Eosinophilic oesophagitis (EoE): hypothetical herbal interventions for a rare and emerging gastrointestinal disorder.
EoE was first described in the early 1990's, with incidence increasing rapidly in recent years in westernised countries (Hruz 2011). Prevalence is often reported to be 1-4 in 10,000 (.01-.04%). Some data, however, indicates that in westernised countries prevalence may be as high as between 0.5% and 1.1% of the population and increasing (Enns 2010, Hruz 2011). This discrepancy may be linked to a poor understanding of the condition by health professionals resulting in misdiagnosis and consequent under-reporting (Doherty 2001). Occurrence is far more prominent in males and atopic patients. All age groups are affected but clinical manifestations can differ. Infants present with reflux, vomiting, food refusal, failure to thrive and signs of epigastric pain; children suffer reflux, heartburn, vomiting, abdominal pain and dysphagia, while adolescents and adults primarily present with food impaction and dysphagia (Straumann 2012). A common initial indicator of EoE in children is gastro-oesophageal reflux disease (GORD) that does not respond to proton pump inhibitor (PPI) therapy (Lucendo 2010). Diagnosis of EoE is determined only by symptoms of oesophageal dysfunction in conjunction with positive oesophageal biopsies (a minimum of 15-24 eosinophils per high-power field), as individually either could be indicative of other disease processes (Enns 2010). Distribution of eosinophils in the oesophagus is not uniform. A 1cm difference in biopsy site can result in either a diagnosis of severe EoE or no diagnosis at all therefore multiple biopsies at multiple sites are crucial (Valent 2012). Given the rapid increase in prevalence and lack of knowledge surrounding the aetiology of EoE, the need for research into non-pharmaceutical interventions is increasing.
The cause of EoE in humans is still unknown but the emerging evidence of mechanisms involved is revealing the complex nature of the disease. Although dietary and environmental allergens are implicated, recent research indicates that a clinical spectrum of different forms of inflammation evolve from various allergens, making the pathophysiology of EoE unique in each patient (Lucendo 2010). Active inflammation of the oesophageal mucosa is most commonly seen in children, with tissue remodelling occurring over time resulting in furrowing, corrugation and strictures (Straumann 2012). The antigen-driven hypersensitivity response seen in EoE involves multiple immunoglobulin E (IgE)-dependent delayed reactions and inflammatory pathways, affecting numerous cells, molecules and genes. Cellular changes are also prevalent, including basal zone hyperplasia, elongated vascular papillae and oesophageal mucosa infiltration (Mulder 2011).
Known mechanisms of disease in EoE
Eosinophils are regulated by the cytokine interleukin (IL)-5 and survive in tissue for approximately 2-14 days. IL-4 and IL-13 are mediators in the recruitment of eosinophils from blood to tissue, as their presence causes the secretion of chemo-attractant and pro-inflammatory cytokines including eotaxin proteins (chemokines) and leukotriene [B.sub.4]. They then recruit eosinophils into oesophageal tissue via integrin-mediated migration (Mulder 2011). Antigen exposure, cytokines and other inflammatory mediators activate eosinophils and lead to the release of reactive oxygen species (ROS), arachidonic acid metabolites, tumour necrosis factor-[alpha] (TNF-[alpha]), additional cytokines (interleukins, chemokines, interferons and growth factors) and protein mediators such as major basic protein, eosinophil-derived neurotoxin, eosinophil peroxidase and eosinophil cationic protein (Busse 2010). Recent evidence suggests that EoE eosinophils might also act as antigen-presenting cells (APCs) leading to activation of T cells, initiating the cytokine cascade (Le-Carlson 2013).
Studies on EoE patients have revealed elevated mast cell numbers in intra-epithelial tissue and defined a link between mast cells, Transforming Growth Factor beta (TGF-P), and smooth muscle (Aceves 2010). Immunoglobulin E (IgE) binds to the high affinity receptor located on the mast cell surface where antigen exposure subsequently causes mast cell activation and degranulation. Degranulation of mast cells results in the release of eosinophil attractants histamine and eicosanoids, perpetuating the inflammatory cycle and causing further oesophageal tissue damage (Mulder 2011). In EoE patients high levels of mast cells are found not only in the superficial tissue but also in the deeper smooth muscle layer of the oesophagus, indicating the high likelihood of mast cell involvement in the pathogenesis of the disease (Abonia 2010).
