Mold Antigens Research Articles

Impact of Antigen Exposure on Outcomes and Treatment Response in Fibrotic Hypersensitivity Pneumonitis

Patients with fibrotic hypersensitivity pneumonitis (fHP) are frequently treated with immunosuppression to slow lung function decline; however, the impact of this treatment has not been studied across different types of antigen exposure. In patients with fHP, do disease outcomes and response to treatment vary by antigen type? A multicenter interstitial lung disease database (Canadian Registry for Pulmonary Fibrosis) was used to identify patients with fHP. The causative antigen was categorized as avian, mold, unknown, or other. Treatment was defined as mycophenolate≥1,000mg/d or azathioprine≥ 75mg/d for≥ 30days. Statistical analysis included t tests, χ2 tests, and one-way analysis of variance. Unadjusted and adjusted competing risks and Cox proportional hazards models were used to assess survival. A total of 344 patients were identified with the following causative antigens: avian (n= 93; 27%), mold (n= 88; 26%), other (n= 15; 4%), and unknown (n= 148; 43%). Patient characteristics and lung function were similar among antigen groups with a mean FVC %predicted of 75 ± 20. The percent of patients treated with immunosuppression was similar between antigens with 58%of patients treated. There was no change in lung function or symptom scores with the initiation of immunosuppression in the full cohort. Immunosuppression was not associated with a change in survival for patients with avian or mold antigen (avian: hazard ratio, 0.41; 95%CI, 0.11-1.59; P= .20; mold: hazard ratio, 1.13; 95%CI, 0.26-4.97; P= .88). For patients with unknown causative antigen, survival was worse when treated with immunosuppression (hazard ratio, 2.65; 95%CI, 1.01-6.92; P= .047). Response to immunosuppression varies by antigen type in patients with fHP. Additional studies are needed to test the role of immunosuppression in fHP, and particularly in those with an unknown antigen.

Impact of number and type of identified antigen on transplant-free survival in hypersensitivity pneumonitis.

Identification of inciting antigen can affect diagnostic confidence, quality of life, and prognosis in patients with HP. It is unknown whether the number and type of antigen affect results of diagnostic testing or prognosis, whether antigen identified by clinical history alone affects prognosis, and whether feather exposure is associated with outcomes similar to those of other antigens. To evaluate whether the number or type of antigen identified by clinical history alone affects clinical outcomes, we evaluated a retrospective cohort of patients with a high or definite probability of HP based on recent guidelines. In our retrospective cohort, 136 patients met high or definite probability of HP and were included in the analysis. Median transplant-free survival was better in patients with antigen identified on clinical history alone than patients without identified antigen. Feather exposure was associated with improved TFS compared to patients without antigen identified; there was no difference in TFS between patients with feather exposure and either mold or live bird exposure. Mold antigen was associated with increased risk of fibrotic HP compared to avian antigen. Among patients with identified antigen, the number and type of antigen did not affect TFS. Our study suggests that clinical history is adequate for providing prognostic information to patients with HP and classifying the diagnostic probability of HP according to recent guidelines. Feather exposure should be considered an inciting antigen in patients with ILD.

COVID-19 patients share common, corticosteroid-independent features of impaired host immunity to pathogenic molds.

Patients suffering from coronavirus disease-2019 (COVID-19) are susceptible to deadly secondary fungal infections such as COVID-19-associated pulmonary aspergillosis and COVID-19-associated mucormycosis. Despite this clinical observation, direct experimental evidence for severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2)-driven alterations of antifungal immunity is scarce. Using an ex-vivo whole blood stimulation assay, we challenged blood from twelve COVID-19 patients with Aspergillus fumigatus and Rhizopus arrhizus antigens and studied the expression of activation, maturation, and exhaustion markers, as well as cytokine secretion. Compared to healthy controls, T-helper cells from COVID-19 patients displayed increased expression levels of the exhaustion marker PD-1 and weakened A. fumigatus- and R. arrhizus-induced activation. While baseline secretion of proinflammatory cytokines was massively elevated, whole blood from COVID-19 patients elicited diminished release of T-cellular (e.g., IFN-γ, IL-2) and innate immune cell-derived (e.g., CXCL9, CXCL10) cytokines in response to A. fumigatus and R. arrhizus antigens. Additionally, samples from COVID-19 patients showed deficient granulocyte activation by mold antigens and reduced fungal killing capacity of neutrophils. These features of weakened anti-mold immune responses were largely decoupled from COVID-19 severity, the time elapsed since diagnosis of COVID-19, and recent corticosteroid uptake, suggesting that impaired anti-mold defense is a common denominator of the underlying SARS-CoV-2 infection. Taken together, these results expand our understanding of the immune predisposition to post-viral mold infections and could inform future studies of immunotherapeutic strategies to prevent and treat fungal superinfections in COVID-19 patients.

