GAITHERSBURG, MD - February 22, 2016 - The Institute for In Vitro Sciences, Inc. (IIVS) has received a grant from the Research Institute for Fragrance Materials
In a previous study, we demonstrated that intravenous administration of adipose tissue stem cells (ASCs) could significantly reduce allergic symptoms and suppress eosinophilic inflammation. To evaluate the secretome of ASCs, we administrated culture supernatant of ASCs (ASC sup, which contains the ASC secretome) and uncultured fresh medium (con sup) into a mouse model of allergic airway inflammation. Subsequently we observed the mice for signs of inflammation and investigated Th1-, Th2-, and Treg-related cytokine levels as well as recruitment of Treg cells into the airway. We found that ASC sup could ameliorate allergic airway inflammation in this model; the value of airway hyperresponsiveness, and the occurrence of inflammatory cell infiltration in the lung, as well as the number of eosinophils, and goblet cells in the lung epithelium were all significantly decreased by ASC sup treatment. In addition, ASC sup treatment significantly decreased the levels of IL-4, IL-5, and IL-13 in the bronchial
Changes in the levels of transforming growth factor (TGF)-beta cytokines or receptors observed during the progression of several inflammatory and fibrotic disorders have been used to implicate these cytokines in the pathophysiology of these diseases. Although correlative, these studies were inconclusive because they were unable to demonstrate actual continuous TGF-beta-mediated signaling in the involved tissues. We reasoned that the phosphorylation state and subcellular localization of Smad2, the intracellular effector of TGF-beta/activin-mediated signaling, could be used as a marker of active signaling mediated by these cytokines in situ. We therefore used an experimental model of ovalbumin-induced allergic airway inflammation and were able to demonstrate a dramatic increase in the numbers of bronchial epithelial, alveolar, and infiltrating inflammatory cells expressing nuclear phosphorylated Smad2 within the allergen-challenged lungs. This was accompanied by strong upregulation of the activin ...
There are no reports of respiratory sensitization from C14-20 aliphatics (,2 % aromatics) in laboratory animals or humans. However, skin sensitization studies utilizing C9-14 aliphatics (,2 % aromatics) found no indication of skin sensitization in guinea pigs. Additional studies on C14-C20 aliphatics (,2% aromatics) in humans also found no indication of skin sensitization. With these observations, it is presumed that C14-20 aliphatics (,2% aromatics) will not be a respiratory sensitizing agents. ...
The Omega Fields blog offers you the best insights for horse & animal care. Visit now to read our post, Feeding Horses with Respiratory Allergies
Unfortunately, recently the diagnosis of bronchial asthma (and this problem is considered to be the most serious manifestation of respiratory allergy)...
Statement of the Problem: Bronchial asthma is more severe in females than in males after puberty because of stronger Th2- oriented immune response in females. ...
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TY - JOUR. T1 - Essential role of TNF receptor superfamily 25 (TNFRSF25) in the development of allergic lung inflammation. AU - Fang, Lei. AU - Adkins, Becky. AU - Deyev, Vadim. AU - Podack, Eckhard R.. PY - 2008/5/12. Y1 - 2008/5/12. N2 - We identify the tumor necrosis factor receptor superfamily 25 (TNFRSF25)/TNFSF15 pair as critical trigger for allergic lung inflammation, which is a cardinal feature of asthma. TNFRSF25 (TNFR25) signals are required to exert T helper cell 2 (Th2) effector function in Th2-polarized CD4 cells and co-stimulate interleukin (IL)-13 production by glycosphingolipid-activated NKT cells. In vivo, antibody blockade of TNFSF15 (TL1A), which is the ligand for TNFR25, inhibits lung inflammation and production of Th2 cytokines such as IL-13, even when administered days after airway antigen exposure. Similarly, blockade of TNFR25 by a dominant-negative (DN) transgene, DN TNFR25, confers resistance to lung inflammation in mice. Allergic lung inflammation - resistant, ...