B-lymphocytes are reliant on T-helper 2 (Th2) cells and are responsible for secretion of IgE (Mulder 2011). Increased levels of B-lymphocytes are found in the epithelial tissue and vascular papillae in EoE indicating a possible role in pathogenesis. On the other hand, elevated B-lymphocytes have been shown to correlate more to mast cell presence than eosinophils (Vicario 2010, Mulder 2011). Increased T cells, CD3+, CD4+ and CD8+ cells are present in the oesophageal mucosa of EoE patients, with Th2, IL-5 responses seen to be due to either food allergy or EoE. Increased numbers of proximal oesophageal CD1a+ cells have been associated with EoE in children (Mulder 2011). EoE appears to be a Th2 associated disease and imbalances of T regulatory cells may be a contributing factor in pathogenesis (Vicario 2010).
TGF-[beta]1 is expressed by eosinophils and mast cells and is potentially a central molecular mediator of EoE (Mulder 2011). It is found in higher numbers in EoE patients and is associated with allergic inflammation and direct regulation of pro-fibrotic processes. This leads to eotaxin-3-mediated eosinophil recruitment and adhesion, along with tissue remodelling thought to be involved in the chronic fibrosis and acute smooth muscle contraction associated with dysphagia (Abonia 2010).
Current recommended treatment options for EoE
Despite numerous pharmaceutical trials, no cure has been found and none of the drugs used are specifically indicated for EoE. The current recommended treatment options involve removal of allergenic triggers, controlling inflammation and modifying structural oesophageal dysfunction via hypoallergenic diets (elimination diet, dietary restriction and elemental formulas), topical corticosteroids, mast-cell stabilisers, leukotriene inhibitors and oesophageal dilation (Lucendo 2010). This paper will examine the research and traditional evidence of herbal medicine to identify hypothetical herbal medicine treatments for reducing inflammation and pain in EoE patients.
Searches of PUBMED, Google Scholar, EBSCO Host, Alt Health Watch, Science Direct and Academic One File databases were conducted in September 2012. Two traditional texts were used: A Modern Herbal (Grieve 1931) for its documenting of traditional English applications for herbal medicine, and the King's American Dispensatory (Felter 1898) for traditional American applications for herbal medicine. Although clinical trials related to herbal interventions in EoE were not found, articles that may be of benefit for the treatment of inflammation and pain caused by EoE inflammatory mediators were extracted and reviewed.
Search terms for this review were defined based on the condition itself and the herbs that are described as anti-allergic, anti-inflammatory and demulcent in common clinical herbal medicine texts as well as those that are often indicated in inflammatory gastrointestinal conditions (Bone 2003): "eosinophil"; "eosinophilic oesophagitis"; "herbal"; "inflammation"; "baical skullcap"; "Scutellaria baicalensis"; "licorice"; "Glycyrrhiza glabra"; "Withania somnifera"; "turmeric"; "Curcuma longa"; "marshmallow"; "Althaea officinalis"; "golden seal" "Hydrastis canadensis"; "Albizia lebbeck" and "Hemidesmus indicus".
Possible herbal interventions for EoE
Although the prevalence of EoE is rapidly increasing, there remains a lack of safe and effective long-term treatments. The use of swallowed topical steroids is not recommended for prolonged periods and has been shown to result in oesophageal candidiasis in 15% of patients, little or no improvement in 40% of patients with identifiable allergies, and recurrence of symptoms in 45% of patients within 12 months following withdrawal of the drug (Nurko 2006). Elimination diets can result in poor compliance and be severely restrictive, with some patients exclusively requiring amino acid--based elemental formulas administered orally or via enteral feeding. Reintroduction of restricted foods results in recurrence of symptoms and inflammation (Straumann 2012). Dilation therapy is an invasive treatment for functional narrowing of the oesophagus that has no impact on the underlying inflammation. It is performed under general anaesthetic and comes with the serious risk of oesophageal perforation (Lucendo 2010). These factors demonstrate the inadequacy of the currently recommended treatment options due to lack of long-term efficacy, poor compliance and safety issues, and they indicate the need for more research into other treatments such as the use of herbal medicine in EoE.
