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Journal articles on the topic 'Airway inflammation'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Finsnes, Finn, Torstein Lyberg, Geir Christensen, and Ole H. Skjønsberg. "Effect of endothelin antagonism on the production of cytokines in eosinophilic airway inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 4 (2001): L659—L665. http://dx.doi.org/10.1152/ajplung.2001.280.4.l659.

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Endothelin (ET)-1 has been launched as an important mediator in bronchial asthma, which is an eosinophilic airway inflammation. However, the interplay between ET-1 and other proinflammatory mediators during the development of airway inflammation has not been elucidated. We wanted to study 1) whether the production of ET-1 precedes the production of other proinflammatory mediators and 2) whether ET-1 stimulates the production of these mediators within the airways. These hypotheses were studied during the development of an eosinophilic airway inflammation in rats. The increase in ET-1 mRNA level

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Boulet, Louis-Philippe, Jamila Chakir, Jean Dubé, Catherine Laprise, Michel Boutet, and Michel Laviolette. "Airway Inflammation and Structural Changes in Airway Hyper-Responsiveness and Asthma: An Overview." Canadian Respiratory Journal 5, no. 1 (1998): 16–21. http://dx.doi.org/10.1155/1998/926439.

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Asthma treatment has moved from bronchodilator therapy to an emphasis on anti-inflammatory therapy. Airway inflammation is believed to induce airway hyper-responsiveness (AHR) through the release of mediators that increase the airway response to agonists. However, the exact contribution of airway inflammation in the physiology of airway hyper-responsiveness remains undefined. Structural modifications in airways resulting from inflammation may contribute to the development and persistence of AHR and the development of asthma. This paper reviews some of the main components of airway inflammation

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3

O'Byrne, Paul M. "Airway Inflammation and the Pathogenesis of Asthma." Canadian Respiratory Journal 1, no. 3 (1994): 189–95. http://dx.doi.org/10.1155/1994/767528.

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Airway inflammation has been recognized for more than l00 years to be present in the airways of patients with severe asthma. Much more recently, airway intlammation has been identified to be central to the pathogenesis of all asthma. The inflammation is of a characteristic type, with the presence of activated eosinophils, mast cells and lymphocytes in bronchoalveolar lavage fluid and airway biopsies from patients with even mild asthma. Stimuli that are known to worsen asthma, such as inhaled allergens, also increase the numbers of mast cells and cosinophils in asthmatic airways. In addition, t

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Zimmermann, Nives, Marc Rothenberg, and Leah Kottyan. "IL-13 is required and sufficient for airway acidification in allergic airway inflammation (141.16)." Journal of Immunology 184, no. 1_Supplement (2010): 141.16. http://dx.doi.org/10.4049/jimmunol.184.supp.141.16.

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Abstract Clinical studies have shown acidification of airways in asthma. Importantly, studies have suggested that acidification contributes to the pathophysiological process. However, the mechanism of acidification is unclear. We developed a novel method for measuring the acidity of mouse airways and demonstrated that mouse airways are acidified during models of allergic airway inflammation. Our studies determined that airway acidification does not develop in IL-13-deficient mice and that IL-13 delivery alone is sufficient to induce airway acidification. There are multiple ways IL-13 could lea

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Takahashi, Kentaro, Koichi Hirose, Saki Kawashima, et al. "IL-22 attenuates IL-25 production by lung epithelial cells and inhibits antigen-induced eosinophilic airway inflammation (59.8)." Journal of Immunology 188, no. 1_Supplement (2012): 59.8. http://dx.doi.org/10.4049/jimmunol.188.supp.59.8.

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Abstract BACKGROUND: IL-22 functions as both a proinflammatory and an anti-inflammatory cytokine in various inflammations. However, the roles of IL-22 in the allergic airway inflammation are still largely unknown. OBJECTIVE: We sought to determine whether IL-22 is involved in the regulation of allergic airway inflammation. METHODS: We examined IL-22 production and its cellular source at the site of antigen-induced airway inflammation in mice. We also examined the effect of IL-22 neutralization, as well as IL-22 administration. We finally examined the effect of IL-22 on IL-25 production from a

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6

Shelhamer, James H. "Airway Inflammation." Annals of Internal Medicine 123, no. 4 (1995): 288. http://dx.doi.org/10.7326/0003-4819-123-4-199508150-00008.