Misalignment between Clinical Mold Antigen Extracts and Airborne Molds Found in Water-damaged Homes

Rationale: Epidemiologic studies have demonstrated that exposure to molds and other fungi can play a role in a variety of allergic and pulmonary diseases in susceptible individuals. Species-specific mold antigen extracts are used in the clinical evaluation of suspected mold-related conditions; however, alignment between these extracts and the species of molds identified in the indoor environment of water-damaged homes has not been rigorously evaluated. Objectives: To identify the predominant genera and species of mold in the air of homes with water damage, mold growth, and/or occupants with respiratory complaints (complaint homes), and to assess their alignment with the mold antigen extracts used in clinical practice. Methods: The genera and species of molds identified in culture-type outdoor and indoor air samples collected from complaint homes throughout the United States and Canada from 2002 to 2017 were examined. Mold antigen extracts available and utilized for skin and serum testing in clinical practice were assessed, and alignment between these data were evaluated. Results: Culture data from 24,455 indoor air samples from 7,547 complaint homes and 29,493 outdoor samples were evaluated. Mean exposure values (colony-forming units [cfu]/m3) were calculated for each genus and species and indoor versus outdoor values were compared. Penicillium was the predominant genus identified in water-damaged homes, with a mean exposure (233.3 cfu/m3) 2.9 times higher than that of the Aspergillus genus (81.4 cfu/m3). Five Penicillium (P. aurantiogriseum, P. brevicompactum, P. citrinum, P. crustosum, and P. variabile) and three Aspergillus (A. versicolor, A. sydowii, and A. niger) species were identified as the predominant indoor water-damage-related fungi. However, none of these Penicillium species and only one of the Aspergillus species is currently available as an antigen extract for use in skin testing or serum testing panels. Conclusions: Significant misalignment exists between the currently available mold antigen extracts and the predominant species of molds found in water-damaged homes. Improving alignment has the potential to enhance diagnosis of mold-related diseases, including allergic asthma and hypersensitivity pneumonitis and to improve patient outcomes via interventions, including antigen avoidance through building remediation and occupant relocation, consistent with the findings of a recent American Thoracic Society Workshop Report.

A Large Case-series of Successful Treatment of Patients Exposed to Mold and Mycotoxin

PurposeThe goal of this study was to present the results of treatment of 100 chemically sensitive and chronically mold-exposed patients, who continued to be disabled even after decontamination of their houses or work places or they were physically removed from their sources of mold. MethodsMolds were identified, serum anti-mold immunoglobulin G antibodies were measured, patients were skin-tested, immunologic abnormalities were recorded, and objective neurologic tests were performed in a subset of patients. FindingsPatient sensitivities and exposures were confirmed by measuring serum immunoglobulin G anti-mold antibodies, intradermal skin testing, and trichothecene toxin breakdown products in the urine. Patients were positive (44%–98%) for individual molds. Abnormalities in T and B cells were found in >80% of patients. Respiratory signs were present in 64% of all patients, and physical signs and symptoms of neurologic dysfunction were present in 70%. Objective autonomic nervous system test results were abnormal in almost 100% of patients tested. Objective neuropsychological evaluations were conducted in 46 of the patients who exhibited symptoms of neurologic impairment and showed typical abnormalities in short-term memory, executive function/judgment, concentration, and hand/eye coordination. Patients (N = 100) with documented mold exposure were divided into 3 groups: (1) those who improved easily, with mold avoidance and antigen injections; (2) those who improved after desensitization to their mold antigens plus additional mycotoxin antigens; and (3) those who had their regular mold antigens, additional mycotoxin antigens, along with regimens that included sauna, oxygen therapy, and nutrients. Approximately 85% of all patients cleared completely; 14% had partial improvement, and 1% remained unchanged. ImplicationsExposure to molds has been increasingly recognized as a major reason for patients presenting with multiple organ symptoms that could not otherwise be explained. Early diagnosis and appropriate treatment could be very successful.

The link between mold sensitivity and asthma severity in a cohort of northern Chinese patients.

