect against sunburn, when the skin is exposed to ultraviolet rays. The clear skin of the inhabitants of Nordic countries allows for faster absorption of vitamin D, even on days when sunlight is scarce. However, excessive exposure to the sun causes burns and, to deal with this situation, the immune system promotes the dilation of blood vessels so that there is greater blood circulation, necessary to transport nutrients to the damaged area. The skin turns red and, immediately afterwards, the TRPV4 protein is activated, which induces the production of keratin type K10. The film that forms on the skin after a sunburn is made up of this type of keratin that accumulates in layers on the skin to protect against infections and UV rays.


However, excess keratin favors the infection of bacteria such as S. aureus which, using another of its 'weapons', the virulent factor Clumping factor B, (11) allows it to adhere to skin tissues to initiate the infection. Not to leave anything to chance, this same bacteria also activates the TRPV4 protein chronically to perpetuate the infection, even when there is no sun exposure. It is therefore very likely that the bacteria S. aureus is the main cause of Rosacea, as the TRPV4 protein is identified in this type of inflammation. (12)

Zonas de inflamação

This characteristic is not unique to this bacteria, as according to scientific research, areas of the body with a high concentration of keratin are preferred by bacteria as it allows them to adhere to tissues and initiate infection. The palms of the hands and soles of the feet have thick layers of keratin forming a waterproof layer that protects against possible injuries. The abundance of keratin facilitates infection by bacteria and, probably, this is where these bacteria release their 'anchor' and initiate the infection.


Naturally, the growth of bacteria in these areas will affect the surrounding muscles and joints, such as the wrists and ankles. Over time, many other muscles connected to these will also be affected. In addition to the palm of the hand and sole of the foot, the S. aureus bacteria prefers moister areas of the body such as the armpit, inguinal area, and the back of the knee and elbow (13) . Maybe it's a coincidence, but these were precisely the areas where the inflammation affecting my muscles was most evident. When, after a lot of effort, I managed to recover the damaged muscles, the inflammation on my face (Rosacea) slowly reduced until the skin recovered noticeably.

Demodex folliculorim

Demodex folliculorum

In many cases of Rosacea, the presence of the Demodex follicolorum mite is responsible for some of the symptoms of this disease. In terms of vision, it manifests itself as itching, burning, blurred vision and a foreign body sensation, symptoms that I felt very frequently. On the face, this microorganism is also responsible for the appearance of pustules that resemble acne. The fact that this mite does not appear in all people affected with Rosacea leads us to believe that the inflammation caused by S. aureus facilitates the development of Demodex folliculorum and this mite is not the cause of Rosacea. In inflammation caused by Staphylococcus aureus, levels of cathelicidin, TRPV4 and MMP-9 (the enzyme that destroys type I and III collagen) are high and are responsible for many of the symptoms that characterize the presence of this bacteria. It is no coincidence that these inflammatory agents are also active when the presence of the Demodex folliculorum mite is noticed on the skin.

Exercise as a means to reduce inflammation


The stiffness and calcification of muscles, due to bacterial infection, hinders blood circulation, which prevents the immune system from recovering damaged muscles. This situation not only perpetuates itself but worsens over time. Stimulating circulation with appropriate exercises promotes the entry of missing nutrients into damaged muscles and allows the immune system access to infection.


Some essential oils such as menthol from Mentha arvensis and carnosol from Rosmarinus officinalis (rosemary), applied as a lotion to affected muscles, enhance the action of exercise, facilitating the muscle regeneration process. While rosemary oil is indicated to stop inflammation caused by Klebsiella p., menthol stimulates circulation, facilitating the entry of nutrients into the muscles. Against the inflammation of S. aureus, and to stimulate the decalcification of affected muscles, the most effective oil, according to my experience, is Limonene, which is easily extracted from the orange peel by macerating in alcohol. As a lotion it is applied on muscles before exercising.


In order to fully recover the damaged muscles and eliminate inflammation, it was important to understand what was happening to me.

Throughout the period I had to deal with this situation, the inflammation always became more intense at night, as this is when adenosine levels are highest. ADENOSINE is a molecule with several physiological functions, among which it induces sleep. To become virulent, the S. aureus bacteria needs high levels of adenosine and therefore inflammation is stronger during the night. Furthermore, the bacteria itself uses another of its many 'weapons', the enzyme Adenosine synthase, which increases adenosine levels to exaggerated values.