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7

Royce, Simon G., Anna M. Tominaga, Matthew Shen, et al. "Serelaxin improves the therapeutic efficacy of RXFP1-expressing human amnion epithelial cells in experimental allergic airway disease." Clinical Science 130, no. 23 (2016): 2151–65. http://dx.doi.org/10.1042/cs20160328.

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We have identified combination cell-based therapies that effectively treat the airway inflammation and airway remodelling (structural changes) that contribute to airway obstruction and related airway hyperresponsiveness in murine chronic allergic airways.

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8

Leff, A. R., K. J. Hamann, and C. D. Wegner. "Inflammation and cell-cell interactions in airway hyperresponsiveness." American Journal of Physiology-Lung Cellular and Molecular Physiology 260, no. 4 (1991): L189—L206. http://dx.doi.org/10.1152/ajplung.1991.260.4.l189.

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Airway hyperresponsiveness results from the conversion of normally reactive airways to a state of augmented responsiveness to constrictor stimuli. Although the mechanism accounting for the induction of airway hyperresponsiveness remains elusive, recent investigations have suggested that inflammation may be a sine qua non for human asthma. Numerous experimental models have demonstrated the necessity of circulating granulocytes as mediators of augmented bronchoconstriction during immune challenge. It is not known how granulocytes are targeted for selective migration to the conducting airways of

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9

O’Byrne, Paul M. "Airway Inflammation and Airway Hyperresponsiveness." Chest 90, no. 4 (1986): 575–77. http://dx.doi.org/10.1378/chest.90.4.575.

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10

Kolahian, Saeed, and Reinoud Gosens. "Cholinergic Regulation of Airway Inflammation and Remodelling." Journal of Allergy 2012 (January 16, 2012): 1–9. http://dx.doi.org/10.1155/2012/681258.

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Acetylcholine is the predominant parasympathetic neurotransmitter in the airways that regulates bronchoconstriction and mucus secretion. Recent findings suggest that acetylcholine regulates additional functions in the airways, including inflammation and remodelling during inflammatory airway diseases. Moreover, it has become apparent that acetylcholine is synthesized by nonneuronal cells and tissues, including inflammatory cells and structural cells. In this paper, we will discuss the regulatory role of acetylcholine in inflammation and remodelling in which we will focus on the role of the air

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11

Shevchenko, M. A., D. E. Murova, and E. A. Servuli. "Spatial characteristics of neutrophils and eosinophils in conducting airway mucosa of mice with induced allergic airway inflammation." Medical Immunology (Russia) 25, no. 3 (2023): 625–30. http://dx.doi.org/10.15789/1563-0625-sco-2830.

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Daily inhaled antigens induce cellular immune response in the airways. In case of allergens, allergic airway inflammation is usually represented by eosinophils, however, neutrophil infiltration is also observed during severe asthma. Animal models contribute to investigation of the mechanisms that involve the switching to eosinophil- or neutrophil-mediated inflammation. Data about the spatial location of eosinophils and neutrophils in the airways are necessary for both the understanding of allergic airway inflammation mechanisms and the drag potential estimation, however, not completely investi

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12

Kanda, Akira, Yoshiki Kobayashi, Mikiya Asako, Koichi Tomoda, Hideyuki Kawauchi, and Hiroshi Iwai. "Regulation of Interaction between the Upper and Lower Airways in United Airway Disease." Medical Sciences 7, no. 2 (2019): 27. http://dx.doi.org/10.3390/medsci7020027.

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The concept of united airway disease comprises allergic rhinitis (AR) with asthma, and eosinophilic chronic rhinosinusitis (ECRS) with asthma. It embodies a comprehensive approach to the treatment of upper and lower airway inflammation. The treatment of upper airway inflammation reduces asthma symptoms and decreases the dose of inhaled corticosteroids (ICS) necessary to treat asthma. However, little is known about the mechanisms of interaction between upper and lower airway inflammation. Here we review these mechanisms, focusing on neural modulation and introduce a novel therapeutic approach t

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Lindley, Alexa R., Margaret Crapster-Pregont, Yanjun Liu та Douglas A. Kuperman. "12/15-Lipoxygenase Is an Interleukin-13 and Interferon-γCounterregulated-Mediator of Allergic Airway Inflammation". Mediators of Inflammation 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/727305.

