Allergic Airway Research Articles

5-BDBD ameliorates an OVA-induced allergic asthma by the reduction of Th2 cytokines production.

Objective(s):P2X4R is expressed in immunocyte and lung tissues. It has been a focus in inflammatory responses recently. This study investigated whether blockage of P2X4R attenuates allergic inflammation by modulating T cell response in ovalbumin-sensitized mice.Materials and Methods:Ovalbumin was used to sensitize and challenge for a mouse model. Intranasal application of 5-BDBD, P2X4R antagonist, were performed 3 hr before each airway allergen challenge. The lung was evaluated for P2X4R by real-time PCR and immunofluorescence. Th1/Th2 cytokines in bronchoalveolar lavage fluid were measured by ELISA. T-bet, Gata-3, and p-p38 MAPK were measured by Western blot or real-time PCR.Results:P2X4R was overexpressed in the lung after allergen challenge compared with the control group. Blockage of P2X4R decreased inflammation in the lung, IL-4 expression was reduced as well as IL-5; IFN-γ expression was elevated in BALF in ovalbumin-sensitized mice. Moreover, blockage of P2X4R inhibited ovalbumin-induced increased Gata-3 level and decreased T-bet level.Conclusion:These findings suggest that 5-BDBD ameliorates an ovalbumin-induced asthmatic attack by the downregulation of cytokines related to the Th2 cell.

Interleukin (IL) 36 gamma induces mucin 5AC, oligomeric mucus/gel-forming expression via IL-36 receptor-extracellular signal regulated kinase 1 and 2, and p38-nuclear factor kappa-light-chain-enhancer of activated B cells in human airway epithelial cells.

Mucin 5AC, oligomeric mucus/gel-forming (MUC5AC) expression is significantly increased in allergic and inflammatory airway diseases. Interleukin (IL) 36 gamma is predominantly expressed in airway epithelial cells and plays an important role in innate and adaptive immune responses. IL-36 gamma is induced by many inflammatory mediators, including cytokines and bacterial and viral infections. However, the association between IL-36 gamma and mucin secretion in human airway epithelial cells has not yet been fully investigated. The objective of this study was to determine whether IL-36 gamma might play a role in the regulation of mucin secretion in airway epithelial cells. We investigated the effect and brief signaling pathway of IL-36 gamma on MUC5AC expression in human airway epithelial cells. Enzyme immunoassay, immunoblot analysis, immunofluorescence staining, reverse transcriptase-polymerase chain reaction (PCR), and real-time PCR were performed in mucin-producing human airway epithelial NCI-H292 cells and in human nasal epithelial cells after pretreatment with IL-36 gamma, several specific inhibitors, or small interfering RNAs (siRNA). IL-36 gamma induced MUC5AC expression and activated the phosphorylation of extracellular signal regulated kinase (ERK) 1 and 2, p38, and nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-kappa B). IL-36 receptor antagonist significantly attenuated these effects. The specific inhibitor and siRNA of ERK1, ERK2, p38, and NF-kappa B significantly attenuated IL-36 gamma induced MUC5AC expression. These results indicated that IL-36 gamma induced MUC5AC expression via the IL-36 receptor-mediated ERK1/2 and p38/NF-kappa B pathway in human airway epithelial cells.

Dexamethasone-Related Perineal Burning in the Prehospital Setting: A Case Series

Dexamethasone is frequently used in the treatment of allergic reactions and airway inflammation because of its potent anti-inflammatory effects and long duration of action. As prehospital use becomes more common, it is important for providers to be aware of unique and potentially distressing associated adverse effects. We report eight cases of intravenous dexamethasone administration associated with perineal or diffuse burning sensation in female patients.

Airway IL-1α promotes development of allergen-specific follicular helper T (Tfh) cells and production of IgE antibody