Mold sensitivity in asthmatic patients has recently attracted clinical interest; however the links between mold sensitivity and asthma severity in the Chinese population have been poorly characterized. In this study, we assess the relationship between asthma severity and airborne mold sensitivity in a cohort of northern Chinese patients. Ninety-three non-smoking adult outpatients with asthma completed a questionnaire and underwent skin prick testing with five aeroallergens. For all patients, eosinophil cell counts, total serum IgE (sIgE) levels, and pulmonary function were measured. An asthma severity score was calculated based on the patient's forced expiratory volume in one second (FEV1), number of asthma attacks, number of hospital admissions, and use of inhaled or oral corticosteroids in the past year. Ninety-three patients were divided into three groups based on the results of their allergy tests: negative results for all tested allergens (group A, n=32); positive reactions to aeroallergens including mold antigens (group B, n=41); and positive reactions to aeroallergens other than molds (group C, n=20). Patients in group B had a lower FEV1 (74.46%±23.09% predicted) compared with group A (85.52%±19.53%, P=0.023). Patients in both group B and C had elevated absolute eosinophil count (AEC) (group A: 3.12%±2.71%, group B: 5.41%±2.85%, group C: 6.1%±4.49%; group A vs. group B, P=0.008; group A vs. group C, P=0.002), and total sIgE values (group A: 117.36±144.90 IU/mL, group B: 195.86±155.87 IU/mL, group C: 253.31±152.41 IU/mL; group A vs. group B, P=0.031; group A vs. group C, P=0.002) compared with patients in group A. Asthma severity scores were higher in patients in group B compared to patients in group C (7 vs. 5.5, P<0.05). Patients allergic to molds were more likely to have severe asthma [odds ratio 3.636, 95% confidence interval (CI): 1.394 to 9.484; for severe versus mild asthma, P<0.05]. There was no association between asthma severity and sensitisation to house mites or weeds. Mold sensitivity is positively correlated with asthma severity in our cohort of northern Chinese patients.

Hypersensitivity pneumonitis by Fusarium vasinfectum in a home environment

Hypersensitivity pneumonitis by Fusarium vasinfectum in a home environment

Immunotherapy for Mold Allergy

The objective of this article is to review the available studies regarding mold immunotherapy. A literature search was conducted in MEDLINE to identify peer-reviewed articles related to mold immunotherapy using the following keywords: mold, allergy, asthma, and immunotherapy. In addition, references cited within these articles were also reviewed. Articles were selected based on their relevance to the topic. Allergic responses to inhaled mold antigens are a recognized factor in allergic rhinitis and asthma. There are significant problems with respect to the production of relevant allergen material for the diagnosis and treatment of mold allergy with immunotherapy. Mold allergens contain proteases and should not be mixed with other allergens for immunotherapy. Most of the immunotherapy studies focus on two molds, Alternaria and Cladosporium. There is a lack of randomized placebo-controlled trials when evaluating the efficacy of mold immunotherapy with trials only focusing on immunotherapy to Alternaria and Cladosporium. Additional studies are needed regarding mold allergy and immunotherapy focusing on which molds are important for causing allergic disease.

Development and Application of Mold Antigen-Specific Enzyme-Linked Immunosorbent Assays (Elisa) to Quantify Airborne Antigen Exposure

The aim of our study was to develop specific enzyme-linked immunosorbent assays (ELISAs) and apply these to assess mold antigen exposure in composting plants. Sandwich ELISAs based on polyclonal antibodies to Aspergillus fumigatus (Af), Penicillium chrysogenum (Pc), and Cladosporium herbarum (Ch) antigens were developed and validated. Reactivity to 18 different mold species was tested. To optimize extraction procedure, inhalable dust samples taken by a parallel sampler were extracted with or without homogenization. In 31 composting plants stationary pumps were installed at 4 sites to collect 124 inhalable dust samples. The newly developed ELISAs were used in addition to an anti β-1,3-glucan ELISA to quantify mold antigens. The Cladosporium ELISA showed less than 0.04% reactivity to extracts from other fungal genera, while the Af ELISA demonstrated a reactivity of up to 3.6% and the Pc ELISA reacted up to 11% to other mold species. Extraction of parallel sampled filters gave higher antigen amounts with homogenization. The increase was highest for Pc-antigens, followed by Af-antigens, and lowest for Ch-antigens. Mean lower detection limits of homogenized inhalable dust samples were 5 ng/m3 (Af), 0.6 ng/m3 (Pc), 0.2 ng/m3 (Ch), and 0.6 ng/m3 (β-1,3-glucan). The ELISAs were able to detect antigens in 43% (Af), 37% (Pc), 94% (Ch), or 100% (β-1,3-glucan) of the 124 airborne dust samples. Inhalable dust, β-1,3-glucan, and Af-, Pc-, and Ch-antigen concentrations were significantly correlated. The newly developed mold antigen ELISAs are thus able to measure airborne exposure levels in composting plants and differentiate between distinct fungi genera.

