Herbal remedies for treating allergies and asthma

Details Herbal remedies for treating allergies and asthma Herbal remedies for treating allergies and asthma

2001-03-07

2003-10-07

Tate, Christopher R. (Department: 1651)

Drug, bio-affecting and body treating compositions

Plant material or plant extract of undetermined constitution...

Containing or obtained from panax or acanthopanax

C424S725000, C424S739000, C424S756000, C424S195160, C514S826000

Reexamination Certificate

active

06630176

ABSTRACT:

BACKGROUND
Allergic and asthmatic reactions pose serious public health problems worldwide. Pollen allergy alone (allergic rhinitis or hay fever) affects about 10-15% of the population, and generates huge economic costs. For example, reports estimate that pollen allergy generated $1.8 billion of direct and indirect expenses in the United States in 1990 (Fact Sheet, National Institute of Allergy and Infectious Diseases, www.niaid.nih.gov/factsheets/allergystat.html; McMenamin,
Annals of Allergy
73:35, 1994; incorporated herein by reference). More serious than the economic costs associated with pollen and other inhaled allergens (e.g., molds, dust mites, animal danders) is the risk of anaphylactic reaction observed with allergens such as food allergens, insect venoms, drugs, and latex.
Allergic reactions occur when an individual's immune system overreacts, or reacts inappropriately, to an encountered antigen. No allergic reaction is thought to occur the first time an individual is exposed to a particular antigen. However, the initial immune response to an antigen primes the system for subsequent allergic reactions. In particular, the antigen is taken up by antigen presenting cells (e.g., macrophages or dendritic cells) that degrade the antigen and then display antigen fragments to T cells. The activated T cells respond by secreting a collection of cytokines that affect other cells of the immune system. The profile of cytokines secreted by responding T cells determines whether subsequent exposures to the particular antigen will induce allergic reactions. When T cells respond by secreting interleukin-4 (IL-4), the effect is to stimulate the maturation of B cells that produce IgE antibodies specific for the antigen. These antigen-specific IgE antibodies then attach to specific receptors on the surface of mast cells and basophils, where they act as a trigger to initiate a rapid reaction to subsequent exposures to the antigen.
When the individual next encounters the antigen, it is quickly bound by these surface-associated IgE molecules. Each antigen typically has more than one IgE binding site, so that the surface-bound IgE molecules quickly become crosslinked to one another through their simultaneous (direct or indirect) associations with antigen. Such cross-linking induces mast cell degranulation, resulting in the release of histamines and other substances that induce the symptoms associated with allergic reaction. Individuals with high levels of IgE antibodies are known to be particularly prone to allergies.
Allergic asthma is a chronic, IgE-mediated lung disease characterized by inflammation and airway hyperresponsiveness (AHR). Asthma is a major public health problem in the United States; nearly 17 million Americans suffer from this often debilitating disease. Moreover, asthma morbidity and mortality have been rising over the last two decades. The prevalence rate increased by 75% from 1980 to 1994, and despite the increased use of medications, deaths from asthma rose 58%.
Clinically, asthma is expressed as episodic breathlessness, wheezing, chest tightness, and cough (U.S. Centers for Disease Control.
Morbidity and Mortality
47:1022, 1998; incorporated herein by reference). The airways of asthmatic subjects are characterized by chronic inflammation with infiltration of the bronchial mucosa by lymphocytes, eosinophils, and mast cells together with epithelial desquamation, goblet cell hyperplasia, and thickening of the submucosa (Steering Committee for International Study of Asthma and Allergies in Childhood,
Lancet
351:1225, 1998; Kay
J. Allergy Clin. Immunol
. 87:893, 1991; each of which is incorporated herein by reference).
Numerous studies have demonstrated that Th2-type cytokines, such as IL-4, IL-5, and IL-13, produced by activated CD4
+