Recent literature suggests that Tfh cells that produce IL-4 play a pivotal role in allergic immune responses. However, the molecular and immunological mechanisms involved in the development of Tfh cells are not fully understood. The goal of this study was to test the hypothesis that IL-1α released from alveolar macrophage plays a pivotal role in respiratory allergy. Naïve wild-type BALB/c mice and IL-4 reporter 4get mice were exposed intranasally (i.n.) to a model antigen ovalbumin (OVA) with or without serial dilutions of IL-1α. Development of allergic immune responses was analyzed by collecting mediastinal lymph nodes (mLNs) and sera, and by challenging the animals i.n. with OVA antigen. Alveolar macrophages were isolated of naïve BALB/c mice and stimulated in vitro with pollens of short ragweed or Japanese cedar. The mice exposed i.n. to OVA with IL-1α produced OVA-specific IgE antibody; the IgE response was dependent on the doses of IL-1α. These mice showed airway eosinophilia and increased lung levels of type 2 cytokines when challenged i.n. with OVA. Marked increase in the IL-4eGFP+CD4+CXCR5+ST2- Tfh cell population was observed in mLNs of mice exposed OVA plus IL-1α as compared to those mice exposed to OVA alone. Furthermore, alveolar macrophages produced and released IL-1α extracellular when they were exposed to allergen pollens in vitro. IL-1α produced by alveolar macrophages by airway allergen exposure may paly a pivotal role to promote generation of antigen-specific Tfh cells and hence development of respiratory allergy.

Immunization with an adenovirus-vectored TB vaccine containing Ag85A-Mtb32 effectively alleviates allergic asthma

Current treatments for allergic asthma primarily ameliorate symptoms rather than inhibit disease progression. Regulating the excessive T helper type 2 (Th2) responses may prevent asthma exacerbation. In this study, we investigated the protective effects of Ad5-gsgAM, an adenovirus vector carrying two mycobacterial antigens Ag85A and Mtb32, against allergic asthma. Using an ovalbumin (OVA)-induced asthmatic mouse model, we found that Ad5-gsgAM elicited much more Th1-biased CD4+T and CD8+T cells than bacillus Calmette-Guérin (BCG). After OVA challenge, Ad5-gsgAM-immunized mice showed significantly lowered airway inflammation in comparison with mice immunized with or without BCG. Total serum immunoglobulin E and pulmonary inducible-nitric-oxide-synthase were efficiently reduced. The cytokine profiles in bronchial-alveolar-lavage-fluids (BALFs) were also modulated, as evidenced by the increased level of interferon-γ (IFN-γ) and the decreased level of interleukin (IL)-4, IL-5, and IL-13. Anti-inflammatory cytokine IL-10 was sharply increased, whereas pro-inflammatory cytokine IL-33 was significantly decreased. Importantly, exogenous IL-33 abrogated the protective effects of Ad5-gsgAM, revealing that the suppression of IL-33/ST2 axis substantially contributed to protection against allergic inflammation. Moreover, regulatory T cells were essential for regulating aberrant Th2 responses as well as IL-33/ST2 axis. These results suggested that modulating the IL-33/ST2 axis via adenovirus-vectored mycobacterial antigen vaccination may provide clinical benefits in allergic inflammatory airways disease.Key messages•Ad5-gsgAM elicits Th1 responses and suppresses Th2-mediated allergic asthma in mice.•Ad5-gsgAM inhibits IL-33/ST2 axis by reducing IL-33 secretion but not ILC2 recruiting.•Treg is essential for modulating Th2 responses and IL-33/ST2 axis by Ad5-gsgAM.

Contributions of direct versus indirect mechanisms for regulatory dendritic cell suppression of asthmatic allergen-specific IgG1 antibody responses.

IL-10-differentiated dendritic cells (DC10) can reverse the asthma phenotype in mice, but how they suppress the asthmatic B cell response is unclear. Herein we assessed the mechanism(s) by which DC10 and DC10-induced Treg affect IgG1 production in asthma. We observed a rapid decline in lung-resident OVA-specific IgG1-secreting B cells on cessation of airway allergen challenge, and intraperitoneal DC10 therapy did not amplify that (p>0.05). It did however increase the loss of IgG1-B cells from the bone marrow (by 45+/-7.2%; p≤0.01) and spleen (by 65+/-17.8%; p≤0.05) over 2 wk. Delivery of OVA-loaded DC10 directly into the airways of asthmatic mice decreased the lung IgG1 B cell response assessed 2 dy later by 33+/-9.7% (p≤0.01), while their co-culture with asthmatic lung cell suspensions reduced the numbers of IgG1-secreting cells by 56.5+/-9.7% (p≤0.01). This effect was dependent on the DC10 carrying intact allergen on their cell surface; DC10 that had phagocytosed and fully processed their allergen were unable to suppress B cell responses, although they did suppress asthmatic Th2 cell responses. We had shown that therapeutic delivery of DC10-induced Treg can effectively suppress asthmatic T and B cell (IgE and IgG1) responses; herein CD4+ cells or Treg from the lungs of DC10-treated OVA-asthmatic mice suppressed in vitro B cell IgG1 production by 52.2+/-8.7% (p≤0.001) or 44.6+/-12.2% (p≤0.05), respectively, but delivery of DC10-induced Treg directly into the airways of asthmatic mice had no discernible impact over 2 dy on the numbers of lung IgG1-secreting cells (p≥0.05). In summary, DC10 treatment down-regulates OVA-specific B cell responses of asthmatic mice. While DC10 that carry intact allergen on their cell surface can dampen this response, DC10-induced Treg are critical for full realization of this outcome. This suggests that infectious tolerance is an essential element in regulatory DC control of the B cell response in allergic asthma.