Topical steroid application has been found more effective than nebulised steroid therapy in EoE (Peterson 2010); therefore, clinical trials into herbal administration in liquid form may be preferable to ensure direct contact with oesophageal mucosa. As inflammation and oesophageal tissue damage is prevalent in EoE patients, research into the use of herbal glycetracts (alcohol removed) may be preferable over ethanolic extracts. Although there appear to be no clinical trials related to herbal interventions in EoE, the following review discusses some potentially beneficial herbs based on the physiological actions of the herbs and the pathogenesis and symptoms of EoE.
The medicinal qualities of S. baicalensis, also known as Huang qin, were first discussed in the ancient Chinese medical text Shen-nung pen ts'ao ching (Divine Husbandman's Materia Medica), where it was said to clear heat and dry dampness in the stomach and intestines (Bensky 2004). The roots of S. baicalensis contain up to 20% flavones, including the lipophilic antioxidant compounds baicalin, baicalein, wogonoside and wogonin (Matkowski 2008). Numerous studies have detailed the mechanisms involved in the anti-inflammatory and antiallergic actions of S. baicalensis.
S. baicalensis has demonstrated anti-inflammatory activity in vitro. Human mast cells stimulated with either IL-1[beta]- (10 ng/ml) or TNF-[alpha] (100 U/ml), then administered baicalein (1.8 to 30[micro]M) resulted in significantly inhibited production of many (EoE related) inflammatory cytokines, and stabilised mast cells via regulation of the NF-Kb pathway (Hsieh 2007). Another in vitro study demonstrated that baicalin brought about significant reductions in neutrophil infiltration and selectively bound to chemokine ligands, interfering with their ability to induce cell migration and resulting in an anti-inflammatory action (Li 2000). The possible use of S. baicalensis in EoE is further supported with findings that baicalin inhibited T-cell proliferation by 98% and reduced production of multiple pro-inflammatory cytokines, including TNF-[alpha], in human peripheral blood mononuclear cells (Krakauer 2001). Further to this, in vitro evidence has shown that at a concentration of 10 [micro]g/ml, a S. baicalensis extract containing baicalein, oroxylin A, baicalin and skullcap flavone II, inhibited the production of eosinophil-specific chemokine eotaxin in (IL-4 and TNF-[alpha]-stimulated) human fibroblasts. Effects were dose dependent with approximately 50% inhibition observed with administration of a 1.8 [micro]g/ml dose (Nakajima 2001). Baicalin and baicalein reduce inflammation and oxidative stress by significantly impairing the production of ROS and preventing leukocyte adhesion while baicalein also has the ability to metabolize hydrogen peroxide (Shen 2003, Matkowski 2008).
Wogonin inhibits nitric oxide (NO) synthase and exhibits a concentration-dependent inhibition of lipopolysaccharide-induced prostaglandin E2 (PGE2) production in murine macrophages. As little as 0.5 [micro]g/ ml concentration of wogonin can result in a decrease of cyclooxygenase-2 (COX-2), and COX-2 protein expression is depressed at concentrations of 10 [micro]g/ ml and over (Wakabayashi 2000). S. baicalensis has been shown to inhibit the arachidonic acid cascade via the 5-lipoxygenase (5-LOX) pathway, subsequently inhibiting EoE inflammatory mediators leukotrienes (Kimura 1987). Further, in vitro and in vivo evidence demonstrates that S. baicalensis acts on mast cells, with oral administration of S. baicalensis extract in rats resulting in significantly reduced histamine release, while human mast cells treated with various concentrations of S. baicalensis extract (1, 10, and 100 [micro]g/ml) significantly inhibited the mitogen-activated protein (MAP) kinase pathway and production of IL-8 and TNF-[alpha]. Inhibition of the MAP kinase pathway reduces the expression of EoE related inflammatory cytokines (Jung 2012).
The anxiolytic action of S. baicalensis is attributed to its ability to bind with the benzodiazepine site of the gamma amino butyric acid (GABA)-A receptor (Liao 2003). This may be of benefit as increased levels of anxiety have been found in children suffering from EoE (Klinnert 2009).