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Interleukin-13 and interferon-γare important effectors of T-helper cells. Interleukin-13 increases expression of the arachidonic acid-metabolizing enzyme, 15-lipoxygenase-1, in a variety of cell types. 15-lipoxygenase-1 is dramatically elevated in the airways of subjects with asthma. Studies in animals indicate that 15-lipoxygenase-1 contributes to the development of allergic airway inflammation but is protective in some other forms of inflammation. We tested the hypothesis that the ability of interleukin-13 and interferon-γto counterregulate allergic airway inflammation was potentially mediat

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14

Singh, Brenal, Wen Lu, Amanda Schmidt-Paustian, and Taku Kambayashi. "The loss of DGK protects against allergic airway inflammation and airway hyperresponsiveness." Journal of Immunology 200, no. 1_Supplement (2018): 44.32. http://dx.doi.org/10.4049/jimmunol.200.supp.44.32.

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Abstract Asthma is a chronic allergic inflammatory airway disease that is caused by aberrant immune responses to inhaled allergens, which leads to airflow obstruction driven in part by increased sensitivity of airway smooth muscle to contractile agonists, a process known as airway hyperresponsiveness (AHR). The inflammation of allergic asthma is driven by type 2 cytokines released by Th2 CD4+ T cells and group 2 innate lymphoid cells (ILC2) in the lung. Here, we report that targeting DAG kinase zeta (DGKζ), a negative regulator of DAG-mediated cell signaling, protects against allergic asthma.

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15

Shapiro, Gail G. "Childhood Asthma: Update." Pediatrics In Review 13, no. 11 (1992): 403–12. http://dx.doi.org/10.1542/pir.13.11.403.

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Definition and Pathophysiology Asthma is a reversible airways disease characterized by both smooth muscle hyperreactivity and airway inflammation. During the 1970s and early 1980s the focus was on smooth muscle constriction, and it was believed that better bronchodilators would greatly diminish our difficulties in controlling this condition. This, unfortunately, was not the case. The emphasis of therapy today has turned to airway inflammation. Lung biopsies from patients who have asthma show destruction of respiratory epithelium, basement membrane thickening, and inflammatory cellular infiltra

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16

Dakhama, Azzeddine, Jung-Won Park, Christian Taube, et al. "Alteration of airway neuropeptide expression and development of airway hyperresponsiveness following respiratory syncytial virus infection." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 4 (2005): L761—L770. http://dx.doi.org/10.1152/ajplung.00143.2004.

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The mechanisms by which respiratory syncytial virus (RSV) infection causes airway hyperresponsiveness (AHR) are not fully established. We hypothesized that RSV infection may alter the expression of airway sensory neuropeptides, thereby contributing to the development of altered airway function. BALB/c mice were infected with RSV followed by assessment of airway function, inflammation, and sensory neuropeptide expression. After RSV infection, mice developed significant airway inflammation associated with increased airway resistance to inhaled methacholine and increased tracheal smooth muscle re

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17

Gochuico, Bernadette R., Kathleen M. Miranda, Edith M. Hessel, et al. "Airway epithelial Fas ligand expression: potential role in modulating bronchial inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 274, no. 3 (1998): L444—L449. http://dx.doi.org/10.1152/ajplung.1998.274.3.l444.

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Epithelium-derived Fas ligand is believed to modulate inflammation within various tissues. In this paper, we report findings that suggest a similar immunoregulatory role for Fas ligand in the lung. First, Fas ligand was localized to nonciliated, cuboidal airway epithelial cells (Clara cells) throughout the airways in the normal murine lung by employing nonisotopic in situ hybridization and immunohistochemistry. Second, gldmutant mice, which express a dysfunctional Fas ligand protein, were noted to develop prominent infiltration of inflammatory cells in submucosal and peribronchial regions of t

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18

Bozkurt, Turgut Emrah. "Endocannabinoid System in the Airways." Molecules 24, no. 24 (2019): 4626. http://dx.doi.org/10.3390/molecules24244626.

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Cannabinoids and the mammalian endocannabinoid system is an important research area of interest and attracted many researchers because of their widespread biological effects. The significant immune-modulatory role of cannabinoids has suggested their therapeutic use in several inflammatory conditions. Airways are prone to environmental irritants and stimulants, and increased inflammation is an important process in most of the respiratory diseases. Therefore, the main strategies for treating airway diseases are suppression of inflammation and producing bronchodilation. The ability of cannabinoid

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19

Chiba, Yoshihiko, Takashi Kusakabe, and Shioko Kimura. "Decreased expression of uteroglobin-related protein 1 in inflamed mouse airways is mediated by IL-9." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 6 (2004): L1193—L1198. http://dx.doi.org/10.1152/ajplung.00263.2004.