Immuno-modulatory and Therapeutic Effect of Curcumin in an Allergensensitized Murine Model of Chronic Asthma

Background: Asthma is a chronic allergic disease of the lung and airways, characterized by persistent inflammation and airway hyper-responsiveness. More than 200 million people are affected with severe asthma worldwide. T cells, especially Th2 cells, secreting IL-4, IL-5 and IL-13, are pivotal in orchestrating the disease process. We herein investigated the inhibition mechanism of curcumin, a polyphenol present in turmeric, and its ability to alleviate allergic asthma in C57BL/6J mice.Methods: Mice were sensitized and challenged with Ovalbumin for 54 days. We investigated cellular infiltration in blood and BALF, assessed levels of serum IgE, assessed structural changes by histological analysis, and determined the levels of expression of relevant genes and proteins.Results: Our data revealed that curcumin has some anti-inflammatory effect and is successful in ameliorating the disease. We found that curcumin most likely acts by inhibiting the activation of NFκB and its subsequent downstream processes. Our data provided evidence in support of therapeutic application of curcumin in allergic inflammation and airway remodeling.

Berufsbedingtes Asthma

Bronchial asthma can be induced and/or worsened by occupational exposure. Approximately 10-15% of all asthmatic diseases in adults are related to the workplace according to international epidemiological studies. Work-related asthmatic diseases can be triggered by airway allergens as well as by chemical irritants and working materials with toxic effects. The diagnostics of work-related bronchial asthma include a comprehensive workplace-related medical history. This is complemented by testing for occupational allergens and an attempt to objectify the reported association of symptoms to the workplace, for example by monitoring lung function with and without exposure at the workplace. If reliable facts for a causal association can be found, a complaint of an occupational disease with respect to work-related asthma must be filed. Furthermore, workplace-related breathing difficulties can be a sign of insufficient workplace safety. In order to optimize management of asthma patients, a collaboration between pneumologists and company physicians is necessary, independent of whether there is a suspicion of a work-related disease or not.

Palmitoylethanolamide Supplementation during Sensitization Prevents Airway Allergic Symptoms in the Mouse.

One important risk factor for the development of asthma is allergen sensitization. Recent increasing evidence suggests a prominent role of mast cells in asthma pathophysiology. Since Palmitoylethanolamide (PEA), an endogenous lipid mediator chemically related to – and co-released with- the endocannabinoid anandamide, behaves as a local autacoid down-regulator of mast cell activation and inflammation, we explored the possible contribution of PEA in allergic sensitization, by using ovalbumin (OVA) as sensitizing agent in the mouse. PEA levels were dramatically reduced in the bronchi of OVA-treated animals. This effect was coupled to a significant up-regulation of CB2 and GPR55 receptors, two of the proposed molecular PEA targets, in bronchi harvested from allergen-sensitized mice. PEA supplementation (10 mg/kg, 15 min before each allergen exposure) prevented OVA-induced bronchial hyperreactivity, but it did not affect IgE plasma increase. On the other hand, PEA abrogated allergen-induced cell recruitment as well as pulmonary inflammation. Evaluation of pulmonary sections evidenced a significant inhibitory action of PEA on pulmonary mast cell recruitment and degranulation, an effect coupled to a reduction of leukotriene C4 production. These findings demonstrate that allergen sensitization negatively affects PEA bronchial levels and suggest that its supplementation has the potential to prevent the development of asthma-like features.

MicroRNA Profiling in Asthma: Potential Biomarkers and Therapeutic Targets.

Asthma is a heterogeneous chronic inflammatory disorder in which different endotypes contribute to define clinical inflammatory phenotypes. MicroRNAs (miRNAs) are a group of minute, endogenous 22-25 nt RNA elements that join to particular mRNAs to reduce translation and increase messenger RNA degradation. miRNAs operate in post-transcriptional control and regulate physiological and pathological processes in several illnesses. The purpose of this work is to review and discuss the current knowledge about the function of miRNAs in asthma, focusing particularly on their biological properties, pathophysiologic actions, and possible use as markers and treatments for asthma.

