Journal articles: 'Airway inflammation'

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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 (April 1, 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 in lung tissue preceded the increase in mRNA levels of tumor necrosis factor-α, interleukin (IL)-1β, and IL-8. Treatment of the animals with the ET receptor antagonist bosentan resulted in a substantial decrease in the concentrations of tumor necrosis factor-α, IL-4, IL-1β, interferon-γ, and ET-1 in bronchoalveolar lavage fluid. In conclusion, the synthesis of ET-1 as measured by increased mRNA level precedes the synthesis of other proinflammatory cytokines of importance for the development of an eosinophilic airway inflammation, and ET antagonism inhibits the production of these mediators within the airways. Whether treatment with ET antagonists will prove beneficial for patients with eosinophilic airway inflammations like bronchial asthma is not yet known.

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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 and structural changes in asthma, and discusses how these processes may interact to modify airway function and induce respiratory symptoms.

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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, treatment with inhaled corticoteroids - the most effective treatment for asthma - improves symptoms and reduces the numbers of eosinophil s, mast cells and lymphocytes in the airways. The precise functions of the cells in promoting inflammation and causing asthma symptoms has not yet been fully elucidated. However, it is very likely that eicosanoids, such as the cysteinyl leukotrienes, are produced by eosinophils and mast cells and are a major cause of bronchoconstriction in asthma. Also, these inflammatory cells can produce proinflammatory cytokines, such as granulocytc-macrophage colony-stimulating factor. interleukin (IL) 3 and IL-5, which may promote continuing inflammation in the airways. Lastly, the persisting inflammatory cell infiltrate and products re leased from these cells arc very likely the cause or the airway structural changes characteristic of asthma, such as epithelial damage, goblet cell hyperplasia. smooth muscle thickening and deposition of collagen below the basement membrane. These changes have been suggested tn he the cause of airway hyperresponsiveness in asthma. An improved understanding of the precise mechanisms by which airway inflammation is initiated, propagates and causes airway damage will hopefully allow more precise treatment strategies to he developed for asthma than currently exist.

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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 (April 1, 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 lead to acidification, including direct effects on epithelial cells or through recruitment of inflammatory cells. We demonstrated a partial role for eosinophils in airway acidification as CCR3 and IL-5-deficient mice had decreased extent of airway acidification in allergen-challenged mice. Furthermore, using dimethyl amiloride, a specific inhibitor of the Na+/H+ exchanger, we demonstrated significant inhibition of airway acidification in allergic airway inflammation, suggesting a role for ion (proton) channels. In summary, our studies demonstrate that mouse airways are acidified during allergic airway inflammation. We also showed that the mechanism of airway acidification in asthma involves IL-13-mediated pathways including eosinophils and proton channels. These results have considerable implications for the development of therapies that target airway acidification.

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Shelhamer, James H. "Airway Inflammation." Annals of Internal Medicine 123, no. 4 (August 15, 1995): 288. http://dx.doi.org/10.7326/0003-4819-123-4-199508150-00008.

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Takahashi, Kentaro, Koichi Hirose, Saki Kawashima, Yusuke Niwa, Hidefumi Wakashin, Arifumi Iwata, Koji Tokoyoda, Toshinori Nakayama, and Hiroshi Nakajima. "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 (May 1, 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 lung epithelial cell line (MLE-15 cells). RESULTS: Antigen inhalation induced IL-22 production in CD4(+) T cells. Only one third of IL-22-producing CD4(+) T cells also produced IL-17A. Anti-IL-22 antibody administration enhanced antigen-induced IL-13 production, eosinophil recruitment, and goblet cell hyperplasia in the airways. On the other hand, intranasal administration of rIL-22 attenuated eosinophil recruitment. Moreover, anti-IL-22 antibody enhanced IL-25 production in the airways, and anti-IL-25 antibody reversed the enhancing effect of anti-IL-22 antibody on eosinophil recruitment into the airways. Finally, IL-22 inhibited IL-13-mediated enhancement of IL-25 expression in IL-1β- or LPS-stimulated MLE-15 cells. CONCLUSION: IL-22 attenuates antigen-induced airway inflammation, possibly by inhibiting IL-25 production by lung epithelial cells.

