Allergy in Atopic Asthma and Rhinitis as a function of a deficiency in the Lu and Kid defensive qi system


Author: Dr. Michael Lind

1.  Introduction 

allergyAllergy is loosely defined as a disorder of the immune system, whereby this system is improperly misguided into a hypersensitive state as a defense against foreign pathogens which, by themselves, are usually considered harmless.This process of hypersensitivity will be examined as it manifests in the airways of individuals as the pathologies of allergic asthma and rhinitis. From the Western standpoint, the focus is on humoral immunity (TH2 cytokines) and the production of immunoglobulin IgE, and its trigger toward inflaming and occluding the airways through bronchoconstriction.

When looking at the conditions through the perspective of Chinese medicine, these trigger agents and events, with the cascade of breathing and sinus difficulties,can be explained by the incipient theory of a deficiency existing in a separate system of Lu and Kid defensive qi mechanisms; which allows the entry of wind to become a sporadic, chronic condition. And it is this atopic association between asthma and rhinitis that suggests a more fundamental causation of all allergies. This paper will try to examine the validity of the theory and efficacy, and the treatment strategies of herbal formulas and acupuncture vis-a-vis Western medical interventions.

2.  The Western Etiology of Allergic Mechanisms

Reprising the definition of allergy in the Western sense, it is said to be an overactivation of the mast cells and basophils in the connective tissues and epithelium by the over represented presence of immunoglobulin, IgE (1). This results in a high degree of inflammation in the surrounding tissues. Out of the four forms of classification of hypersensitivity, this immediate reaction is considered to be type 1(1). The trigger for this inflammation cascade is usually an exogenous substance, in the form of a foreign macromolecule (the antigen). Predominantly, they consist of airborne particles, targeting areas in contact with the outside environment, such as the nose and lungs (1).

3.  Initiation of the Immune Response

The procedure of invasion and reaction is as such. In the presence of exogenous antigens (humoral immunity), the initial immune response begins with the T lymphocyte. On the surface of these cells are receptors that bind to the complex present at the corresponding surface of an antigen-presenting cell (APC), which also include dendritic cells and macrophages (2). The antigens are enveloped by the APC’s, employing phagocytosis, which fragment the antigen and present the antigenic peptides within a transmembrane class II histocompatibility molecule (MHC) on the cell surface (2). These processed antigens can now be recognized by other T cells, being mainly CD4 T cells. For internally derived cellular antigens (cell-mediated immunity), they are similarly reduced and fragmented and presented at the cell surface, but are paired with a class I histocompatibilty molecule (MHC), which can be recognized, but also destroyed by another type of T cell, being a cytotoxic CD8 cell (2).

Faced with the numbers of allergens and their associated antigens, the immune system has to make more T cells through a process of differentiation and proliferation. Monocytes in peripheral tissues dispense monocyte growth factor, which changes the monocytes into macrophages, and then these macrophages cause dendritic cells to mature, which migrate into lymph nodes carrying the antigen, which increases the concentration of antigen and cytokines, which stimulate these dendritic cells to interact with the undifferentiated, premature T helper cells into the pathway of either TH1,TH2, or TREG cells (2). TH1 cells control cell-mediated immunity, and TH2 cells control humoral immunity; and both activities are overseen and counterbalanced by TREG cells (2).

There is a fine balance between the reciprocal responses of humoral and cell-mediated immunity (see fig.1), with each having the ability to restrain the others functioning through inhibitory pathways, as well as also having the ability of self-inhibition (2). 

fig.1. The Immune response and its mediators, undifferentiated T cells, and TH1 and TH2 cytokines(2)

 The antigen first causes Type 1 hypersensitivity by stimulating a TH2 lymphocyte, called a T helper cell, also known as a CD4 T cell, and is essential for antibody-mediated immunity, which is needed to control extracellular pathogens (3). These cells, when activated, help immune responses of other lymphocytes by costimulating B cells. These cells also have specific receptors which fasten and engulf soluble antigens through receptor-mediated phagoctytosis, and the antigen is fragmented and presented at the cell surface in a class II histocompatibility molecule (MHC)(2). Now, TH2 cells with complementary receptors fasten to the B cell and secrete lymphokines that produce B cell differentiation into plasma cells and secrete identical antibodies. And it is these that bind to the active part of the antigen and initiate a response.