Function of the airway epithelium in asthma.

Function of the airway epithelium in asthma.

Identification of fungal DNA in BALF from patients with home-related hypersensitivity pneumonitis

In Japan, a major type of home-related hypersensitivity pneumonitis (HP) is summer-type HP, which is caused by Trichosporon asahii (T. asahii) or Trichosporon mucoides. Some patients with home-related HP test negative for antibodies against Trichosporon; yet, a causative mold antigen cannot be identified. We analyzed 19 patients with home-related HP, 8 healthy volunteers, and 35 patients with other diseases. We extracted DNA from cell pellets of bronchoalveolar lavage fluid (BALF), amplified the DNA by PCR using Trichosporon-specific primers or other fungus-specific primers, and cloned as well as sequenced the PCR amplicon. Other primers used were specific for Acremonium chrysogenum, Aspergillus fumigatus, Aspergillus niger, Fusarium napiforme, Humicola fuscoatra, Penicillium corylophilum, and Pezizia domiciliana. We detected Trichosporon DNA (n = 17) and F. napiforme DNA (n = 2) by PCR in 19 patients with home-related HP; however, these species were not identified in healthy volunteers. After sequencing of the PCR amplicon for Trichosporon species, we identified T. asahii (n = 11), Trichosporon japonicum (n = 1), and Cryptococcus uzbekistanesis (n = 4). We could detect fungal DNA in BALF cell pellets from patients with home-related HP. These data suggest that this method might be useful to detect antigens responsible for home-related HP.

Factors influencing patterns of airway response after allergen challenge in patients with bronchial asthma

We examined patterns of airway response of thirty nine asthma patients who had positive responses on allergen inhalation tests. Six types of inhaled allergens were used: house dust mite, animal, pollen, plant, mold, and others. Three patterns of responses were found: isolated immediate asthmatic response (IAR), immediate and late response (Dual), and isolated late asthmatic response (LAR). No relationship was found between the pattern of response and pulmonary function, airway sensitivity, IgE RIST titers, numbers of eosinophils, or concentration of inhaled antigens. Animal antigens tended to cause a dual response, and molds did only rarely. Ten of 39 challenged patients had an isolated LAR, half of which were caused by mold antigen inhalation. RAST scores were lower in isolated LAR than in other responses. Changes in the number and proportion of peripheral leukocytes during the challenge tests were also studied. Total leukocyte count had increased significantly in the isolated LAR group by 24 hours after the inhalation. These results suggest that the pattern of airway response after inhalation depended in part on the type of inhaled antigen, and that non-IgE mediated immune reactions have some role in the isolated LAR.

IgE‐bearing Cells in Bronchoalveolar Lavage Fluid and Allergen‐specific IgE Levels in Sera from RAO‐affected Horses

Recurrent airway obstruction (RAO) is a common condition in stabled horses characterized by small airway inflammation, airway neutrophilia and obstruction following exposure of susceptible horses to mouldy hay and straw and is thus regarded as a hypersensitivity reaction to mould spores. However, the role of immunoglobulin E antibodies (IgE) in the pathogenesis of RAO is unclear. We hypothesized that the number of cells with receptor-bound IgE in bronchoalveolar lavage fluid (BALF) and IgE levels in serum would be higher in RAO-affected than in healthy horses living in the same environment. Therefore, IgE-positive (+) cells were identified by immunocytochemistry on cytospins from BALF and counted. IgE levels against the mould extracts Aspergillus fumigatus (Asp. f.) and Alternaria alternata (Alt. a.) and the recombinant mould allergen Aspergillus fumigatus 8 (rAsp f 8) were measured by enzyme-linked immunosorbent assay (ELISA) in the sera of seven RAO-affected and 22 clinically healthy mature horses housed in the same conventional stable environment. After correcting for the number of neutrophils, there were no significant differences in IgE+ cells on cytospins from BALF between both groups of horses (5% versus 7%, P > 0.1). Serum IgE levels against the mould extracts were significantly higher in RAO-affected than in clinically healthy horses [median = 119 versus 66 relative ELISA units (REU), P < 0.05]. Furthermore, significantly more RAO-affected than healthy horses had detectable serum IgE against the recombinant allergen rAsp f 8 (4/7 and 3/22, respectively, P < 0.05). Age had no significant effect on BALF cell ratios or on specific serum IgE levels. These results show that high IgE levels against mould antigens are associated with RAO under controlled environmental conditions but ranges of mould-specific serum IgE levels overlapped too much between diseased and clinically healthy animals to be of any diagnostic value. Further studies are needed to assess whether IgE-mediated reactions contribute to the pathogenesis of RAO.