Exacerbation of Ventilation-Induced Lung Injury and Inflammation in Preterm Lambs by High-Dose Nanoparticles

Mechanical ventilation of preterm neonates causes lung inflammation and injury, with potential life-long consequences. Inert 50-nm polystyrene nanoparticles (PS50G) reduce allergic inflammation in the lungs of adult mice. We aimed to confirm the anti-inflammatory effects of PS50G in a sheep asthma model, and investigate the effects of prophylactic administration of PS50G on ventilation-induced lung injury (VILI) in preterm lambs. We assessed lung inflammatory cell infiltration, with and without PS50G, after airway allergen challenge in ewes sensitised to house dust mite. Preterm lambs (0.83 gestation) were delivered by caesarean section for immediate tissue collection (n = 5) or ventilation either with (n = 6) or without (n = 5) prophylactic intra-tracheal administration of PS50G nanoparticles (3% in 2 ml). Ventilation was continued for a total of 2 h before tissue collection for histological and biomolecular assessment of lung injury and inflammation. In ewes with experimental asthma, PS50G decreased eosinophilic infiltration of the lungs. Ventilated preterm lambs showed molecular and histological signs of lung injury and inflammation, which were exacerbated in lambs that received PSG50G. PS50G treatment decreased established inflammation in the lungs of asthmatic sheep. However, prophylactic administration of PSG50 exacerbated ventilation-induced lung injury and lung inflammation in preterm lambs.

Cell Penetrating Peptide Derived from Human Eosinophil Cationic Protein Decreases Airway Allergic Inflammation

Cell penetrating peptide derived from human eosinophil cationic protein (CPPecp) is a 10-amino-acid peptide containing a core heparan sulfate (HS)-binding motif of human eosinophil cationic protein (ECP). It binds and penetrates bronchial epithelial cells without cytotoxic effects. Here we investigated airway-protective effects of CPPecp in BEAS-2B cell line and mite-induced airway allergic inflammation in BALB/c mice. In BEAS-2B cell, CPPecp decreases ECP-induced eotaxin mRNA expression. CPPecp also decreases eotaxin secretion and p-STAT6 activation induced by ECP, as well as by IL-4. In vivo studies showed CPPecp decreased mite-induced airway inflammation in terms of eosinophil and neutrophil count in broncho-alveolar lavage fluid, peri-bronchiolar and alveolar pathology scores, cytokine production in lung protein extract including interleukin (IL)-5, IL-13, IL-17A/F, eotaxin; and pause enhancement from methacholine stimulation. CPPecp treated groups also showed lower serum mite-specific IgE level. In this study, we have demonstrated the in vitro and in vivo anti-asthma effects of CPPecp.

Sensitization to dust mite defines different phenotypes of asthma: A multicenter study.

Indoor allergens are risk factors for asthma: Thus, the characterization of indoor air quality is important for studying environment-health relationships in children. In particular, Dermatophagoides pteronyssinus is the dominant allergen for asthma. We cross-sectionally investigated the relationships among respiratory symptoms and function, airway inflammation, allergen sensitization, and indoor allergen concentration. One hundred and thirty-two children aging 10-14years and living in a Southern Mediterranean area were evaluated by parental questionnaires. Spirometry, exhaled nitric oxide (FeNO), skin prick tests, total, and specific serum IgE analyses were performed along with the evaluation of home dust samples for the content in Der p 1 allergen. Three clusters were created on the basis of the presence/absence of wheeze in the last 12months (Wh12m) and Der p 1-specific IgE level. Cluster 1 (Wh12m+/high Der p 1 IgE) presented higher FeNO and poorer pulmonary function (lower FEV1 and FEF25%-75% ), while its symptom score was not different from Cluster 2 (Wh12m+/low Der p 1 IgE). Cluster 3 (Wh12m-/low IgE) showed the lowest FeNO values and pulmonary function similar to Cluster 2. Within Cluster 1, both Der p 1-specific IgE and FeNO were positively correlated with dust Der p 1. Similar asthma phenotypes may occur in children despite differences in their atopic state. In atopic children, sensitizing allergens in the indoor environment may increase airway inflammation worsening pulmonary function. Moreover, environmental exposures may contribute to the development of asthma-like symptoms also in the absence of atopic sensitization, thus contributing to asthma overdiagnosis.