The integrin CD103 is the αE chain of integrin αEβ7 that is important in the maintenance of intraepithelial lymphocytes and recruitment of T cells and dendritic cells (DC) to mucosal surfaces. The role of CD103 in intestinal immune homeostasis has been well described, however, its role in allergic airway inflammation is less well understood. In this study, we used an ovalbumin (OVA)-induced, CD103-knockout (KO) BALB/c mouse model of experimental allergic airways disease (EAAD) to investigate the role of CD103 in disease expression, CD4+ T-cell activation and DC activation and function in airways and lymph nodes. We found reduced airways hyper-responsiveness and eosinophil recruitment to airways after aerosol challenge of CD103 KO compared to wild-type (WT) mice, although CD103 KO mice showed enhanced serum OVA-specific IgE levels. Following aerosol challenge, total numbers of effector and regulatory CD4+ T-cell subsets were significantly increased in the airways of WT but not CD103 KO mice, ...
The Brown Norway (BN) rat model for respiratory sensitisation has used both dermal and inhalation routes for induction. The elicitation phase was typically four inhalation exposures, spaced at approximately 15-day intervals. After the last challenge the measurements made included: respiratory responses using whole body plethysmography, analysis of inflammatory endpoints using lung lavage fluid and IgE levels in lung lavage fluid or serum. Lung and lymph node weights were measured post mortem and the respiratory tract was used for histopathological investigations. Controls did not receive the induction treatment but were challenged by inhalation as for the test groups, to control for short term irritation effects. On occasion respiratory methacholine challenge was performed the day following MDI challenge to test for non-specific respiratory hyperreactivity. The test material in these studies was polymeric MDI. Both inhalation and dermal routes of induction were investigated in a study in BN ...
commonly used for some types of disposable surgical gloves) can also give rise to skin or respiratory sensitisation (see Section 8.4). Further information on Health Surveillance available can be obtained from Occupational Health.. For some work activities there may be standard procedures to ensure safe working with the chemical. On the other hand there could be situations where each chemical reaction or process requires a unique assessment which should be recorded permanently. In most cases this record should be written into the experimental notebook adjacent to the details of the process undertaken. The School or Departmental arrangements for your work area should be consulted as to which course of action is needed.. For the hazards associated with particular substances refer to the manufacturers hazards data sheets or consult a reference book. "Dangerous Properties of Industrial Materials" by N.I. Sax, "The Registry of Toxic Effects of Chemical Substances" by R.J. Lewis, "Hazards in the ...
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TY - JOUR. T1 - Novel immunomodulatory oligonucleotides prevent development of allergic airway inflammation and airway hyperresponsiveness in asthma. AU - Agrawal, Devendra K.. AU - Edwan, Jehad. AU - Kandimalla, Ekambar R.. AU - Yu, Dong. AU - Bhagat, Lakshmi. AU - Wang, Daqing. AU - Agrawal, Sudhir. PY - 2004/1. Y1 - 2004/1. N2 - Oligodeoxynucleotides containing unmethylated CpG motifs (CpG oligos) have been shown to prevent development of allergic airway inflammation and airway hyperresponsiveness (AHR) in mouse models of asthma. Recently, we reported immunomodulatory oligonucleotides (IMOs) containing novel structures (immunomers) and synthetic immunostimulatory CpR (R=2′-deoxy-7- deazguanosine) motifs show potent stimulatory activity with distinct cytokine secretion profiles. Since type 2 T cells predominate in asthma and increase in type 1 cells can prevent the differentiation of naïve T lymphocytes to a type 2 phenotype, we hypothesized that IMOs can prevent the development of allergic ...
From MSDS EYE: May cause moderate eye irritation. May cause very slight transient (temporary) corneal injury. SKIN: Prolonged or repeated exposure may cause slight skin irritation. May cause allergic skin reaction in susceptible individuals. Animal studies have shown that skin contact with isocyanates may play a role in respiratory sensitization. May stain skin. A single prolonged exposure is not likely to result in the material being absorbed in harmful amounts. INGESTION: Single dose oral toxicity is considered to be low. No hazards anticipated from swallowing small amounts incidental to normal handling operations. INHALATION: At room temperature, PMDI vapors are minimal due to low vapor pressure. However, certain operations may generate vapor or aerosol concentrations sufficient to cause irritation or other adverse effects. Excessive exposure may cause irritation to upper respiratory tract and lungs, and pulmonary edema (fluid in the lungs). May cause respiratory sensitization in susceptible ...