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Uteroglobin-related protein 1 (UGRP1) is a secretory protein, highly expressed in epithelial cells of airways. Although an involvement of UGRP1 in the pathogenesis of asthma has been suggested, its function in airways remains unclear. In the present study, a relationship between airway inflammation, UGRP1 expression, and interleukin-9 (IL-9), an asthma candidate gene, was evaluated by using a murine model of allergic bronchial asthma. A severe airway inflammation accompanied by airway eosinophilia and elevation of IL-9 in bronchoalveolar lavage (BAL) fluids was observed after ovalbumin (OVA) c

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20

Ruiz, Beatriz León, and Andre Ballesteros Tato. "Age difference in the immune response to endotoxin (LPS) shapes Th2-mediated airway inflammation and development of asthma." Journal of Immunology 198, no. 1_Supplement (2017): 220.9. http://dx.doi.org/10.4049/jimmunol.198.supp.220.9.

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Abstract In addition to genetic factors, environmental exposures is also of primary importance for the development of asthma/allergy disorders in children, as demonstrated by epidemiological data showing children growing up in traditional farms seem to develop asthma less often than children growing up in urban areas. According to the hygiene hypothesis, this is due to increased exposure to endotoxin (LPS) and other farm-related microorganism-derived compounds. However little is known about how early-life contact to microbial compounds influence the development of asthma. Here we show that hou

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21

Gundel, R. H., C. D. Wegner, H. O. Heuer, and L. G. Letts. "A PAF receptor antagonist inhibits acute airway inflammation and late-phase responses but not chronic airway inflammation and hyperresponsiveness in a primate model of asthma." Mediators of Inflammation 1, no. 6 (1992): 379–84. http://dx.doi.org/10.1155/s0962935192000577.

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We have examined the effects of a PAF receptor antagonist, WEB 2170, on several indices of acute and chronic airway inflammation and associated changes in lung function in a primate model of allergic asthma. A single oral administration WEB 2170 provided dose related inhibition of the release of leukotriene C4(LTC4) and prostaglandin D2(PGD2) recovered and quantified in bronchoalveolar lavage (BAL) fluid obtained during the acute phase response to inhaled antigen. In addition, oral WEB 2170 treatment in dual responder primates blocked the acute influx of neutrophils into the airways as well as

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22

Dolovich, J., and F. E. Hargreave. "Airway Mucosal Inflammation." Journal of Asthma 29, no. 3 (1992): 145–49. http://dx.doi.org/10.3109/02770909209099022.

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23

Kalla, Ismail S. "Measuring Airway Inflammation." Clinical Pulmonary Medicine 22, no. 2 (2015): 53–61. http://dx.doi.org/10.1097/cpm.0000000000000081.

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24

Taylor, D. R., and D. C. Cowan. "Assessing airway inflammation." Thorax 65, no. 12 (2010): 1031–32. http://dx.doi.org/10.1136/thx.2009.132985.

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25

Sexton, D. W., and G. M. Walsh. "Airway inflammation resolution." Clinical Experimental Allergy 35, no. 7 (2005): 838–40. http://dx.doi.org/10.1111/j.1365-2222.2005.02282.x.

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26

Balter, Meyer S. "Treating airway inflammation." Asthma Magazine 1, no. 5 (1996): 24–26. http://dx.doi.org/10.1016/s1088-0712(96)80011-2.

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27

Marianne, Frieri. "Human Airway Inflammation." Annals of Allergy, Asthma & Immunology 88, no. 3 (2002): 343. http://dx.doi.org/10.1016/s1081-1206(10)62020-0.

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28

Agrawal, Devendra K., and Arpita Bharadwaj. "Allergic airway inflammation." Current Allergy and Asthma Reports 5, no. 2 (2005): 142–48. http://dx.doi.org/10.1007/s11882-005-0088-7.

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29

Hargreave, Frederick E., Peter G. Gibson, and E. Helen Ramsdale. "Airway Hyperresponsiveness, Airway Inflammation, and Asthma." Immunology and Allergy Clinics of North America 10, no. 3 (1990): 439–48. http://dx.doi.org/10.1016/s0889-8561(22)00287-9.