Sublingual house dust mite immunotherapy has no impact on decrease of circulating erythrocytes upon airway allergen challenge in allergic rhinitis

House dust mite (HDM) allergy is a predominant cause for perennial allergic rhinitis (AR) in Europe. We recently reported that circulating erythrocyte numbers decrease after airway allergen challenge in a murine asthma model and in grass-pollen sensitized AR subjects. Consequently, we aimed to evaluate these findings in HDM sensitized AR subjects and the influence of preceding allergen immunotherapy. Seventy-seven (age 26.8 ± 7.3 years; 54.5% female) HDM-allergic rhinitis subjects previously enrolled in a randomized, monocentric sublingual immunotherapy (SLIT) trial at the Vienna Challenge Chamber (VCC) were included. Subjects had either received placebo (n = 22), low-dose HDM (n = 29) or high-dose HDM specific sublingual immunotherapy (n = 26) daily for 24 weeks. Blood sampling was performed before and after 6 hours of HDM allergen exposure. Overall, specific airway allergen challenge resulted in a significant decrease in circulating erythrocytes and hematocrit (p < 0.001), and elevation of leukocytes (p < 0.001), particularly segmented neutrophils (p < 0.001). Gender had no significant effect on the observed changes in circulating blood cells. Erythrocytes decreased and neutrophil counts increased significantly after airway allergen challenge regardless of preceding immunotherapy. These findings imply a rapid systemic mobilization of neutrophils occurring within immediate type hypersensitivity response upon a specific allergen challenge, which is possibly inversely linked with the erythrocyte numbers.

Allergic Rhinitis and Sexual Dysfunction

Sexual dysfunction is perhaps an important co-morbidity of allergic rhinitis and other upper airway diseases in adults; however, its prevalence and importance are underestimated mainly due to lack of assessment by the physician and lack of reporting by the patients. The clue for a successful treatment relies in adequate diagnosis and understanding of the mechanisms involved in the generation of the symptoms.

Exposure to Bacterial CpG DNA Protects from Airway Allergic Inflammation by Expanding Regulatory Lung Interstitial Macrophages

Living in a microbe-rich environment reduces the risk of developing asthma. Exposure of humans or mice to unmethylated CpG DNA (CpG) from bacteria reproduces these protective effects, suggesting a major contribution of CpG to microbe-induced asthma resistance. However, how CpG confers protection remains elusive. We found that exposure to CpG expanded regulatory lung interstitial macrophages (IMs) from monocytes infiltrating the lung or mobilized from the spleen. Trafficking of IM precursors to the lung was independent of CCR2, a chemokine receptor required for monocyte mobilization from the bone marrow. Using a mouse model of allergic airway inflammation, wefound that adoptive transfer of IMs isolated from CpG-treated mice recapitulated the protective effects of CpG when administered before allergen sensitization or challenge. IM-mediated protection was dependent on IL-10, given that Il10-/- CpG-induced IMs lacked regulatory effects. Thus, the expansion of regulatory lung IMs upon exposure to CpG might underlie the reduced risk of asthma development associated with a microbe-rich environment.

IL-15-deficient mice develop enhanced allergic responses to airway allergen exposure.

Interleukin-15 is a pleiotropic cytokine that is critical for the development and survival of multiple haematopoietic lineages. Mice lacking IL-15 have selective defects in populations of several pro-allergic immune cells including natural killer (NK) cells, NKT cells, and memory CD8+ T cells. We therefore hypothesized that IL-15-/- mice will have reduced inflammatory responses during the development of allergic airway disease (AAD). To determine whether IL-15-/- mice have attenuated allergic responses in a mouse model of AAD. C57BL/6 wild-type (WT) and IL-15-/- mice were sensitized and challenged with ovalbumin (OVA), and the development of AAD was ascertained by examining changes in airway inflammatory responses, Th2 responses, and lung histopathology. Here, we report that IL-15-/- mice developed enhanced allergic responses in an OVA-induced model of AAD. In the absence of IL-15, OVA-challenged mice exhibited enhanced bronchial eosinophilic inflammation, elevated IL-13 production, and severe lung histopathology in comparison with WT mice. In addition, increased numbers of CD4+ T and B cells in the spleens and bronchoalveolar lavage (BAL) were also observed. Examination of OVA-challenged IL-15Rα-/- animals revealed a similar phenotype resulting in enhanced airway eosinophilia compared to WT mice. Adoptive transfer of splenic CD8+ T cells from OVA-sensitized WT mice suppressed the enhancement of eosinophilia in IL-15-/- animals to levels observed in WT mice, but had no further effects. These data demonstrate that mice with an endogenous IL-15 deficiency are susceptible to the development of severe, enhanced Th2-mediated AAD, which can be regulated by CD8+ T cells. Furthermore, the development of disease as well as allergen-specific Th2 responses occurs despite deficiencies in several IL-15-dependent cell types including NK, NKT, and γδ T cells, suggesting that these cells or their subsets are dispensable for the induction of AAD in IL-15-deficient mice.

