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Sinus probiotics are being investigated for chronic rhinosinusitis (CRS). In this article, I am going to address the conventional approach to CRS, the underlying cause of CRS that research has illuminated, some factors that contribute to the cause, and general ways, including the use of sinus probiotics, to improve sinus and nasal health. |
Chronic rhinosinusitis (CRS) is a persistent inflammatory condition of the nasal passages and the paranasal sinuses, air-filled extensions of the nasal cavity. It is said to affect approximately 11% of the European population, cause costly medical expenses, and result in significant morbidity in young and middle-aged adults with substantial decreases in quality of life.
If you go to an ear-nose-throat (ENT) doctor for CRS, you most likely will be placed on antibiotics, not sinus probiotics. I cannot count the number of rounds of antibiotics I took, along with three sinus surgeries, before I got my CRS under control with diet changes and gut restoration. Most ENT's automatically assume that a bacterial infection is present and antibiotics are warranted. But is it? And are they? What does research show?
Many, many sinus microbiome studies have been performed prior to 2015 comparing people with CRS to healthy controls. Almost all of the studies focused on bacteria.
Some studies have implicated the Corynebacterium genus as a potential cause of CRS. The problem with those studies is that they are too broad because this genus of bacteria contains pathogenic, opportunistic, and non-pathogenic species.
Other studies have suggested changes in the pathogen Staphylococcus aureus, decreased Prevotella species, lower microbial diversity, and/or increased microbial abundance as the causes of CRS, with seemingly contradictory results.
Complicating the picture is the effect that polyps, immune-cell dominance type, genetics, sampling location in the sinuses, virus or fungi habitation, antibiotic treatments, and corticosteroid treatments have on CRS. No clear answer on the cause of CRS has been found until recently.
A very interesting 2020 study used data from 410 sinus swabs from the International Sinonasal Microbiome Study plus 97 sinus swabs from a different set of people. The researchers determined that there are three basic "microbiotypes" of the sinuses:
This study showed that most people (54%) have the first microbiotype, 29% have the second, and 17% have the third. There was no significant difference between those microbiotypes in healthy control versus CRS patients, meaning that these microbiotypes cannot be used by themselves as disease markers.
The pathogen Staphylococcus aureus is known to hide in biofilms, produce toxins, and is perceived to be important in inflammatory sinus disease. This study and other studies have shown a competitive inhibition between Corynebacterium as a genus and the pathogen Staphylococcus aureus, and also have shown an ability of Corynebacterium to not only control S. aureus, but also to resist the very contagious Respiratory Syncytial Virus and the pathogen Streptococcus pneumoniae. In fact, one strain of Corynebacterium pseudodiphtheriticum demonstrated potential as sinus probiotics in an animal model.
Continuing to focus on the bacterial sinus microbiome, another study worth highlighting was performed in 9 patients with CRS and 6 non-CRS controls, ages 21 to 80, who were about to undergo endoscopic sinus surgery. The patients had to be off antibiotics for at least 4 weeks prior to surgery. The beauty of this study is that it used samples from various sites in each individual to look at variations among patients as well as variations at different sites in the same patient.
Duplicate surface mucosa samples were taken from each individual from 3 sites on each side of the nose: anterior nares (nostrils), inferior turbinate (one of the first bones encountered inside the nose), and middle meatus (a space important for drainage from the maxillary, anterior ethmoid, and frontal sinuses). Bacterial primers were used to match bacteria.
The results showed that most healthy samples were dominated by the Actinobacteria phylum (specifically the Corynebacterium genus) and Firmicutes phylum (mostly Staphylococcus or Dolosigranulum), with Betaproteobacteria and Gammaproteobacteria (particularly Moraxella) being detected to a lesser extent. Importantly, the results showed considerable variation among the microbiota of different individuals with and without CRS, but no significant differences in bacterial diversity, composition or abundance among different sites within the same individual with or without CRS.
Also, importantly and surprisingly, disease status did not explain the variations. The majority of differences between CRS samples could not be explained as the results varied considerably and were not predictable, except for the overall impression that the bacterial diversity of CRS patients was reduced.
Thus, importantly, there was no signature CRS bacterial community. nstead, CRS is thought to be a mix of disease states that share clinical symptoms.
A more stable bacterial community in healthy patients suggests that dysbiosis is linked to CRS occurrence. Dysbiosis can cause chronic inflammatory disease in the absence of acute infection, as well as cause acute infection. Disrupting the interactions of healthy commensal bacteria with the local immune system by dysbiosis appears to be critical for CRS progression.
Thus, an emerging view at the time of the study and today is that CRS is a state of altered ecological landscape interacting with an abnormal immune response to cause a disease state. In other words, although earlier studies that isolated pathogens from the sinuses of CRS patients pointed to a pathogen-related infection, CRS is regarded in the recent research literature as a disease of inflammation rather than infection.