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30

Morianos, Ioannis, and Maria Semitekolou. "Dendritic Cells: Critical Regulators of Allergic Asthma." International Journal of Molecular Sciences 21, no. 21 (2020): 7930. http://dx.doi.org/10.3390/ijms21217930.

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Allergic asthma is a chronic inflammatory disease of the airways characterized by airway hyperresponsiveness (AHR), chronic airway inflammation, and excessive T helper (Th) type 2 immune responses against harmless airborne allergens. Dendritic cells (DCs) represent the most potent antigen-presenting cells of the immune system that act as a bridge between innate and adaptive immunity. Pertinent to allergic asthma, distinct DC subsets are known to play a central role in initiating and maintaining allergen driven Th2 immune responses in the airways. Nevertheless, seminal studies have demonstrated

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31

Banno, Asoka, Aravind T. Reddy, Sowmya P. Lakshmi, and Raju C. Reddy. "Bidirectional interaction of airway epithelial remodeling and inflammation in asthma." Clinical Science 134, no. 9 (2020): 1063–79. http://dx.doi.org/10.1042/cs20191309.

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Abstract Asthma is a chronic disease of the airways that has long been viewed predominately as an inflammatory condition. Accordingly, current therapeutic interventions focus primarily on resolving inflammation. However, the mainstay of asthma therapy neither fully improves lung function nor prevents disease exacerbations, suggesting involvement of other factors. An emerging concept now holds that airway remodeling, another major pathological feature of asthma, is as important as inflammation in asthma pathogenesis. Structural changes associated with asthma include disrupted epithelial integri

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32

Henderson, A. C., E. P. Ingenito, H. Atileh, E. Israel, B. Suki, and K. R. Lutchen. "Selected Contribution: How does airway inflammation modulate asthmatic airway constriction? An antigen challenge study." Journal of Applied Physiology 95, no. 2 (2003): 873–82. http://dx.doi.org/10.1152/japplphysiol.00075.2003.

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During the late-phase (LP) response to inhaled allergen, mediators from neutrophils and eosinophils are released within the airways, resembling what occurs during an asthma attack. We compared the distribution of obstruction and degree of reversibility that follows a deep inspiration (DI) during early-phase (EP) and LP responses in nine asthmatic subjects challenged with allergen. Heterogeneity of constriction was assayed by determining frequency dependence of dynamic lung resistance and elastance, airway caliber by tracking airway resistance during a DI, and airway inflammation by measuring i

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33

Ferrini, Maria, Soram Hong, Kevan Roberts, and Zeina Jaffar. "Cannabinoid CB2 receptors as novel target for inhibiting house dust mite induced allergic airway inflammation (P6023)." Journal of Immunology 190, no. 1_Supplement (2013): 120.12. http://dx.doi.org/10.4049/jimmunol.190.supp.120.12.

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Abstract Asthma is a chronic lung inflammatory disorder characterized by airflow obstruction, airway hyperreactivity (AHR) and bronchial inflammation in response to environmental stimuli including allergens. Allergic asthma is associated with the presence in the airways of CD4+ Th2 cells and eosinophils, together with goblet cell hyperplasia and epithelial desquamation. Recent studies have indicated that cannabis-derived compounds and cannabinoid receptor agonists have immunosuppressive and anti-inflammatory properties. In this study, we examined the effect of CB2 selective agonists on allergi

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Dulek, Daniel E., Dawn C. Newcomb, Kasia Goleniewska, et al. "Allergic Airway Inflammation Decreases Lung Bacterial Burden following Acute Klebsiella pneumoniae Infection in a Neutrophil- and CCL8-Dependent Manner." Infection and Immunity 82, no. 9 (2014): 3723–39. http://dx.doi.org/10.1128/iai.00035-14.

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ABSTRACTThe Th17 cytokines interleukin-17A (IL-17A), IL-17F, and IL-22 are critical for the lung immune response to a variety of bacterial pathogens, includingKlebsiella pneumoniae. Th2 cytokine expression in the airways is a characteristic feature of asthma and allergic airway inflammation. The Th2 cytokines IL-4 and IL-13 diminishex vivoandin vivoIL-17A protein expression by Th17 cells. To determine the effect of IL-4 and IL-13 on IL-17-dependent lung immune responses to acute bacterial infection, we developed a combined model in which allergic airway inflammation and lung IL-4 and IL-13 exp

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35

Alqarni, Saleh A., Abdulwahab Bineid, Sheikh F. Ahmad, et al. "Blockade of Tyrosine Kinase, LCK Leads to Reduction in Airway Inflammation through Regulation of Pulmonary Th2/Treg Balance and Oxidative Stress in Cockroach Extract-Induced Mouse Model of Allergic Asthma." Metabolites 12, no. 9 (2022): 793. http://dx.doi.org/10.3390/metabo12090793.