From MSDS EYE: May cause moderate eye irritation. May cause very slight transient (temporary) corneal injury. SKIN: Prolonged or repeated exposure may cause slight skin irritation. May cause allergic skin reaction in susceptible individuals. Animal studies have shown that skin contact with isocyanates may play a role in respiratory sensitization. May stain skin. A single prolonged exposure is not likely to result in the material being absorbed in harmful amounts. INGESTION: Single dose oral toxicity is considered to be low. No hazards anticipated from swallowing small amounts incidental to normal handling operations. INHALATION: At room temperature, PMDI vapors are minimal due to low vapor pressure. However, certain operations may generate vapor or aerosol concentrations sufficient to cause irritation or other adverse effects. Excessive exposure may cause irritation to upper respiratory tract and lungs, and pulmonary edema (fluid in the lungs). May cause respiratory sensitization in susceptible ...
To study the role of CD8+ T cells in allergic sensitization, we examined the effects of in vivo depletion of CD8+ T cells prior to sensitization on IgE production, immediate type cutaneous hypersensitivity and development of altered airway responsiveness. BALB/c mice were thymectomized and treated with anti-CD8 antibody resulting in depletion of CD8+ T cells (,1%) in spleen and lymphoid tissues. In these mice, sensitization to ovalbumin (OVA) via the airways still resulted in IgE anti-OVA responses and immediate cutaneous reactions to OVA, but the animals were unable to develop airway hyperresponsiveness, eosinophil infiltration of the lung parenchyma, or IL-5 production in the local lymph nodes of the airway. Transfer of CD8+ T cells from naive animals during sensitization (on day 8 of the 10-d protocol) fully restored the ability to develop airway hyperresponsiveness and this was accompanied by IL-5 production and eosinophil accumulation in the lung. These data indicate a critical role for ...
In the present study, we demonstrate that lung macrophages rather than Th17 or other types of immune cells are the main producer of IL-17 in the OVA-induced allergic inflammation in the lung. Moreover, it is alveolar macrophages rather than interstitial macrophages that are the main source of IL-17 in this situation. Either depleting alveolar macrophages or neutralizing IL-17 in lung effectively inhibits OVA-induced allergic inflammation related to asthma, which is consistent with previous reports on the role of IL-17 in OVA-induced airway hypersensitivity response (12).. Enhanced macrophage recruitment during asthmatic process may result in the accumulation of tissue macrophages, which are activated by Th2 cytokines, leading to Th2 polarized reaction and inflammation (32, 33). Thus, the recruited lung macrophages have the potential to promote asthmatic development. However, the inconsistent results have been obtained from different studies. Several reports suggest that macrophages are crucial ...
An integrated investigative team of environmental and biomedical scientists from Michigan State University (MSU) and the Southern California Particle Center and Supersite (SCPCS) will conduct atmospheric and toxicologic research at three sites in the Los Angeles Basin (LAB), each of which have distinct air-pollution profiles. One designated site in the LAB contains locally generated PM and gaseous co-pollutants (source emission site). Another site contains transported PM and gaseous co-pollutants (receptor site). The third site is geographically located between the source and the receptor sites. The team will use a recently built, state-of-the-art mobile air research laboratory (AirCARE 1), parked at the LAB sites, to conduct inhalation toxicology studies exposing laboratory rodents with and without pre-existing allergic airway disease (animal model of human asthma) to concentrated PM (CAPs) from the local environment. Brown Norway (BN) rats with and without allergic airway disease will be ...
Particulate matter (PM), a component of air pollution, has been shown to enhance allergen-mediated airway hypersensitivity and inflammation. Surprisingly, exposure to PM during the sensitization to allergen is sufficient to produce immunological changes that result in heightened inflammatory effects upon future allergen exposures (challenge) in the absence of PM. This suggests that PM has the ability to modulate the allergic immune response, thereby acting as an adjuvant by enhancing the immunological memory formed during the adaptive immune response; however, the mechanisms through which this occurs remain elusive. Establishing a reproducible animal model to study the PM-mediated immunotoxicological effects that enhance allergy, may provide insights to understand how air pollution activates the immune system and thereby modulates the pathophysiology of asthma. The basic protocol can be used to study various characteristics of air pollution, such as PM size, source, or chemical composition, to ...