Chronic environmental exposure to &lt;i&gt;Alternaria tenuis&lt;/i&gt; may manifest symptoms of neuropsychological illnesses: a study of 12 cases

Toxigenic mold exposures are shown to lead to illnesses most of which are just being unraveled. This paper reports the findings in cases of 12 white female office workers who presented with symptoms of neuropsychological illnesses, most likely, due to indoor environmental toxigenic mold exposures. Their major complaints were: weakness and numbness in legs, dizziness, loss of memory, light-headedness and vertigo, fatigue, getting lost in familiar territory, and confused thoughts. The subjects were evaluated by testing immunologic, basic EEG, and comprehensive neuropsychological tests. Abnormal antibodies to Alternaria tenuis, Pullularia pullulans, and Epicoccum nigrum antigens were found in all the subjects' serum, and they were quite different from the abnormal levels of Aspergillus, Stachybotrys, and Penicillium, Cladiosporium genera found in their indoor environment. EEG examination was abnormal all the subjects with 10 Hz posterior dominant activities in 6 out of 12, which were synchronous, symmetrical and attenuated on eye opening and eye-closure. There was an evidence of tremor of the extremities in 3 subjects. These particular subjects' reflex was abnormal, and they had accommodation paresis. Gross neuropsychological abnormalities including those observed in the brain-damaged population and significantly below non-brain damaged functioning was observed. These findings seem to indicate that chronic exposures to Alternaria tenuis, Pullularia pullulans, and Epicoccum nigrum might have neuropsychological effects, and that most likely, only one abnormal antibody to toxigenic mold antigen could have the most dominant adverse toxic exertion leading to the observed neuropsychological effects. It is concluded therefore, that chronic exposures to certain toxigenic molds might lead to neuropsychological manifestations and that although, it is acknowledged that the contaminations of the indoor environment by toxigenic molds are directly related to the adverse health effects on the occupants, there could be a situation where such relationship does not exist. Journal of Applied Sciences and Environmental Management Vol. 9(3) 2005: 45-51

The medical effects of mold exposure

Exposure to molds can cause human disease through several well-defined mechanisms. In addition, many new mold-related illnesses have been hypothesized in recent years that remain largely or completely unproved. Concerns about mold exposure and its effects are so common that all health care providers, particularly allergists and immunologists, are frequently faced with issues regarding these real and asserted mold-related illnesses. The purpose of this position paper is to provide a state-of-the-art review of the role that molds are known to play in human disease, including asthma, allergic rhinitis, allergic bronchopulmonary aspergillosis, sinusitis, and hypersensitivity pneumonitis. In addition, other purported mold-related illnesses and the data that currently exist to support them are carefully reviewed, as are the currently available approaches for the evaluation of both patients and the environment.

Comparison of Intradermal Dilutional Testing with the Multi‐Test II Applicator in Testing for Mold Allergy

To compare and correlate wheal size using the Multi-Test II applicator with the endpoint obtained by intradermal dilutional testing (IDT) for common mold allergens. To validate the safety and efficacy of modified quantitative testing (MQT) for determining immunotherapy starting doses. Prospective study of 86 subjects with Multi-Test II and IDT for 6 common mold antigens. There was 84% concordance between IDT results and the results expected from the MQT method. When IDT and MQT results differed, the MQT algorithm predicted a safer endpoint for starting immunotherapy in all but 2 cases. The correlation between Multi-Test II and IDT is not strong enough to infer IDT endpoint from Multi-Test II results for molds. MQT is nearly as effective as formal IDT in determining endpoint. MQT appears to be a safe method for determining starting doses for immunotherapy with fungal allergens.

Results of allergen-specific immunotherapy in 117 dogs with atopic dermatitis

The success of the treatment of 117 dogs with atopic dermatitis with allergen-specific immunotherapy for up to 48 months was assessed. An excellent response (remission with exclusive immunotherapy) was recorded...