Addressing the symptoms of CRS by randomly giving patients antibiotics without ultimately knowing what is causing it is… silly, at the very least, and has the potential to do more harm than good. Infections are not always the cause of CRS, as the studies have illuminated.
If CRS is a disease of inflammation, and if dysbiosis contributes to the inflammation, then we have to take a step back, deal with the causes of the dysbiosis, and study if sinus probiotics can help. There are actually many causes of dysbiosis, and more than one may play a role in a person's altered sinus microbiome. Numerous causes are summarized below.
An obvious cause of sinonasal dysbiosis is a structural abnormality that narrows the already very narrow nasal passages. This can lead to oxygen depletion in the sinuses and an unfavorable change in the microbial community, as explained in the next possible cause of dysbiosis. While many sinus and nasal pathogens prefer oxygen-depleted environments, commensal bacteria that live in the sinuses, such as many Corynebacterium, prefer aerobic conditions.
Another possible explanation for the cause of dysbiosis may be impaired mucus clearance, which allows oxygen levels in the sinuses to plummet, which then allows mucin-fermenting anaerobes to proliferate and cause dysbiosis, which ultimately leads to proliferation of sinus pathogens feasting on the fermentation products. Indeed, one study with mucus samples from 9 CRS patients and 6 controls showed that short-chain fatty acid levels in patients with CRS were significantly higher than in controls, suggesting enhanced bacterial fermentation in a hypoxic environment.
Another explanation may be a virus or allergen that disrupts the immune barrier. Nasal tissue has a high concentration of capillaries it in, and changes in these capillaries can lead to nasal congestion and significantly block the already very narrow nasal passages, as well as secrete inflammatory immune molecules to counter the virus or allergen. Sinus flushing may help with thick mucus and viral or allergen loads.
Smoking may also cause dysbiosis in the sinuses.
Genetics may play a role. One example is a common polymorphism (SNP) in a bitter taste receptor that is associated with gram-negative bacterial infection and biofilm formation in CRS. This polymorphism results in reduced signaling through the receptor, thus decreasing nitric oxide production and ciliary beat frequency, which are important in host immune defense against gram-negative pathogens.
Immune status may contribute to dysbiosis, as reductions in antimicrobial peptides and/or exaggerated inflammatory responses can affect microbial colonization and CRS. Conversely, dysbiosis influences immune status. Sinus probiotics can address both.
Sinus Squeeze may cause microbiome imbalances. Sinus Squeeze, also known as barosinusitis, is the irritation of the mucosal lining in the paranasal sinuses due to an inability to equalize intrasinus pressure with ambient pressure with a rapid ascent or descent in altitude. If the irritation and resulting inflammation do not subside, dysbiosis may establish.
Fungi may upset the balance. Most studies focused on bacterial communities since antibiotics are the first line of therapy in conventional ENT. However, fungi involvement is a real possibility. Although most people have evidence of fungal colonization in the sinuses, more recent research shows that fungi may be important, particularly in CRS with nasal polyps. The fungi cause an imbalance in the immune system resulting in chronic inflammation that may or may not proceed to a bacterial infection.
In most cases, the immune response keeps the fungi under control, albeit with uncomfortable symptoms, but in immune-suppression cases, the fungi can become life-threatening. However, studies using topical or systemic antifungal drug treatments in CRS did not show any benefit compared to placebo to support their use clinically, and in fact, showed adverse reactions compared to placebo.
Another explanation for sinonasal dysbiosis is gut dysbiosis due to wide-reaching effects of the gut on the entire body. One study that focused on sinus inflammation is of interest here. A retrospective, controlled, 4-week multicenter study on inflammatory non-allergic rhinitis in 93 patients showed that oral sinus probiotics containing Lactobacillus acidophilus NCFM and Bifidobacterium lactis combined with a prebiotic, fructo-oligosaccharides (FOS), significantly reduced the percentages of patients with symptoms and endoscopy findings, and also diminished inflammatory cells, compared to controls. The sinus probiotics symbiotic was used as an adjunct therapy to nasal corticosteroid, oral antihistamine, and isotonic saline.
The two sinus probiotics in the last study are found in Metagenics UltraFlora in my online supplement dispensaries, Wellevate and Fullscript.
This article has shown that inflammation, and not necessarily infection, is the culprit behind CRS. Dysbiosis is a cause of inflammation, and there are multiple causes of dysbiosis. It takes detective work to expose the contributing factors and determine if sinus probiotics may be helpful.
A good place to start to reduce inflammation of many kinds is with gut health since most of the immune system resides in the gut and affects multiple parts of the body. Identifying pathogens, parasites, imbalances in normal flora, and intestinal permeability through a stool test, and addressing them with a gut restoration protocol that includes sinus probiotics has the potential to improve sinus/nasal health and symptoms.
If you would like to schedule a stool test and one-time consultation with me with recommendations for improving your gut health, please contact me.
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