Our First Line of Defense Against Respiratory Infections is a Clean nose! 

When the kitchen floor is dirty the first thing we do is sweep it.  

For example, the highest incidence of ear infections in this country, and probably the world, is in the Native American children in Alaska. 

Doctors think that these people get ear infections because they are genetically disposed to them by the shape of the Eustachian Canal in the back of the nose. But the same tribal elders point out that children from the same genetic pool living in a more traditional environment in Nome's sister city of Provideniya, Siberia do not have trouble with their ears today. Our doctors say they are just not diagnosed, but it does not take a doctor to tell that a screaming child that pulls on his ear or complains of an ear ache has a problem, especially when it drains a few days later. Tribal elders often have more wisdom than some like to acknowledge.

Besides the environmental factors, things that hurt the cilia will also lead to more problems.

The cilia and mucus working together clean out the great majority of bacteria and other pollutants that enter the nose. When we look at the back of the nose with a microscope we can see the bacteria caught in the mucus and riding on top of the cilia. These bacteria are not going to cause problems. In normal cleaning they are swallowed along with the mucus and are killed by the acid in our stomachs. In order to cause infections bacteria must find a place in the back of the nose where there is no mucus protecting the cells. The first step in any infection is bacteria or viruses that are holding on, the scientific word is adhering, to our cells. Even most of these bacteria are killed by our own antibacterial substances in the airway surface fluid that bathes these cells. 

Sweeping back-up: If  we cannot remove the dirt from the kitchen floor with sweeping we need to get out the soap and water.  

It's the same with the nose. 

Defenses help us to deal with insults from our environmentthey should be honored and supported because they function to keep us healthy. But researchers in the 1940's weren't interested in defenses. They found that histamine was associated with a runny nose and that antihistamines stopped the nose from draining. They sanitized the snotty nose by turning off its defensive washing. Two things happened in the early 1970's to promote these problems:

    These drugs act to block our normal, but bothersome, nasal cleaning. Antihistamines block the effects of histamine so the washing never gets turned on and decongestants close down the blood vessels that histamine has opened so the water gets turned off. It does not require a whole lot of training to see that if we stop the washing we will have more dirt. 

This is also suggested by the side effect studies of one of these drugs.

While two weeks is enough time to evaluate the side effects for the drug, such as dry nose or sedation, it is hardly long enough to see the side effects of taking the drug for its intended purpose. 

We have now had an uncontrolled thirty year trial of what happens when we block a normal defense and we ought to pay attention.

Blocking defenses is not new in our medical history. When a person gets infected or injured our immune system recognizes a problem and signals that more blood is needed to deal with it. This is called the inflammatory reaction. In an injury it causes swelling and pain so the area is splinted by the swelling and we know from the pain to stay off it until it is better. In an infection the increased  blood helps the body deal more effectively with the infection. 

For almost 4000 years a person who went to the doctor with these symptoms would usually be bled; their arm would be cut and allowed to bleed into a bowl until the swelling and the redness went away. It was a very effective therapy for the symptoms because loss of blood is potentially much more serious than infection; shock trumps the immune system. The symptoms would rapidly disappear. But in the mid-19th Century, when we finally got around to asking the question, we found that more people treated this way died. It probably did not harm those bled for a sprain or gout, but bleeding someone with an infection allows the infecting agent some time to spread and get a better hold in the person. More of them died. 

When we finally get around to asking this question about our current practices I'm sure that we will find that more people die today from infections that could have been washed away, or from asthma that is triggered by pollutants that could have been similarly removed. We're continuing the mistake we made when we bled people and it's time to stop.

We need to ask the question we asked about bleeding—why did this symptom develop and is it defensive; does it help us deal with environmental insults? If the answer is "Yes" then we ought to honor rather than block those symptoms.

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Read about more examples where we block our normal body functions of fever and diarrhea.

Go on to read about helping clean the nose.



Am J Rhinol 1998 Jan-Feb;12(1):37-43

Nasal mucosal endorgan hyperresponsiveness.

Svensson C, Andersson M, Greiff L, Persson CG

Department of Otorhinolaryngology, Head & Neck Surgery, University Hospital, Lund, Sweden.