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Royce, Simon G., Anna M. Tominaga, Matthew Shen, Krupesh P. Patel, Brooke M. Huuskes, Rebecca Lim, Sharon D. Ricardo, and Chrishan S. Samuel. "Serelaxin improves the therapeutic efficacy of RXFP1-expressing human amnion epithelial cells in experimental allergic airway disease." Clinical Science 130, no. 23 (October 20, 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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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 (April 1, 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 the lung during hyperresponsive states; however, recent evidence implicates the upregulation of granulocyte adhesion molecules on both the endothelial and epithelial surfaces of the airway. There is evidence that during migration diapedesis, granulocytes interact with epithelial and endothelial cells to produce regionally secreted mediators that upregulate the responsiveness of adjacent airway smooth muscle and/or cause lumenal edema, thus augmenting the effect of constrictor stimuli. Most evidence suggests that the eosinophil is the most important granulocyte in these responses and that eosinophilic infiltration and activation may account for the unique, spasmodic, and cyclic nature of hyperreactive airways. The molecular biology of the eosinophil granule proteins has characterized four distinct substances, each of which exerts potential cytotoxic effects on airway epithelium by different mechanism. In addition, at least one of these proteins, the major basic protein, appears to cause direct, noncytotoxic stimulation of epithelial secretion that upregulates nonspecifically the response of airway smooth muscle to contractile stimuli. The recognition of inflammation as the essential component to airway hyperresponsiveness provides a fresh approach to a difficult problem and suggests a host of novel therapies for human asthma.

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

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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 airway smooth muscle cell as a target cell for acetylcholine that modulates inflammation and remodelling during respiratory diseases such as asthma and COPD.

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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 (June 1, 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 investigated. In the present study, we characterized the model of Aspergillus fumigatus extract-induced allergic airway inflammation that allowed investigating the early stage of inflammation development. The model adequacy was confirmed according to the blood and bronchoalveolar lavage eosinophilia. Using immunohistochemical staining of conducting airway as a whole-mount and confocal laser scanning microscopy, we estimated neutrophil and eosinophil spatial location: in the luminal side of the epithelium, in the airway wall or in the submucosal compartment close to the smooth muscle layer. An allergic airway response activation was detected upon significant elevation of blood eosinophil percentage compared to intact mice. Simultaneously, the number of eosinophils in the bronchoalveolar lavage was also significantly increased compared to the intact mice. At this time point, eosinophils predominated both in bronchoalveolar lavages and in conducting airway mucosa compared to neutrophils. Spatial location of conducting airway mucosal cell analysis demonstrated that eosinophils mostly located in the submucosal compartment, in a lesser extent in the airway wall, and a few eosinophils were detected in the luminal side of the epithelium. Neutrophils mainly infiltrated the luminal side of the epithelium, and a few neutrophils were detected in the submucosal compartment, while no neutrophils were detected in the airway wall. The data suggests that in response to the further allergen challenge, evidently eosinophils but not neutrophils will migrate through the airway wall to the airway lumen. Thus, eosinophils can be expected to damage airway epithelium in allergic airway inflammation development. Simultaneously, neutrophils located in close proximity to the smooth muscle layer together with eosinophils can contribute to bronchoconstriction induction.

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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 (February 11, 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 to united airway disease using a fine-particle ICS. Our understanding of the relationship between the upper and lower airways and its contribution to T helper 2 (Th2)-skewed disease, such as AR and/or ECRS with asthma, has led us to this novel therapeutic strategy for a comprehensive approach to the treatment of upper airway inflammation with asthma.

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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 mediated by counterregulation of 12/15-lipoxygenase, the mouse ortholog of 15-lipoxygenase-1. The airways of mice were treated with interleukin-13 or interferon-γone day prior to each of the four allergen exposures. Interleukin-13 augmented and interferon-γinhibited allergic airway inflammation independently of systemic IgE and mucosal IgA responses but in association with counterregulation of 12/15-lipoxygenase. Interleukin-13 and interferon-γcounterregulate 12/15-lipoxygenase potentially contributing to the effects of these cytokines on allergic airway inflammation.

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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 (May 1, 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. DGKζ knockout (KO) mice exhibited reduced type 2 airway inflammation and were completely resistant to AHR induction in a mouse model of allergic asthma. Surprisingly, the mechanism by which DGKζ protected against airway inflammation and AHR were separable. Targeted deletion of DGKζ in T cells led to decreased type 2 inflammation with no attenuation of AHR. In contrast, conditional deletion of DGKζ in airway smooth muscle cells led to decreased AHR despite no changes in airway inflammation. Importantly, the pharmacological inhibition of DGK provided protection against airway inflammation and AHR in mice, and also reduced bronchoconstriction of human airways. Together, our data suggest that DGKζ is potentially a novel therapeutic target for allergic asthma. Moreover, the targeted deletion of DGKζ reveals that the inflammatory and AHR components of allergic asthma are not as interdependent, as generally believed.