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Asthma is one of the most common inflammatory diseases affecting the airways. Approximately 300 million individuals suffer from asthma around the world. Allergic immune responses in the asthmatic airways are predominantly driven by Th2 cells and eosinophils. Lymphocyte-specific protein tyrosine kinase (LCK) is a non-receptor tyrosine kinase which regulates several key intracellular events through phosphorylation of its substrates. Some of the intracellular signaling pathways activated by LCK phosphorylation help in differentiation of Th2 cells which secrete allergic cytokines that amplify airw

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Royce, Simon G., Yu R. Miao, Melissa Lee, Chrishan S. Samuel, Geoffrey W. Tregear, and Mimi L. K. Tang. "Relaxin Reverses Airway Remodeling and Airway Dysfunction in Allergic Airways Disease." Endocrinology 150, no. 6 (2009): 2692–99. http://dx.doi.org/10.1210/en.2008-1457.

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Mice deficient in the antifibrotic hormone relaxin develop structural changes in the airway that resemble airway remodeling, and demonstrate exaggerated remodeling changes in models of allergic airways disease (AAD). Relaxin expression in asthma has not been previously studied. We evaluated the efficacy of relaxin in the treatment of established airway remodeling in a mouse model of AAD. Relaxin expression in mouse AAD was also examined by immunohistochemistry and real-time PCR. BALB/c mice with established AAD were treated with relaxin or vehicle control (sc for 14 d), and effects on airway r

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Yanagisawa, Haruhiko, Mitsuo Hashimoto, Shunsuke Minagawa, et al. "Role of IL-17A in murine models of COPD airway disease." American Journal of Physiology-Lung Cellular and Molecular Physiology 312, no. 1 (2017): L122—L130. http://dx.doi.org/10.1152/ajplung.00301.2016.

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Small airway fibrosis is a major pathological feature of chronic obstructive pulmonary disease (COPD) and is refractory to current treatments. Chronic inflammatory cells accumulate around small airways in COPD and are thought to play a major role in small airway fibrosis. Mice deficient in α/β T cells have recently been shown to be protected from both experimental airway inflammation and fibrosis. In these models, CD4+Th17 cells and secretion of IL-17A are increased. However, a pathogenic role for IL-17 in specifically mediating fibrosis around airways has not been demonstrated. Here a role fo

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38

Ribeiro, Carla M. P., and Martina Gentzsch. "Impact of Airway Inflammation on the Efficacy of CFTR Modulators." Cells 10, no. 11 (2021): 3260. http://dx.doi.org/10.3390/cells10113260.

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Defective CFTR biogenesis and activity in cystic fibrosis airways leads to airway dehydration and impaired mucociliary clearance, resulting in chronic airway infection and inflammation. Most cystic fibrosis patients have at least one copy of the F508del CFTR mutation, which results in a protein retained in the endoplasmic reticulum and degraded by the proteosomal pathway. CFTR modulators, e.g., correctors, promote the transfer of F508del to the apical membrane, while potentiators increase CFTR activity. Corrector and potentiator double therapies modestly improve lung function, whereas triple t

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Shevchenko, Marina A., Ekaterina A. Servuli, Dina E. Murova, et al. "IL-4R and CXCR2 Contribute to Downregulating Neutrophil-Mediated Response in the Early Stage of Fungal Extract-Induced Allergic Airway Inflammation." Biomedicines 12, no. 12 (2024): 2743. https://doi.org/10.3390/biomedicines12122743.

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Background/Objectives: Airborne exogenous antigen inhalation can induce neutrophil infiltration of the airways, while eosinophils migrate to the airways in allergic airway inflammation. During a bacterial infection, Th2-associated cytokine IL-4, by binding to the IL-4 receptor (IL-4R), can suppress neutrophil recruitment to the site of inflammation. In the present study, we estimated whether the IL-4-dependent suppression of neutrophil recruitment contributed to the development of an immune response in asthma. Methods: Using a mouse model of Aspergillus fumigatus extract-induced allergic airwa

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40

Lambrecht, Bart N., Benoı̂t Salomon, David Klatzmann, and Romain A. Pauwels. "Dendritic Cells Are Required for the Development of Chronic Eosinophilic Airway Inflammation in Response to Inhaled Antigen in Sensitized Mice." Journal of Immunology 160, no. 8 (1998): 4090–97. http://dx.doi.org/10.4049/jimmunol.160.8.4090.