Fritillaria cirrhosa bulbus, Anemarrhena rhizoma and Lee-Mo-Tang
The traditional Korean herbs Fritillaria cirrhosa bulbus, Anemarrhena rhizoma and Lee-Mo-Tang (a traditional herbal formulae composed by a ratio of 50 to 50), have been shown in vivo to significantly reduce inflammation via lowered levels of numerous EoE inflammatory mediators. Eosinophil, histamine, IgE and Th2 cytokine (IL-4, IL-5 and IL-13) levels were all significantly reduced and increases in interferon-y production were observed when eosinophilia-induced mice were orally administered 200mg/kg of each herb three times a week for 8 weeks (Yeum 2007).
G. glabra is a herb with anti-inflammatory, mucoprotective and demulcent actions. Traditionally G. glabra root has been used as an emollient, demulcent and nutritive due to its ability to reduce mucosal irritation and relieve intestinal pain (Felter 1898, Grieve 1931). Its gastro-protective effects are due to an increase in mucous secretion from elevated prostaglandin levels. This action may be beneficial in EoE by soothing and protecting damaged and inflamed gastrointestinal mucosa (Baker 1994). G. glabra has steroid-like anti-inflammatory effects, possibly reducing the need for corticosteroid medication in EoE; however, its long-term use is not recommended as it has been known to cause hypertension, hypokalemia and quadriparesis when used in high doses for prolonged periods (Omar 2012).
Many of the physiological actions of W. somnifera, such as its adaptogenic and anti-inflammatory properties, may theoretically be of benefit in the treatment of EoE. W. somnifera has also been shown to decrease immunosuppression and regulate corticosteroid levels, while also acting as an immune modulator and anxiolytic (Bhattacharya 2003, Davis 2000, Gutpa 2007).
W. somnifera has demonstrated anti-inflammatory, immune modulating and eosinophil lowering activity in vivo and in vitro. The active constituent withanolides are anti-inflammatory via inhibition of COX enzymes. W. somnifera root extract (500 [micro]g/ml in vitro) significantly inhibited lipid peroxidation and demonstrated NO and hydrogen peroxide scavenging activity when administered to inflammatory bowel disease (IBD) induced rats, and at a concentration of 1000mg/kg a significant muco-restorative effect was seen (Pawar 2011). An additional in vivo study in an asthma-induced mouse model resulted in immune modulating, eosinophil lowering and anti-inflammatory actions comparable to corticosteroid medication, attributed to phytosteroid withaferin A (Oberholzer 2008). Further in vivo trials in stress-induced mice that were administered W. somnifera daily at graded doses of 0.25, 0.5, 1 and 2 mg/kg led to improvements in altered T-lymphocyte subset distribution and cytokine secretion patterns, demonstrating its effectiveness as an anti-inflammatory agent and possible therapeutic benefit in EoE (Kour 2009). W. somnifera may also play a role in the treatment of IgE mediated reactions as it has been shown to down-regulate OVA-specific IgE antibody and antigen-specific IgE antibody responses in mice, indicating its possible effectiveness in an antigen driven disease such as EoE (Amara 1999).
C. longa is a potent antioxidant via direct scavenging of free radicals and its ability to enhance the activity of certain endogenous antioxidants such as glutathione peroxidase (Fiorillo 2008). It causes inhibition of inflammatory prostaglandin PGE2 via PGE2 synthase-1 enzyme and stimulates nuclear transcription molecule NrF2, enhancing cell antioxidant defences and reducing inflammation (Oksman 2006). C. longa inhibits NF-[kappa]B, COX and LOX, decreasing the breakdown of arachidonic acid into the EoE inflammatory mediators, leukotrienes, prostaglandins, and prostacyclins (Blaylock 2012). In vivo evidence showed that an oral dose of 550 mg of curcumin twice daily for one month and then for an additional month three times daily resulted in significantly reduced inflammatory indicators (erythrocyte sedimentation rate and c-reactive protein) in patients with ulcerative colitis, a disease which shares many of the inflammatory mediators seen in EoE (Jurenka 2009).
Although clinical trials are lacking, A. officinalis has traditionally been used for mucous membrane related disease states and gastrointestinal inflammation and irritation due to its demulcent and emollient actions, which are attributed to mucilage (acidic polysaccharides) (Felter 1898, Grieve 1931). Topical use in EoE may be soothing to inflamed oesophageal mucosa (Bone 2003).