T cells, play a central role in the pathogenesis of allergic asthma (see, for example, Lemanske et al., in
Allergy: Principles and Practice
. C. V. Mosby, Co., St. Louis, Mo., pg. 320, 1993; Mosmann et al.,
J. Immunol
. 136:2348, 1986; Mosmann et al.,
Annu. Rev. Immunol
. 7:145, 1989; Walker et al.,
Am. Rev. Respir. Dis
. 146:109, 1992; Robinson et al.,
N. Engl. J. Med
. 326:298, 1992; Finkleman et al.,
J. Immunol
. 141:2335, 1988; Schleimer et al.,
J. Immunol
. 148:1086, 1992; Hamaguchi et al.,
J. Exp. Med
. 165:268, 1987; Campbell et al.,
Proc. Natl. Acad. Sci. USA
84:6629, 1987; Zurawski et al.,
Immunol. Today
15:19, 1994; each of which is incorporated herein by reference).
Atopic human subjects, when exposed to the relevant asthmatic antigen, suffer an acute IgE-dependent response, often followed by a late-phase inflammatory response 6-12 hours later (Beasley et al.,
Am. Rev. Respir. Dis
. 139:806, 1989; Metzger et al.,
Clin. Rev. Allergy
3:145, 1985; each of whichlis incorporated herein by reference). The early (immediate) phase response is associated with mast cell degranulation and release of mediators such as histamine, tryptase, leukotrienes, and platelet-activating factor (Busse et al.,
Agents Actions Suppl
. 28:41, 1989; Lemanske et al., in
Allergy: Principles and Practice
. C. V. Mosby, Co., St. Louis, Mo., pg. 320, 1993; each of which is incorporated herein by reference); the late phase response is associated with the infiltration of inflammatory cells, predominantly eosinophils, which release eosinophil major basic protein and other mediators that damage the epithelium and induce bronchoconstriction (Beasley et al.,
Am. Rev. Respir. Dis
. 139:806, 1989; Busse et al.,
Agents Actions Suppl
. 28:41, 1989; each of which is incorporated herein by reference).
As the significance of inflammation has become recognized in the pathogenesis of airway hyperresponsiveness, efforts have been made to treat asthma by reducing the inflammatory process. Corticosteroids are the most potent known non-specific anti-inflammatory agents and have been found to produce notable improvement in objective lung function of asthmatics. In view of the substantial side effects associated with systemic corticosteroids, inhaled corticosteroids are currently the first line of treatment. Inhaled steroids can be effective in decreasing inflammation and bronchoconstriction in patients, but the lack of specificity of their effects can also have negative results. Although the most frequently reported side effects of inhaled corticosteroids are local, systemic effects have also been reported. Thinning of the skin, bruising, adrenal suppression, decreased bone metabolism, and decreased growth (Barnes,
N. Engl. J. Med
. 332:868, 1995; incorporated herein by reference) are of particular concern, especially among children, in whom asthma appears to be rapidly increasing in frequency.
One approach to treating allergies is antigen immunotherapy, which attempts to “vaccinate” a sensitive individual against a particular allergen by periodically injecting or treating the individual with a crude suspension of the raw allergen. The goal is to modulate the allergic response mounted in the individual through controlled administration of known amounts of antigen. If the therapy is successful, the individual's allergic response is diminished, or can even disappear. However, the therapy can require several rounds of vaccination, over an extended time period (3-5 years), and very often does not produce the desired results. Moreover, certain individuals suffer anaphylactic reactions to the vaccines, despite their intentional, controlled administration.
Another commonly used approach to treating allergic symptoms is the administration of histamine antagonists. These drugs are widely available in over-the-counter formulations, but unfortunately they merely mask the symptoms of the allergic response rather than providing any type of permanent cure or protection against recurrence.
Efforts are underway to develop more specific treatments for allergy and asthma (see, for example, Fahy et al.,
Am. J. Respir. Crit. Care Med
. 155:1828, 1997; Boulet et al.,
Am. J. Respir. Crit. Care Med
. 155:1835, 1997; Kung et al.,
Am. J. Respir. Cell Mol. Bio
. 1

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