Nonspecific hyperresponsiveness of the upper and lower airways is a well-known characteristic of different inflammatory airway diseases but the underlying mechanisms have not yet been satisfactorily explained. In attempts to elucidate the relation of hyperresponsiveness to disease pathophysiology we have particularly examined the possibility that different airway endorgans may alter their function in allergic airway disease. The nose, in contrast to the bronchi, is an accessible part of the airways where in vivo studies of airway mucosal processes can be carried out in humans under controlled conditions. Different endorgans can be defined in the airway mucosa: subepithelial microvessels, epithelium, glands, and sensory nerves. Techniques may be applied further in the nose to determine selectively the responses/function of these endorgans. Topical challenge with methacholine will induce a glandular secretory response, and topical capsaicin activates sensory c-fibers and induces nasal smart. Topical histamine induces extravasation of plasma from the subepithelial microvessels. The plasma exudate first floods the lamina propria and then moves up between epithelial cells into the airway lumen. This occurs without any changes in the ultrastructure or barrier function of the epithelium. We have therefore forwarded the view of mucosal exudation of bulk plasma as a physiological airway tissue response with primarily a defense function. Since the exudation is specific to inflammation, we have also suggested mucosal exudation as a major inflammatory response among airway endorgan functions. Using a "nasal pool" device for concomitant provocation with histamine and lavage of the nasal mucosa we have assessed exudative responses by analyzing the levels of plasma proteins (e.g., albumin alpha 2-macroglobulin) in the returned lavage fluids. A secretory hyperresponsiveness occurs in both experimental and seasonal allergic rhinitis. This type of nasal hyperreactivity may develop already 30 minutes after allergen challenge. It is attenuated by topical steroids and oral antihistamines. We have demonstrated that exudative hyperresponsiveness develops in both seasonal allergic rhinitis and common cold, indicating significant changes of this important microvascular response in these diseases. An attractive hypothesis to explain airway hyperresponsiveness has been increased mucosal absorption permeability due to epithelial damage, possibly secondary to the release of eosinophil products. However, neither nonspecific nor specific endorgan hyperresponsiveness in allergic airways may be explained by epithelial fragility or damage since nasal absorption permeability (measured with 51CR-EDTA and dDAVP) was decreased or unchanged in our studies of allergic and virus-induced rhinitis, respectively. Thus, the absorption barrier of the airway mucosa may become functionally tighter in chronic eosinophilic inflammation.

Publication Types:
  • Review
  • Review, tutorial

PMID: 9513658
American Academy of Allergy, Asthma and Immunology.
The Allergy Report. Vol. 1, page 4.
Q Rev Biol. 1991 Mar;66(1):23-62.

The function of allergy: immunological defense against toxins.

Profet M.

Division of Biochemistry & Molecular Biology, University of California, Berkely 94720.

This paper proposes that the mammalian immune response known as "allergy" evolved as a last line of defense against the extensive array of toxic substances that exist in the environment in the form of secondary plant compounds and venoms. Whereas nonimmunological defenses typically can target only classes of toxins, the immune system is uniquely capable of the fine-tuning required to target selectively the specific molecular configurations of individual toxins. Toxic substances are commonly allergenic. The pharmacological chemicals released by the body's mast cells during an IgE antibody-mediated allergic response typically cause vomiting diarrhea, coughing, tearing, sneezing, or scratching, which help to expel from the body the toxic substance that triggered the response; individuals frequently develop aversions to substances that have triggered such responses. A strong allergic response often includes a decrease in blood pressure, which slows the rate at which toxins circulate to target organs. The immune system identifies as toxic the following kinds of substances: (1) those low-molecular-weight substances that bind covalently to serum proteins (e.g., many plant toxins); (2) nontoxic proteins that act as carriers of toxins with low molecular weights (e.g., plant proteins associated with plant toxins); (3) specific substances of high molecular weight that harmed individuals in ancestral mammalian populations for a span of time that was significant from the standpoint of natural selection (e.g., the toxic proteins of bee venom. Substances that bind covalently to serum proteins generally are acutely toxic, and because many of these substances also bind covalently to the DNA of target cells, they are potentially mutagenic and carcinogenic as well. Thus, by protecting against acute toxicity, allergy may also defend against mutagens and carcinogens. The toxic hypothesis explains the main phenomena of allergy; why IgE-mediated allergies usually occur within minutes of exposure to an allergen and why they are often so severe; why the manifestations of allergy include vomiting, diarrhea, coughing, sneezing, scratching, tearing, and a drop in blood pressure; why covalent binding of low-molecular-weight substances to serum proteins frequently causes allergy; why allergies occur to many foods, pollens, venoms, metals, and drugs; why allergic cross-reactivity occurs to foods and pollen from unrelated botanical families; why allergy appears to be so capricious and variable; and why allergy is more prevalent in industrial societies than it is in foraging societies. This hypothesis also has implications for the diagnosis, prevention, and treatment of allergy.

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