H. canadensis is a mucous membrane trophorestorative, anti-inflammatory and vulnerary herb that has been shown to inhibit production of TNF-[alpha], IL-6, IL-10, and IL-12 in a dose-dependent manner in vitro (ClementKruzel 2008). Traditionally it has been used for sub-acute and chronic gastrointestinal inflammation and gastric irritability (Felter 1898, Grieve 1931). H. canadensis may be of particular benefit in EoE, given that active inflammation of the oesophageal mucosa is common (Straumann 2012).
A. lebbeck is a powerful anti-allergic herb via inhibition of IL-4, IL-5, IL-13, histamine receptor 1, histidine decarboxylase signalling, Th2-cytokine signalling and alteration of the histamine-cytokine network (Nurul 2011). In vivo studies (rats) show that A. lebbeck is effective in treating atopic allergy, as it has been shown to reduce T and B-lymphocytes and stabilise mast cells (Tripathi 1979).
H. indicus has been used in traditional Ayurvedic medicine as a topical anti-inflammatory herb (Bone 2003). Although there appear to be no clinical studies on H. indicus, it is thought to have potent anti-inflammatory, immune-modulating/suppressing and antioxidant properties. Phenolic acids are thought to be responsible for its effective use in gastrointestinal ailments and diseases in which high levels of oxidative stress are indicated (Jayaram 2011).
EoE is a chronic antigen-driven inflammatory disease. Herbs with anti-allergic, anti-inflammatory and demulcent actions should be considered for future clinical trials into possible herbal interventions. As the precise aetiology of EoE is still unknown, there is much scope for additional herbs that may have appropriate actions in prevention or treatment as more information is discovered. The research reviewed has demonstrated that various herbs may be effective in reducing certain EoE inflammatory mediators. The anti-inflammatory abilities of certain herbs can work on the same inflammation pathways as many of the currently recommended pharmaceutical treatment options for EoE, such as corticosteroids, mast cell stabilizers and leukotriene inhibitors. To date there has been no research evaluating the efficacy and safety of any herbal medicines and likewise there is no traditional evidence describing the herbal medicine management for the treatment of EoE. In conjunction with this, EoE is a rare condition with large variability in symptom severity and sensitivity. Consequently, considerable caution must be taken when using herbal medicine to manage this condition. The rapidly increasing prevalence of the disease and the lack of long-term efficacy, poor compliance and safety issues associated with the currently recommended treatment options all support the call for more research into the use of herbal medicine in EoE.
Abonia JP, Franciosi JP, Rothenberg ME. 2010. TGF-[beta]1: Mediator of a feedback loop in eosinophilic esophagitis ... or should we really say mastocytic esophagitis? J Allergy Clin Immunol 126:6;1205-07.
Aceves SS, Chen D, Newbury RO, Dohil R, Bastian JF, Broide DH. 2010. Mast cells infiltrate the esophageal smooth muscle in patients with eosinophilic esophagitis, express TGF-b1, and increase esophageal smooth muscle contraction. J Allergy Clin Immunol 126:6;1198-204.
Amara S, Kumar P, Athota R. 1999. Suppressive effect of Withania somnifera root extract on the induction of anti-ovalbumin IgE antibody response in mice. Pharmaceutical Biology 37:4;253-59.
Baker ME. 1994. Licorice and enzymes other than 11 betahydroxysteroid dehydrogenase: An Evolutionary Perspective. Steroids 59:2;136-41.
Bhattacharya SK, Muruganandam AV. 2003. Adaptogenic activity of Withania somnifera: an experimental study using a rat model of chronic stress.
Pharmacol Biochem Behav 75:3;547-55.
Blaylock RL, Maroon, J. 2012. Natural plant products and extracts that reduce immunoexcitotoxicity-associated neurodegeneration and promote repair within the central nervous system. Surg Neurol Int 3:19;1-12.
Bone K. 2003. A Clinical Guide to Blending Liquid Herbs: Herbal Formulations for the Individual Patient. St. Louis: Churchill Livingstone.
Busse WW, Ring J, Huss-Marp J & Kahn JE. 2010. A review of treatment with Mepolizumab, an anti-IL-5 Mab, in hypereosinophilic syndromes and asthma. J Allergy Clin Immunol 125:4;803-13.