This study examines the role of interleukin 23 (IL-23) in airway inflammation in asthma, focusing on the ability of IL-23 to promote inflammation independently of the known IL-17 pathway and via its effect on T helper 2 (Th2) polarisation. These interactions are studied using in vitro and in vivo techniques.. Mice exposed to allergen showed a significant increase in IL-23-specific p19 mRNA and IL-23 receptor mRNA. In mice induced to overexpress IL-23, an increased inflammatory cell infiltrate was observed after allergen challenge. In IL-23 knockout mice, exposure to the same allergen challenge resulted in a significant reduction in airway inflammation.. Having established a role for IL-23 in airway inflammation the authors next examined its signalling pathway. No significant alteration in IL-17 expression was seen between the IL-23 knockout and IL-23-expressing mice, thus suggesting a possible pathway independent of IL-17. In contrast, the levels of Th2 cytokines (IL-4, IL-5 and IL-13) were seen ...
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TY - JOUR. T1 - Airway hyperresponsiveness. T2 - From molecules to bedside. AU - Sieck, Gary C. PY - 2003/7/1. Y1 - 2003/7/1. UR - http://www.scopus.com/inward/record.url?scp=0038309533&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0038309533&partnerID=8YFLogxK. M3 - Article. C2 - 12794089. AN - SCOPUS:0038309533. VL - 95. SP - 1. EP - 2. JO - Journal of Applied Physiology. JF - Journal of Applied Physiology. SN - 8750-7587. IS - 1. ER - ...
The overall goal of this laboratory over the past 20 years has been the elucidation of mechanisms regulating allergic inflammation and thereby identification of...
Dr Omi Narayan, Consultant Respiratory Paediatrician, FRCPCH, MSc (Respiratory & Allergy), MBBS at Spire Healthcare. Learn more about this consultant here.
With the increase in production and use of engineered nanoparticles (NP; ≤ 100 nm), safety concerns have risen about the potential health effects of occupational or environmental NP exposure. Results of animal toxicology studies suggest that inhalation of NP may cause pulmonary injury with subsequent acute or chronic inflammation. People with chronic respiratory diseases like asthma or allergic rhinitis may be even more susceptible to toxic effects of inhaled NP. Few studies, however, have investigated adverse effects of inhaled NP that may enhance the development of allergic airway disease. We investigated the potential of polyethylene glycol coated amorphous silica NP (SNP; 90 nm diameter) to promote allergic airway disease when co-exposed during sensitization with an allergen. BALB/c mice were sensitized by intranasal instillation with 0.02% ovalbumin (OVA; allergen) or saline (control), and co-exposed to 0, 10, 100, or 400 μg of SNP. OVA-sensitized mice were then challenged intranasally with 0.5%
The NF-κB/Rel family of transcription factors regulates the expression of multiple genes that have been implicated in immune and inflammatory responses, including asthma (8, 16). Analyzing the effects of germline deletions or mutations of specific NF-κB/Rel subunits will elucidate their roles in various inflammatory diseases, including asthma. The present study demonstrates that absence of c-Rel is associated not only with significant attenuation of allergen-induced pulmonary and BAL eosinophilia but also with inhibition of total IgE and the physiological correlate of allergic airway inflammation, AHR. p50−/− mice do not develop eosinophilic airway inflammation in response to allergen sensitization and challenge, concomitant with a lack of IL-5 and eotaxin production; total serum IgE and AHR were not examined (27). The phenotype and immune system defects of c-Rel−/− mice are distinct from those of p50−/− mice (23, 24).. One explanation for the blunted response of c-Rel−/− mice ...
Epithelial mast cells are generally present in the airways of patients with allergic asthma that are inadequately controlled. Airway mast cells (MCs) are critically involved in allergic airway inflammation and contribute directly to the main symptoms of allergic patients. Phosphodiesterase 3 (PDE3) tailors signaling of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), which are critical intracellular second messenger molecules in various signaling pathways. This paper investigates the pathophysiological role and disease-modifying effects of PDE3 in mouse bone marrow-derived MCs (bmMCs), human LAD2- and HMC1 mast cell lines, human blood basophils, and peripheral blood-derived primary human MCs (HuMCs). In a chronic house dust mite (HDM)-driven allergic airway inflammation mouse model, we observed that PDE3 deficiency or PDE3 inhibition (PDE3i) therapy reduced the numbers of epithelial MCs, when compared to control mice. Mouse bone marrow-derived MCs (bmMCs) and the ...