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Abstract Asthma is characterized by chronic eosinophilic inflammation of the airways, and allergen-specific Th2 lymphocytes are thought to play a major role in the development and maintenance of this type of inflammation in allergic asthma. It is generally accepted that airway dendritic cells (DC) are essential for stimulating naive T cells in a primary immune response to inhaled Ag and for the development of allergic sensitization. We have examined the role of airway DC in stimulating memory T cells in a secondary response to inhaled Ag and the subsequent development of chronic airway inflamm

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41

Jha, Aruni, Pawan Sharma, Vidyanand Anaparti, Min H. Ryu, and Andrew J. Halayko. "A role for transient receptor potential ankyrin 1 cation channel (TRPA1) in airway hyper-responsiveness?" Canadian Journal of Physiology and Pharmacology 93, no. 3 (2015): 171–76. http://dx.doi.org/10.1139/cjpp-2014-0417.

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Airway smooth muscle (ASM) contraction controls the airway caliber. Airway narrowing is exaggerated in obstructive lung diseases, such as asthma and chronic obstructive pulmonary disease (COPD). The mechanism by which ASM tone is dysregulated in disease is not clearly understood. Recent research on ion channels, particularly transient receptor potential cation channel, subfamily A, member 1 (TRPA1), is uncovering new understanding of altered airway function. TRPA1, a member of the TRP channel superfamily, is a chemo-sensitive cation channel that can be activated by a variety of external and in

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42

Hanania, N. "Airway inflammation in asthma: current and future targets and therapies." Breathe 6, no. 3 (2010): 245–52. http://dx.doi.org/10.1183/18106838.0603.245.

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Educational aimsTo provide an overview of airway inflammation in asthma.To review current management guidelines' recommendations for the use of anti-inflammatory therapies in asthma.To discuss current treatment options for airway inflammation in asthma.To outline unmet needs for treating airway inflammation in asthma.To describe novel targets for treating airway inflammation in asthma based on current knowledge.SummaryAsthma is a chronic inflammatory disease of the airways that requires long-term anti-inflammatory therapy. Inhaled corticosteroids (ICS) are recommended for first-line treatment

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Almolki, Abdelhamid, Camille Taillé, Gillian F. Martin, et al. "Heme oxygenase attenuates allergen-induced airway inflammation and hyperreactivity in guinea pigs." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 1 (2004): L26—L34. http://dx.doi.org/10.1152/ajplung.00237.2003.

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Heme oxygenase (HO), the heme-degrading enzyme, has shown anti-inflammatory effects in several models of pulmonary diseases. HO is induced in airways during asthma; however, its functional role is unclear. Therefore, we evaluated the role of HO on airway inflammation [evaluated by bronchoalveolar lavage (BAL) cellularity and BAL levels of eotaxin, PGE2, and proteins], mucus secretion (evaluated by analysis of MUC5AC gene expression and periodic acid-Schiff staining), oxidative stress (evaluated by quantification of 4-hydroxynonenal adducts and carbonylated protein levels in lung homogenates),

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Xu, K. F., R. Vlahos, A. Messina, T. L. Bamford, J. F. Bertram, and A. G. Stewart. "Antigen-induced airway inflammation in the Brown Norway rat results in airway smooth muscle hyperplasia." Journal of Applied Physiology 93, no. 5 (2002): 1833–40. http://dx.doi.org/10.1152/japplphysiol.00738.2001.

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Asthma is characterized by chronic airways inflammation, airway wall remodeling, and airway hyperresponsiveness (AHR). An increase in airway smooth muscle has been proposed to explain a major part of AHR in asthma. We have used unbiased stereological methods to determine whether airway smooth muscle hyperplasia and AHR occurred in sensitized, antigen-challenged Brown Norway (BN) rats. Ovalbumin (OA)-sensitized BN rats chronically exposed to OA aerosol displayed airway inflammation and a modest level of AHR to intravenously administered ACh 24 h after the last antigen challenge. However, these

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Hunt, E. B., A. Sullivan, J. Galvin, J. MacSharry, and D. M. Murphy. "Gastric Aspiration and Its Role in Airway Inflammation." Open Respiratory Medicine Journal 12, no. 1 (2018): 1–10. http://dx.doi.org/10.2174/1874306401812010001.