Clement-Kruzel S, Hwang SA, Kruzel MC, Dasgupta A, Actor JK. 2008. Immune modulation of macrophage pro-inflammatory response by goldenseal and astragalus extracts. J Med Food 11:3;493-98.
Davis L, Kuttan G. 2000. Immunomodulatory activity of Withania somnifera. J Ethnopharmacol 71:1-2;193-200.
Doherty J, Grenier D. The Canadian Paediatric Surveillance Program: Beyond collecting numbers. Paediatr Child Health 6:5;263-268.
Enns R, Kazemi P, Chung W, Lee M. 2010. Eosinophilic esophagitis: clinical features, endoscopic findings and response to treatment. Can J Gastroenterol 24:9;547-51.
Felter H, Lloyd J. 1898. King's American Dispensatory, 18th edn. Ohio Valley, Cincinnatti.
Fiorillo C, Becattia M, Pensalfinia A, Cecchia C, Lanzilaoa L, Donzellib G et al. 2008. Curcumin protects cardiac cells against ischemia-repurfusion injury: effects on oxidative stress. Free Radic Biol Med 45:6;839-46.
Grieve M. 1931. A Modern Herbal. New York: Harcourt, Brace & Company
Hruz P, Straumann A, Bussmann C, Heer P, Simon HW, Zwahlen M et al. 2011. Escalating incidence of eosinophilic esophagitis: a 20 year prospective, population-based study in Olten County Switzerland. J Allergy Clin Immunol 128:6;1349-50.
Hsieh CJ, Hall K, Ha T, Li C, Krishnaswamy G, Chi DS. 2007. Baicalein inhibits IL-1[beta]- and TNF-[alpha] -induced inflammatory cytokine production from human mast cells via regulation of the NF-Kb pathway. Clin Mol Allergy 5:5;1-10.
Jayaram S, Dharmesh SM. 2011. Assessment of antioxidant potentials of free and bound phenolics of Hemidesmus indicus (L) R.Br against oxidative damage. Pharmacognosy Res 3:4;225-31.
Jung HS, Kim MH, Gwak NG, Im YS, Lee KY, Sohn Y, Choi H, Yang WM. 2012. Antiallergic effects of Scutellaria baicalensis on inflammation in vivo and in vitro. J Ethnopharmacol 141:1;345-349.
Jurenka JS. 2009. Anti-inflammatory properties of curcumin, a major constituent of Curcuma longa: a review of preclinical and clinical research. Altern Med Rev 14:2;141-53.
Kimura Y, Okuda H, Arichi S. 1987. Effects of baicalein on leukotriene biosynthesis and degranulation in human polymorphonuclear leukocytes. Biochim Biophys Acta 922:3;278-86.
Klinnert MD. 2009. Psychological impact of eosinophilic esophagitis on children and families. Immunol Allergy Clin North Am 29:1;99-107.
Kour K, Pandey A, Suri KA, Satti NK, Gupta KK, Bani S. 2009. Restoration of stress-induced altered t cell function and corresponding cytokines patterns by withanolide A. Int Immunopharmacol 9:10;1137-44.
Krakauer T, Li BQ, Young HA. 2001. The flavonoid baicalin inhibits superantigen-induced inflammatory cytokines and chemokines. FEBS Lett 500:1-2;52-5.
Le-Carlson M, Seki S, Abarbanel D, Quiros A, Cox K, Nadeau KC.
Markers of antigen presentation and activation on eosinophils and T cells in the esophageal tissue of patients with eosinophilic esophagitis. J Pediatr Gastroenterol Nutr 56:3;257-62.
Li BQ, Fu T, Gong WH, Dunlop N, Kung H, Yan Y, Kang J, Wang JM. 2000. The flavonoid baicalin Exhibits anti-inflammatory activity by binding to chemokines. Immunopharmacology 49:3;295-306.
Liao JF, Hung WY, Chen CF. 2003. Anxiolytic-like effects of baicalein and baicalin in the vogel conflict test in mice. Eur J Pharmacol 464:2-3;141-6.
Lucendo AJ, Gonzalez-Castillo S, Guagnozzi D, Yague-Compadre JL, Arias A. 2010. Eosinophilic esophagitis: current aspects of a recently recognized disease. Gastroenterol Res 3:2;52-64.
Mulder DJ, Justinich CJ. 2011. Understanding eosinophilic esophagitis: the cellular and molecular mechanisms of an emerging disease. Mucosal Immunol 4:2;139-47.