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Asian sand dust (ASD) containing microbiological materials, sulfate (SO42), and nitrate (NO3−) derived from air pollutants in East China, reportedly cause adverse respiratory health effects. ASD aggra
Principal Investigator:OBOKI Keisuke, Project Period (FY):2010 - 2011, Research Category:Grant-in-Aid for Young Scientists (B), Research Field:膠原病・アレルギー・感染症内科学
The human body is the most complex machine that works in seamless synchronicity to ensure optimum health. The body constantly battles against various germs and disease-causing microbes involuntarily which we dont even realize. The white blood cells work as the czar that protects the body from the attacks of the unknowns.. Eosinophils. Among the different types of WBC, Eosinophils are responsible for destroying foreign substances and regulating inflammation. They fight substances related to parasitic infection that has been flagged for destruction by your immune system.. Eosinophilia. Eosinophilia is a condition in which a large number of eosinophils are recruited to a specific site in the body or when the bone marrow produces too many eosinophils. The root cause of this condition may vary from some mere infection to fatal disease like cancer.. Treatment of eosinophils is very crucial as it might lead to severe conditions if left untreated. However, the synthetic medicines used to address the ...
Critical role for IL-13 in the development of allergen-induced airway hyperreactivity.: Airway hyperresponsiveness to a variety of specific and nonspecific stim
Trends of air pollutant concentrations that influence the incidence of respiratory diseases and might be influential for respiratory hypersensitivity are presented and discussed. Data for these trends are collected in UNEP/WHO s Global Environmental Monitoring System GEMS/Air which recently has been revitalized and redirected to become a tool...
Asthma is a chronic disease of the airways characterized by airway hyperresponsiveness, airway inflammation, and airway remodeling. Eosinophils migrate to the airways and play a significant role in the pathogenesis of ...
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TY - JOUR. T1 - Requirement for neuropeptide Y in the development of type 2 responses and allergen-induced airway hyperresponsiveness and inflammation. AU - Oda, Naohiro. AU - Miyahara, X. Nobuaki. AU - Taniguchi, Akihiko. AU - Morichika, Daisuke. AU - Senoo, Satoru. AU - Fujii, Utako. AU - Itano, Junko. AU - Gion, Yuka. AU - Kiura, Katsuyuki. AU - Kanehiro, Arihiko. AU - Maeda, Yoshinobu. PY - 2019/3. Y1 - 2019/3. N2 - Neuro-peptide Y (NPY) is a neurotransmitter that is widely expressed in the brain and peripheral nervous system. Various immune cells express the NPY Y 1 receptor. NPY modulates these cells via its Y 1 receptor; however, involvement of NPY in the pathophysiology of bronchial asthma, particularly airway hyperresponsiveness (AHR), has not been defined. NPY-deficient and wild-type mice were intranasally sensitized and challenged to house dust mite (HDM) extract, and airway responses were monitored. After sensitization and challenge, NPY-deficient mice showed significantly lower AHR ...
Allergic airway inflammation is a complex disease, and multiple immune and nonimmune contribute to development and progression. Here, using a house dust mite-induced mouse model of allergic inflammation, Patel et al. report that depletion of neutrophils worsens airway inflammation. Neutrophil depletion, as expected, led to enhanced myelopoiesis that was driven by granulocyte colony-stimulating factor (G-CSF). By carrying out experiments to understand how neutrophil depletion and systemic increase in G-CSF levels drive airway inflammation, the authors have uncovered a previously unsuspected link between G-CSF and type 2 innate lymphoid cells (ILC2s). They report that G-CSF acts directly on both human and mouse ILC2s to promote production of TH2 cytokines interleukin-5 (IL-5) and IL-13. ...
Lin, J.T., Hiroshi, I., Suzuki, T., et al. (1994) Eosinophilic Airway Inflammation and Airway Hyperresponsiveness. Chinese Journal of Tuberculosis and Respiratory Diseases, 17, 213-215.
OBJECTIVES: To study the role of exposure, atopy, and smoking in the development of laboratory animal allergy (LAA) in a retrospective cohort study. METHODS: Between 1977 and 1993, 225 people received a pre-employment screening when they started a job at a Dutch research institute where they were going to work with laboratory animals. After active follow up 136 of them (60.4%) could be traced and were sent a questionnaire with extensive questions on allergic symptoms, smoking habits, and job history. 122 people (89.7%) sent back a completed questionnaire. Those who were accepted for a job at the institute and did not have allergic symptoms at the start of the job were selected as cohort members. After selecting people with complete data on start and end date of jobs, exposure intensity, atopy, and smoking, the cohort consisted of 99 people with an average time of follow up of 9.7 years. LAA was defined as a positive response to a set of questions in the questionnaire. The mean number of hours a ...