From here, more lymphokines are released, such as interleukin-4 (IL-4), which cause B cells to switch to plasma cells to secrete an immunoglobulin, IgE, and promotes premature T cells to enter the TH2 pathway and also inhibit the TH1 pathway(3).Interleukin 13 also promotes the production of IgE. Interleukin 5 (IL-5) gathers eosinophils, and interleukin 10 (IL-10) inhibits IL-12 production and the TH1 pathway.Then IgE enters the bloodstream and eventually attaches itself to IgE specific receptors on mast cells and basophils These cells are now said to be sensitized to the allergen. Subsequent exposure to the same allergens will activate the mast cells and basophils, causing them to undergo a process called degranulation (see fig.2); whereby, histamine, cytokine, prostaglandins, leukotrienes, interleukins, and other inflammatory molecules are released from the granules inside these cells to the surrounding tissues to cause vasodilation, mucous secretion, nerve stimulation, and smooth muscle contraction (1). If the response is all encompassing to the individual anaphylaxis is the result, but if it is localized in the respiratory system, atopic asthma is symptomatic, and if it is just confined to the nasal area, rhinorhea will be indicated.


fig. 2. A representation of a mast cell responding to an allergen.
1.antigen (substance form allergen) 2.IgE 3. IgE specific receptor 4. inflammatory molecules of histamine 5. granules 6. mast cell 7. other inflammatories, such as prostaglandins (1).

These atopic individuals can possibly have up to ten times the amount of serum IgE in their blood compared to individuals not displaying atopy (4).

4.  The Hygiene Hypothesis and TH1 - TH2 Balance

In order to explain allergy (atopy) in a large cross section of the population an environmental theory, the hygiene hypothesis, originated from observations showing an inverse association between family size and allergy in early childhood. Further studies linked changing microbial environments in home surroundings, and a diminishment in infectious disease, as well as some vaccinations as the factors responsible for an increase of atopic symptoms in the population (5).

The theory on the mechanisms behind this is that in infancy the human immune system is immature and is geared more toward TH2 cytokine production. With increasing exposure to environmental stimuli, such as parasitic worms (helminth) and viruses, transmitted from other children and siblings, an increase in TH1 cytokine production occurs. This has the effect of balancing the TH1-TH2 response, or “down-regulating” an exclusive, overactive TH2 pathway (6). If there is not enough of this TH1 stimuli and immunomodulating early in life, then it is the TH2 pathway that will come to dominate immune response late in life, resulting in inappropriate type 1 allergy responses(6).

The protective effects of early exposure to a microbial environment has shown to be beneficial if this exposure occurrs early in childhood. Individuals who grow up on dairy farms seem to display lower prevalence of allergic diseases; subsequently, the focus is on gram-negative bacteria, lipopolysaccharide, an endotoxin that is present in their bloodstream(5). It turns out that this endotoxin is a major TH1 stimulator (5). So, an endotoxin can provide protection from allergy, such as in atopic asthma, but it can also aggravate a condition in a later period of life. For instance, asthmatics can become hypersensitive to endotoxin exposure, and inflammatory symptoms can become more pronounced (5).

There are clearly other factors involved in determining the extent of TH1-TH2 balance and allergic sensitization, other than the genetics of the individual, or the point in life that individual receives microbial exposure. Future studies will have to winnow out the main protective factors.

5.  Atopic Asthma Definition and Etiology 

Atopic asthma is a malady with variable progression, which is characterized by periods of cough, wheezing and shortness of breath, reversible airflow limitation, and bronchial hyper-responsiveness (8) It is a chronic inflammatory disease of the airway, that becomes inflamed, may constrict the lumen, and may become lined with mucous, and is mostly reversible (7). In short, it is an immune response (TH2 specific), as it has an allergy trigger, confined to the bronchial tract. For many, it begins in childhood with sporadic symptoms, and occurs with other viral respiratory tract infections. For those genetically susceptible to allergy the malady becomes unremitting, occurring without the presence of respiratory tract infections. Children with persistent wheezing are, in the end, diagnosed with asthma, with those at greatest risk having developed allergic sensitization early in life (8).

6.  Bronchoconstriction

Therefore, in atopic asthma the increased hypersensitivity of the bronchial airways causes them to react to a stimulus, usually an environmental one such as pollen, and the normal bronchial openings or diameter are compromised. The mechanism of bronchoconstriction involves the afferent nerve endings of the parasympathetic reflex loop in the inner lining of the bronchus (7). These nerve endings become stimulated and send signals to the brain stem vagal center, which then sends a signal back to release acetylcholine, which causes a overproduction of cyclic guanine monophospahte (GMP), which begins the cascade of smooth muscle spasm and constriction in the bronchia (7).

Also, it has been found that the beta-2 receptors of pulmonary smooth muscle are impeded by IgE, which is amply produced in type 1 hypersensitivities (7).

7.  Airway Inflammation

The other characteristic of asthma events is the inflammation. This characteristic is now understood to be chronic, with acute inflammatory events exacerbating an already inflamed state in the bronchial tissues (9). Additionally, this chronic inflammation also affects tissue repair, and is said to compromise and reduce lung function over time(9). Inflammatory cells, such as eosinophils and other lymphocytes, invade tissues and interact with the mast cells, macrophages, epithelial and endothelial cells, causing the release of histamine and prostaglandins (refer to fig. 1), further contributing to an inflammation process, bronchospasm, mucous secretion, and bronchial microvascular leakage, leading to further narrowing (9).