Chronic Exposure To Alternaria Tenuis, Pullularia Pullulans, And Epicoccum Nigrum May Lead To Symptoms Of Neuropsychological Illnesses: Evidence From A Comprehensive Evaluation

Background: Toxigenic mold exposures are shown to lead to illnesses most of which are just being unraveled. This paper reports the findings in cases of 12 white female office workers who presented with symptoms of neuropsychological illnesses, most likely, due to indoor environmental toxigenic mold exposures. Their major complaints were: weakness and numbness in both legs, dizziness, loss of memory, light-headedness and vertigo, fatigue, getting lost in familiar territory, and confused thoughts. Methods: Immunologic, basic EEG, and comprehensive neuropsychological tests were carried out on the subjects to evaluate determine the extent of their neuropsychological impairments. Results: Abnormal antibodies to Alternaria tenuis, Pullularia pullulans, and Epicoccum nigrum antigens were found in all the subjects' serum. EEG examination was abnormal all the subjects with 10 Hz posterior dominant activities in 6 out of 12, which were synchronous, symmetrical and attenuated on eye opening and eye-closure. There was an evidence of tremor of the extremities in 3 subjects. Gross neuropsychological abnormalities including those observed in the brain-damaged population and significantly below nonbrain damaged functioning were observed. These findings seem to indicate that chronic exposures to Alternaria tenuis, Pullularia pullulans, and Epicoccum nigrum might have neuropsychological effects, and that most likely, only one abnormal antibody to toxigenic mold antigen could have the most dominant adverse toxic exertion leading to the observed neuropsychological effects. Conclusion: It is concluded therefore, that chronic exposures to certain toxigenic molds might lead to neuropsychological manifestations and that although, it is acknowledged that the contaminations of the indoor environment by toxigenic molds are directly related to the adverse health effects on the occupants, there could be a situation where such relationship does not exist.

Specific IgE to indoor molds in patients with respiratory allergies

Rationale To evaluate the importance of sensitivity to molds in patients living in Caracas with persistent allergic rhinitis (PAR) and/or bronquial asthma (BA). Methods We evaluated 139 patients from the outpatient clinic of the Institute of Immunology, 6 to 55 years old, with PAR and/or BA, and positive questionnaire for molds exposures in their houses. A panel of inhalants and molds skin tests (Prick) were performed to all patients. Total serum IgE was measured and specific IgE to indoor molds was evaluated by RAST, basophil histamine release test (BHRT) and basophil activation test (BAT) in 10 patients with positive mold skin test. Results Thirty two patients were positive to at least one mold antigen (Prick), being the most frequents: Candida, Aspergillus, Rhizopus, Neurospora and Alternaria. The presence of damping was the most common inciting factor found in the questionnaire (p<0.0001). The group of patients aged 11 to 20 years old had the highest incidence of molds sensitivity (43.75%). All patients showed elevated total IgE levels (‘X=719.61 UI/ml). By RAST, most of the patients were positive for Alternaria (70%) and Neurospora (50%) with no significant correlation to Prick. To explore BHRT and BAT we used Aspergillus, Neurospora and Alternaria as antigens. Significant correlations between RAST and BAT (r=0.9063; p=0.0003), BHRT and BAT (r=0.9407; p=0.0016) and RAST and BHRT (r=0.96; p=0.01) were found only for Alternaria. Conclusions We suggest that in fungi mediated respiratory allergies, a careful questionnaire is critical. In addition, several IgE specific test should be performed for definitive diagnosis and establishment of therapeutics measures.

A novel model for equine recurrent airway obstruction

Equine recurrent airway obstruction (RAO; a term combining both chronic obstructive pulmonary disease (COPD) and summer pasture associated obstructive pulmonary disease (SPAOPD)) is one of the most common equine respiratory diseases with up to 50% of horses affected worldwide. The etiopathogenesis of RAO is unknown although pulmonary hypersensitivity to inhaled mold antigens may be involved. Recent work in our laboratory demonstrating elevated levels of IL-4 and IL-13 mRNA in the airways and peripheral blood of horses with RAO is consistent with an atopic component to RAO. Little is known regarding the earliest phases of RAO in horses. Here we describe the development of a novel airway model for equine RAO that utilizes ovalbumin-coated polystyrene beads for airway sensitization and challenge. Aerosol challenge of sensitized ponies with OVA-coated microbeads resulted in decreased airway compliance, increased percentage of lymphocytes and neutrophils in the bronchoalveolar lavage fluid, and evidence of a Th2 cytokine response in the bronchoalveolar cells. These results suggest that this approach may be useful in describing the initial stages of RAO development in the horse.