Allergic respiratory disease tends to occur in older horses and we dont tend to see chronic respiratory diseases like RAO and SPAOPD (Summer Pasture Associated Obstructive Pulmonary Disease - essentially like RAO but horses are better inside as they develop allergy to primarily outdoor allergens such as pollen) developing until 6-7 years of age. With allergic respiratory disease this can be a risk all year round. More time in the stable in Winter and increased hay intake can increase exposure to moulds, forage mites and bacterial endotoxin - all potent respiratory allergens and especially for horses with RAO (horses with RAO are better out than stabled - opposite to SPAOPD affected horses). During Spring, Summer and Autumn even when out horses can be susceptible to exposure to pollen and moulds. Again, older horses with RAO in particular can be worse at certain times of the year when turned out as they may be sensitive to both moulds and pollens ...
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The early life period represents a time of immunological plasticity whereby the functionality immature immune system is highly susceptible to environmental stimulation. Perennial aeroallergen and respiratory viral infection induced sporadic episodes of lung inflammation during this temporal window represent major risk factors for initiation of allergic asthmatic disease. Murine models are widely used as an investigative tool to examine the pathophysiology of allergic asthma; however, models in current usage typically do not encapsulate the early life period which represents the time of maximal risk for disease inception in humans. To address this issue, this protocol adapted an experimental animal model of disease for sensitization to ovalbumin during the immediate post-weaning period beginning at 21 days of age. By initially sensitizing mice during this early life post-weaning period, researchers can more closely align experimental allergic. ...
The AusPollen Australian Pollen Allergen Partnership will establish the inaugural national pollen monitoring program in eight Australian state and territory capital cities. Innovative molecular and immunological techniques will be applied to assess the grass pollen source and allergen content. Total and grass pollen counts will be forecast to help patients manage their exposure to triggers of hay fever and asthma. Access to this information has potential to reduce the social, medical and financial burden of allergic respiratory disease.
Severe, steroid-resistant asthma is clinically and economically important since affected individuals do not respond to mainstay corticosteroid treatments for asthma. Patients with this disease experience more frequent exacerbations of asthma, are more likely to be hospitalized, and have a poorer qua …
What is feline asthma?. Feline asthma is a common cause of lower airway disease with signs beginning in young to middle age cats. The disease is triggered by breathing in environmental particles that trigger an allergic reaction. Once these allergens are inhaled, they are recognized by the immune system and inflammation begins. Inflammatory cells are recruited to the airway and produce chemicals that make the inflammation even worse. This vicious cycle leads to more and more inflammation. With more inflammation comes more disease. This excessive inflammatory response leads to narrowing of the airway, allergic airway inflammation, and eventually to structural changes to the airways themselves, all of which are hallmark findings in patients with asthma.. What do cats with asthma look like?. The most likely symptom that you will notice if your cat develops asthma is a cough. It may also have an increased breathing rate or difficulty breathing. The severity of signs is highly variable between pets, ...
November 2014. Attenuation of allergic airways inflammation by an extract of Hymenocardia acida Tracheal hyperresponsiveness, airway mucus production and bronchoalveolar inflammation are the major components of asthma. Here, we aim to investigate the role in the control of asthma of a bioactive plant extracted from Hymenocardia acida in a physiological and pathophysiological model. The effect of H. acida crude extract (HACE) on total cellular components of bronchoalveolar (BAL) fluids was performed on ovalbumin.... Author(s): Fatou Bintou Sar, Mamadou Sarr, Mama S.Y. Diallo, Saliou Ngom, Lamine Gueye, Abdoulaye Samb, Ramaroson Andriantsitohaina and Annelise Lobstein ...
Affecting mostly older horses, heaves arises when lung cells react to allergens by swelling & thickening air passage linings and increasing mucus secretions
An important advance in our understanding of the pathophysiology of asthma has been the discovery that airway inflammation is not confined to severe asthma but also characterizes mild and moderate asthma. Inflammation in asthma may be the result of a