8.  Western Diagnosis of Atopic Asthma

Other than family history and the patient’s own medical history, airway function is assessed with peak flow rates (impractical before age 6), and if the patient responds to bronchodilator medication (7). Additionally, clues to an atopic constitution can be had if there are other allergies, or if the patient suffers from atopic eczema or rhinitis (10). In this case, the degree of atopy can be assessed by skin-prick testing, measurement of specific IgE antibodies, and measurement of eosinophil counts (10). A more obvious indicator is to ascertain if there is an identifiable allergy trigger, or triggers, that initiate an asthmatic attack (7).

9.  Western Prevention and Treatment

The most easily implemented treatment for atopic asthma is to identify the allergen triggers and eliminate or reduce exposure to them (7). Failing that, medical treatment for relief and prevention can be implemented, as well as emergency treatment. To minimize wheezing bronchodilators are used to give short term relief. For those that have more than two episodes of an asthmatic attack a week the preferred choice for a prophylactic is inhaled glucocorticoids, which dampens chronic inflammation (11).

When the frequency of attacks becomes daily, a short acting beta2-adrenoceptor agonist is prescribed along with a higher dose of glucocorticoids . Longer acting beta2- adrenoceptor agonists have a 12 hour effect and are used to even out symptomatic relief, but there is still the necessity to use shorter acting agonists because of their more immediate action (11).

Modern, Western asthma therapies still function as controls, and not cures. For instance, glucocorticoids are effective in controlling some of the inflammatory aspects of asthma, but have a multitude of side effects with long term use, and do nothing further inside the airway path to affect bronchial inflammation and healing (remodeling). Future treatments are being directed at modulating the T cell pathway, targeting TH2 recruitment and activation, as well as dampening the mediators for inflammation (11).

But, Western medical science, in essence, still does not know what causes atopic asthma.

10.  Breathlessness and Wheezing

Most Chinese concepts relating to asthma point to its etiological origins being best explained by the Chinese categories of breathlessness (Chuan) and Wheezing (Xiao).

For the most part, the matter of Phlegm obstructing Lu Qi descending is the centerpiece. The wheezing and breathlessness is the result of bronchspasms narrowing the airways, with mucous further obstructing the opening, but does not point to a cause (12). Further discrediting Phlegm as a cause of atopic asthma are pulse and tongue signs of patients, which do not display the slippery character or the sticky and swollen signs, respectively. Additionally, in between attacks breathing is fairly normal. A Phlegm dominant condition would have breathing difficulty constant (12). 

11.  Lu and Kid Defensive Qi 

Without a good fit of asthma to Wheezing and Breathlessness, a different focus is on a different deficiency. In this case, it has to do with Lu and Kid Qi -- Defensive Qi, to be precise. This is not a deficiency involving the whole gamut of Kidney Yin,Yang, and Essence; but, in effect, only involves a defect relating to a separate category of Kidney Defensive Qi (12). Therefore, the usual signs of Kid deficiency, such as dizziness, lower back ache, week knees, do not apply. However, even in young children, geographic tongue may be found (12).

For the most part, asthma that occurs early in life, and is associated with an allergy, is considered to be extrinsic (atopic) asthma; and asthma that occurs late in life, and not associated with allergy is considered intrinsic asthma (12). Intrinsic asthma would be more compatible with Breathlessness and Wheezing criteria, in most cases. It can also sometimes have an early onset, as a case of retention of residual pathogenic factor, with Wind-Cold or Wind-Heat invading the upper respiratory tract, and failing to be completely expunged. This leads to an impairment of the diffusing and descending of Lu Qi, manifesting as Breathlessness and Phlegm (12).

Unfortunately, many children with repeating invasions of Wind, with no associated allergen, are misdiagnosed as having asthma. For those with true atopic asthma, there is a Kid Defensive Qi deficiency right from the start. 

12.  Bibliography

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  3. Tortora, Gerard J. et al. Principles of Anatomy and Physiology. Tenth edition. pp.780-794. John Wiley and Sons, Inc. 2003.
  4. Wikipedia. (2008). IgE. Wikipedia. The Free Encyclopedia
  5. The Hygiene Hypothesis Revisited: The Pros and Cons
  6. Wikipedia. (2008). The Hygiene Hypothesis. Wikipedia, The Free Encyclopedia
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  12. Maciocia, Giovanni. The Practice of Chinese Medicine. Second edition. pp.114-199. Churchill Livingstone. 2008.