Nakajima T, Imanishi M, Yamamoto K, Cyong JC, Hirai K. 2001. Inhibitory effect of baicalein, a flavonoid in scutellaria root, on eotaxin production by human dermal fibroblasts. Planta Med 67:2;132-5.
Nurko S, Furuta GT. 2006. Eosinophilic esophagitis. GI Motility online doi:10.1038/gimo49.
Nurul IM, Mizuguchi H, Shahriar M, Venkatesh P, Maeyama K, Mukherjee P et al. 2011. Albizia Lebbeck Suppresses Histamine Signaling by the Inhibition of Histamine H1 Receptor and Histidine Decarboxylase Gene Transcriptions. Int Immunopharmacol 11:11;1766-72.
Oberholzer HM, Pretorius E, Smit E, Ekpo OE, Humphries P, Auer RE, Bester MJ. 2008. Investigating the effect of Withania somnifera, selenium and hydrocortisone on blood count and bronchial lavage of experimental asthmatic BALB/c mice', Scand J Lab Anim Sci 35:4;239-48.
Oksman M, Livonen H, Hogyes E, Amtul Z, Penke B, Leenders I et al. 2006. Impact of different saturated fatty acids, polyunsaturated fatty acid and cholesterol containing diets on beta-amyloid accumulation in app/ps1 transgenic mice. Neurobiol Dis 23:3;563-72.
Omar HR, Komarova I, El-Ghonemi M, Fathy A, Rashad R, Abdelmalak HD, Yerramadha MR, Ali Y, Helal E, Camporesi EM. 2012. Licorice abuse: time to send a warning message. Ther Adv Endocrinol Metab 3:4;125-38.
Pawar P, Gilda S, Sharma S, Jagtap S, Paradkar A, Mahadik K, Ranjekar P, Harsulkar A. 2011. Rectal gel application of Withania somnifera root extract expounds anti-inflammatory and mucorestorative activity in TNBS-induced inflammatory bowel disease. BMC Complement Altern Med 11:34;1-9.
Peterson KA, Thomas KL, Hilden K, Emerson LL, Wills JC, Fang JC. 2010. Comparison of esomeprazole to aerosolized, swallowed fluticasone for eosinophilic esophagitis. Dig Dis Sci 55:5;1313-9.
Shen YC, Chiou WF, Chou YC, Chen CF. 2003. Mechanisms in mediating the anti-inflammatory effects of baicalin and baicalein in human leukocytes. Eur J Pharmacol 465:1-2;171-81.
Straumann A. 2012. Eosinophilic esophagitis: rapidly emerging disorder. Swiss Med Wkly 142:1-8.
Tripathi RM, Sen PC, Das PK. 1979. Studies on the mechanism of action of Albizzia lebbeck, an Indian indigenous drug used in the treatment of atopic allergy. J Ethnopharmacol 1:4;385-96.
Valent P, Klion AD, Horny HP, Roufosse F, Gotlib J, Weller PF et al. 2012. Contemporary consensus proposal on criteria and classification of eosinophilic disorders and related syndromes. J Allergy Clin Immunol 130:3;607-612.
Vicario M, Blanchard C, Stringer KF, Collins MH, Mingler MK, Ahrens A et al. 2010. Local B cells and IgE production in the oesophageal mucosa in eosinophilic oesophagitis. Gut 59:1;12-20.
Wakabayashi I, Yasui K. 2000. Short communication: Wogonin inhibits inducible prostaglandin e2 production in macrophages. Eur J Pharmacol 406:3;477-81.
Yeum HS, Lee YC, Kim SH, Roh SS, Lee JC, Seo YB. 2007. Fritillaria cirrhosa, Anemarrhena asphodeloides, Lee-Mo-Tang and Cyclosporine a inhibit ovalbumin-induced eosinophil accumulation and Th2-mediated bronchial hyperresponsiveness in a murine model of asthma. Basic Clin Pharmacol Toxicol 100:3;205-13.
Nicole Hannan BSc (Sports Med)
Surfers Paradise, QLD
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|Title Annotation:||Herbal medicine hypothesis|
|Publication:||Australian Journal of Herbal Medicine|
|Date:||Jun 1, 2013|
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