It didn't take long to discover that the only way to combat inflammation at night was to exercise, in moderation, the affected muscles. To my surprise, the exercise I was doing, together with the essential oils I applied to the affected area, stimulated the decalcification of muscles. However, muscles that had been stiff for many years, when they lost calcification, they didn't gain flexibility immediately. They felt loose, without action and I felt a sensation of tightness as if, after being freed from calcification, these muscles suddenly needed to take up more space.

This sensation allowed me to identify the affected muscles and, whenever this happened, I had to react immediately, otherwise, the inflammation would become unbearable. I had to exercise muscles very slowly and little by little muscles regained their flexibility.

This was a very long and scary process because the end result was unpredictable. I have no doubt that I owe my success to the combination of three things: choosing foods rich in nutrients (which were lacking in my body), the many physiotherapy sessions and also the essential oils I applied when I exercised at home.

At all times I had the unconditional support of my family, who gave me the strength not to be tempted to give up, and, despite all the uncertainties and difficulties that surrounded my situation, I always had the professional support of the EQUILIBRIUM physiotherapy clinic. I owe a lot to the physiotherapists, and all the staff at this clinic, as I am sure that, without their support, this journey would have been much more difficult.





BIBLIOGRAFIA

  1. In conclusion, extensive scientific evidence suggests an important role of Klebsiella in AS. The presence of HLA antigens and elevated Klebsiella antibodies in AS could be helpful in the identification of patients with this condition during the early stages of disease. The use of new therapeutic modalities in the form of anti-microbial therapies in conjunction with the currently available treatments should be evaluated in longitudinal studies. https://link.springer.com/article/10.1007%2Fs10067-006-0488-7

  2. Stimulation of cells with BMP-7 induced HAS2 mRNA expression and decreased the expression of Hyal1 and Hyal2. https://www.researchgate.net/publication/8605106_BMP-7_modulates_hyaluronan-mediated_proximal_tubular_cell-monocyte_interaction

  3. In conclusion significant progressive increase in serum BMP-7 was noted in AS (Ankylosing spondylitis) patients that correlated with markers of bone formation.” (1) https://www.ncbi.nlm.nih.gov/pmc/articles/

  4. These results suggest that H. pylori-associated urease functions to produce a potent ONOO− scavenger, CO2/HCO3−, that defends the bacteria from ONOO− cytotoxicity. The protective effect of urease may thus facilitate sustained bacterial colonization in the infected gastric mucosa. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC98327/

  5. High CO2 induced AMPKα2 activation, triggering the phosphorylation and nuclear translocation of FoxO3a, and leading to an increase in MuRF1 expression and myotube atrophy. Accordingly, we provide evidence that high CO2 activates skeletal muscle atrophy via AMPKα2-FoxO3a-MuRF1, which is of biological and potentially clinical significance in patients with lung diseases and hypercapnia. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4423704/

  6. Moreover, Asp (ácido aspártico) decreased phosphorylation of AMPKα but increased phosphorylation of Akt and Forkhead Box O (FOXO) 1 in the muscles. Our results indicate that Asp suppresses LPS-induced MAFbx and MuRF1 expression via activation of Akt signaling, and inhibition of AMPKα and FOXO1 signaling. https://www.researchgate.net/publication/309299808_Aspartate_inhibits_LPS-induced_MAFbx_and_MuRF1_expression_in_skeletal_muscle_in_weaned_pigs_by_regulating_Akt_AMPKa_and_FOXO1