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Gastro-Oesophageal Reflux (GOR) has been associated with chronic airway diseases while the passage of foreign matter into airways and lungs through aspiration has the potential to initiate a wide spectrum of pulmonary disorders. The clinical syndrome resulting from such aspiration will depend both on the quantity and nature of the aspirate as well as the individual host response. Aspiration of gastric fluids may cause damage to airway epithelium, not only because acidity is toxic to bronchial epithelial cells but also due to the effect of digestive enzymes such as pepsin and bile salts. Experi

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Henderson, W. R., D. B. Lewis, R. K. Albert, et al. "The importance of leukotrienes in airway inflammation in a mouse model of asthma." Journal of Experimental Medicine 184, no. 4 (1996): 1483–94. http://dx.doi.org/10.1084/jem.184.4.1483.

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Inhalation of antigen in immunized mice induces an infiltration of eosinophils into the airways and increased bronchial hyperreactivity as are observed in human asthma. We employed a model of late-phase allergic pulmonary inflammation in mice to address the role of leukotrienes (LT) in mediating airway eosinophilia and hyperreactivity to methacholine. Allergen intranasal challenge in OVA-sensitized mice induced LTB4 and LTC4 release into the airspace, widespread mucus occlusion of the airways, leukocytic infiltration of the airway tissue and broncho-alveolar lavage fluid that was predominantly

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van Rijt, Leonie S., Steffen Jung, Alex KleinJan, et al. "In vivo depletion of lung CD11c+ dendritic cells during allergen challenge abrogates the characteristic features of asthma." Journal of Experimental Medicine 201, no. 6 (2005): 981–91. http://dx.doi.org/10.1084/jem.20042311.

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Although dendritic cells (DCs) play an important role in sensitization to inhaled allergens, their function in ongoing T helper (Th)2 cell–mediated eosinophilic airway inflammation underlying bronchial asthma is currently unknown. Here, we show in an ovalbumin (OVA)-driven murine asthma model that airway DCs acquire a mature phenotype and interact with CD4+ T cells within sites of peribronchial and perivascular inflammation. To study whether DCs contributed to inflammation, we depleted DCs from the airways of CD11c-diphtheria toxin (DT) receptor transgenic mice during the OVA aerosol challenge

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Tirouvanziam, Rabindra, Ibrahim Khazaal, and Bruno Péault. "Primary inflammation in human cystic fibrosis small airways." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 2 (2002): L445—L451. http://dx.doi.org/10.1152/ajplung.00419.2001.

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Most cystic fibrosis (CF) patients die of lung failure, due to the combined effects of bacterial infection, neutrophil-mediated inflammation, and airway obstruction by hyperviscous mucus. To this day, it remains unclear where and how this pathological vicious circle is initiated in vivo. In particular, it has proven difficult to investigate whether inflammatory pathways are dysregulated in CF airways independently of infection. Also, the relative involvement of large (tracheobronchial) vs. small (bronchiolar) airways in CF pathophysiology is still unclear. To help address these issues, we used

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Szczepankiewicz, Dawid, Wojciech Langwiński, Paweł Kołodziejski, et al. "Allergic Inflammation Alters microRNA Expression Profile in Adipose Tissue in the Rat." Genes 11, no. 9 (2020): 1034. http://dx.doi.org/10.3390/genes11091034.

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Adipose tissue is a major source of circulating exosomal microRNAs (miRNAs) that are modulators of the immune response in various types of tissues and organs, including airways. Still, no evidence exists if allergic airway inflammation may affect fat tissue inflammation via alterations in the miRNA expression profile. Therefore, we investigated the miRNA expression profile in the adipose tissue upon induced allergic inflammation in the airways in the rat. Brown Norway rats were chronically sensitized to house dust mite extract for seven weeks. Body composition was performed using MiniSpec Plus

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Pavord, I. D. "Asthma control, airway responsiveness and airway inflammation." Clinical & Experimental Allergy 39, no. 12 (2009): 1780–82. http://dx.doi.org/10.1111/j.1365-2222.2009.03395.x.

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