Chemorepellent Semaphorin 3E Negatively Regulates Neutrophil Migration In Vitro and In Vivo.

Neutrophil migration is an essential step in leukocyte trafficking during inflammatory responses. Semaphorins, originally discovered as axon guidance cues in neural development, have been shown to regulate cell migration beyond the nervous system. However, the potential contribution of semaphorins in the regulation of neutrophil migration is not well understood. This study examines the possible role of a secreted chemorepellent, Semaphorin 3E (Sema3E), in neutrophil migration. In this study, we demonstrated that human neutrophils constitutively express Sema3E high-affinity receptor, PlexinD1. Sema3E displayed a potent ability to inhibit CXCL8/IL-8-induced neutrophil migration as determined using a microfluidic device coupled to real-time microscopy and a transwell system in vitro. The antimigratory effect of Sema3E on human neutrophil migration was associated with suppression of CXCL8/IL-8-mediated Ras-related C3 botulinum toxin substrate 1 GTPase activity and actin polymerization. We further addressed the regulatory role of Sema3E in the regulation of neutrophil migration in vivo. Allergen airway exposure induced higher neutrophil recruitment into the lungs of Sema3e-/- mice compared with wild-type controls. Administration of exogenous recombinant Sema3E markedly reduced allergen-induced neutrophil recruitment into the lungs, which was associated with alleviation of allergic airway inflammation and improvement of lung function. Our data suggest that Sema3E could be considered an essential regulatory mediator involved in modulation of neutrophil migration throughout the course of neutrophilic inflammation.

Entire Course Monitoring and Evaluation of Asthma Attack Following Allergen Airway Challenge In A Rat Model

Entire Course Monitoring and Evaluation of Asthma Attack Following Allergen Airway Challenge In A Rat Model

Effect of Angelica glauca essential oil on allergic airway changes induced by histamine and ovalbumin in experimental animals

Objective:Angelica glauca Edgew (Apiaceae) is used in traditional medicine for treatment of several diseases including bronchial asthma. The present investigation was aimed to evaluate broncho-relaxant activity of A. glauca essential oil in histamine and ovalbumin (OVA)-induced broncho constriction in experimental animals.Materials and Methods:Airway was induced using histamine aerosol in guinea pigs (n = 24) and OVA aerosol in albino mice (n = 24). The number of inflammatory cells, namely, absolute eosinophils count in blood, total immunoglobulin E (IgE) in serum, eosinophils, and neutrophils in bronchoalveolar lavage fluid (BALF) and histopathological examination of lung tissues were investigated in A. glauca oil and dexamethasone-treated groups. A. glauca oil 200 μL/kg was given orally, and dexamethasone 2 mg/kg was given intraperitoneal. Both the treatments were repeated daily for 7 days. Results were analyzed by one-way ANOVA, and P ≤ 0.05 was considered statistically significant.Results:Treatment with A. glauca essential oil significantly (P < 0.001) increased the time of preconvulsive dyspnea in histamine-induced guinea pigs. Oral treatment of A. glauca oil significantly (P < 0.001) decreased absolute blood eosinophil count (from 325 ± 3.69 to 200 ± 3.05 cells/mm3), serum level of IgE (from 6.10 ± 0.05 to 0.70 ± 0.08 IU/L), and the number of eosinophils (from 11.0% ±1.41% to 3.0% ±0.51%), neutrophils (from 13.0% ±1.12% to 5.0% ±1.39%) in BALF. Histopathological changes observed in lungs of untreated group were marked suppressed by treatment with A. glauca oil.Conclusion:The essential oil of A. glauca has bronchorelaxation in both histamine and OVA-induced bronchoconstriction in animals. The traditional use of A. glauca against asthma could be attributed to its bronchodilator property as observed in the present study.