  7. We have demonstrated that the presence of abundant F-actin and DNA in a neutrophil-rich environment is exploited by P. aeruginosa to ensure survival via biofilm development. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2677169/ Neutrophils are short-lived cells under steady condition but, once migrated into tissue, they are exposed to survival signals to increase their life-span. It has long been accepted that, in a successful acute inflammatory response that completely resolves, neutrophils are cleared from inflamed tissue in a timely fashion (Soehnlein and Lindbom 2010). When this clearance does not occur appropriately, neutrophils undergo necrosis and release intracellular contents that can damage the tissue and extend the inflammatory phase. https://link.springer.com/article/10.1007/s00441-017-2785-7 The inefficacy of neutrophils to penetrate Pseudomonas biofilm leads to the production and release of NETs as an attempt to avoid bacteria spreading https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6769795/ ...neutrophilic recruitment to corneal infections limits P. aeruginosa biofilms to the outer eye surface, preventing bacterial dissemination. Neutrophils moved to the base of forming biofilms, where they underwent neutrophil extracellular trap formation (NETosis) in response to high expression of the bacterial type-3 secretion system (T3SS). NETs formed a barrier "dead zone," confining bacteria to the external corneal environment and inhibiting bacterial dissemination into the brain. Once formed, ocular biofilms were resistant to antibiotics and neutrophil killing, advancing eye pathology. However, blocking both Psl and T3SS together with antibiotic treatment broke down the biofilm and reversed keratitis, suggesting future therapeutic strategies for this intractable infection. https://pubmed.ncbi.nlm.nih.gov/30930127/ Although NETs may protect the host against microbes, excessive NETosis can be detrimental to the host. Recent discoveries in in vitro experiments and animal models demonstrated the crucial role of NETs in the pathogenesis of some metabolic, autoimmune, and autoinflammatory diseases and certain septic conditions increasing morbidity and mortality https://link.springer.com/article/10.1007/s12016-020-08804-7

  8. https://microbeonline.com/virulence-factors-staphylococcus-aureus/

  9. In this study, enhanced SOX9 expression induced by GSK1016790A was apparently suppressed by the pre-incubation with HAase, which would suggest that ATDC5 cells require the intact CD44-HA interaction for the chondrogenesis induced by the mechanical stress loading. The appropriate extent of mechanical stress loading in the presence of the adequate amount of HA would affect the differentiation and maintenance of articular cartilage and chondrocytes. (…) This study demonstrated that the HAase pre-treatment clearly suppressed the SOX9 expression induced by TRPV4 specific agonist in ATDC5. Our results may help to elucidate the mechanisms of chondrogenesis through the potential relationship between TRPV4 and HA-CD44 interaction. http://www.ors.org/Transactions/61/0340.pdf

  10. Dysregulation of Bmp4 signaling and/or its receptor has been implicated in heterotopic ossification and myositis ossificans,36, 37 and several studies have suggested that Bmp4 plays a key role in the development of these diseases. (…) Ac3tivated Bmp signaling initiated endochondral ossification at the site of muscle injury.40 Although it is still unclear if FOXC2 plays a role in the development of conditions such as heterotopic ossification, we show that FOXC2 is expressed in areas of ectopic bone development in muscle biopsies from patients diagnosed with myositis ossificans. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705598/

  11. The commensal Staphylococcus aureus permanently colonizes the anterior part of the nasal cavity. The staphylococcal surface receptor clumping factor B (ClfB) plays a pivotal role in this process. It was shown that ClfB binds to epidermal K10 [52,72,73], which is typically found in cornified stratified epithelia [74,75]. The interaction between ClfB and K10 enhanced adherence of Staphylococcus aureus to epithelial cells and thereby supported epithelial colonization, notably in the squamous epithelial cells of the nasal epithelium https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5040971/

  12. "Mascarenhas et al. report that TRPV4 expression is upregulated in mast cells in response to the proteolytic cathelicidin fragment LL37 in a murine rosacea model and that TRPV4 loss of function attenuates mast cell degranulation. These findings render TRPV4 a translational-medical target in rosacea. However, signaling mechanisms causing increased expression of TRPV4 await elucidation. Moreover, we ask whether TRPV4-mediated Ca++-influx evokes mast cell degranulation." https://irosacea.org/forums/topic/3457-trigeminal-sensory-malfunction-theory/

  13. Staphylococcus aureus (S. aureus) is found on about a third of the population. It usually lives in the moist areas such as armpits, groin and nose, although it can be found on other parts of the body such as your hands https://www.wchc.nhs.uk/services/infection-prevention-and-control/meticillin-resistant-staphylococcus-aureus-mrsa/#:~:text=aureus%29%20is%20found%20on%20about%20a%20third%20of,like%20any%20other%20germ%2C%20it%20can%20cause%20infections.





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