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Shapiro, Gail G. "Childhood Asthma: Update." Pediatrics In Review 13, no. 11 (November 1, 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 infiltrate. Among the infiltrating cells are eosinophils, macrophages, and neutrophils that are called to the site of inflammation by the chemotactic products released by activated mast cells. Upon their arrival, these cells release their own products of inflammation, which amplify this immunologic response. A variety of neuropeptides also play a role, some serving to stabilize and others to destabilize the airway. One result of this airway inflammation is airways reactivity, also known as bronchial hyperresponsiveness. A common example of this scenario is the child who has allergic asthma and encounters a problematic allergen. This child has immunoglobulin E (IgE) to this allergen bound to mast cells in his or her airway. Upon exposure to the allergen, the binding of IgE and antigen triggers mast cell mediator release within minutes.

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Dakhama, Azzeddine, Jung-Won Park, Christian Taube, Mohamed El Gazzar, Taku Kodama, Nobuaki Miyahara, Katsuyuki Takeda, 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 (April 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 responsiveness to electrical field stimulation. In these animals, substance P expression was markedly increased, whereas calcitonin gene-related peptide (CGRP) expression was decreased in airway tissue. Prophylactic treatment with Sendide, a highly selective antagonist of the neurokinin-1 receptor, or CGRP, but not the CGRP antagonist CGRP(8–37), inhibited the development of airway inflammation and AHR in RSV-infected animals. Therapeutic treatment with CGRP, but not CGRP(8–37) or Sendide, abolished AHR in RSV-infected animals despite increased substance P levels and previously established airway inflammation. These data suggest that RSV-induced airway dysfunction is, at least in part, due to an imbalance in sensory neuropeptide expression in the airways. Restoration of this balance may be beneficial for the treatment of RSV-mediated airway dysfunction.

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Gochuico, Bernadette R., Kathleen M. Miranda, Edith M. Hessel, Joris J. De Bie, Antoon J. M. Van Oosterhout, William W. Cruikshank, and Alan Fine. "Airway epithelial Fas ligand expression: potential role in modulating bronchial inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 274, no. 3 (March 1, 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 the upper and lower airways. Third, during allergic airway inflammation induced by ovalbumin in mice, cell-associated staining for Fas ligand mRNA and protein was markedly reduced in the airway epithelium. These data suggest that Clara cell-derived Fas ligand may control immune activity in the airway; thus alterations in this protective mechanism may be involved in the pathogenesis of certain inflammatory conditions of the airway, such as asthma.

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Bozkurt, Turgut Emrah. "Endocannabinoid System in the Airways." Molecules 24, no. 24 (December 17, 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 cannabinoids to induce bronchodilation and modify inflammation indicates their importance for airway physiology and pathologies. In this review, the contribution of cannabinoids and the endocannabinoid system in the airways are discussed, and the existing data for their therapeutic use in airway diseases are presented.

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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 (December 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) challenge to OVA-sensitized mice. In this animal model of airway inflammation, lung Ugrp1 mRNA expression was greatly decreased compared with control mice. A significant inverse correlation between lung Ugrp1 mRNA levels and IL-9 levels in BAL fluid was demonstrated by regression analysis ( r = 0.616, P = 0.023). Immunohistochemical analysis revealed a distinct localization of UGRP1 in airway epithelial cells of control mice, whereas UGRP1 staining was patchy and faint in inflamed airways. Intranasal administration of IL-9 to naive mice decreased the level of Ugrp1 expression in lungs. These findings suggest that UGRP1 is downregulated in inflamed airways, such as allergic asthmatics, and IL-9 might be an important mediator for modulating UGRP1 expression.

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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 (May 1, 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 house dust mite (HDM) allergen sensitization in adult mice (8 weeks-old) induced T-helper type 2 (Th2)- driven airway inflammation, i.e., influx of activated Th2 cells into the airways, airway eosinophilic inflammation and increased IgE-producing plasmablasts. In contrast, HDM allergen sensitization with low-dose LPS (10 μg) abrogated HDM-driven Th2-mediated allergic airway inflammation without increasing antigen-specific Th1 cell trafficking into the airways. Importantly, unlike adults, infant mice (3 weeks-old) exposed to HDM with low-dose LPS (10 μg) developed Th2 responses allergic airway inflammation and required allergen sensitization with high-dose LPS (100 μg) to effectively suppress allergen-specific Th2 responses and allergic inflammation. These results show that airway exposure levels of endotoxin provide different protection against asthma and allergies in adults and infants and suggest that Infants are more vulnerable to prime type 2 cell dominant responses to inhaled allergens in the presence of low dose endotoxin, which will shape future effector Th2 responses and Th2-mediated airway inflammation throughout adult life.

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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 the associated late-phase airway obstruction occurring 6 h after antigen inhalation. In contrast, a multiple dosing regime with WEB 2170 (once a day for 7 consecutive days) failed to reduce the chronic airway inflammation (eosinophilic) and associated airway hyperresponsiveness to inhaled methacholine that is characteristic of dual responder monkeys. Thus, we conclude that the generation of PAF following antigen inhalation contributes to the development of lipid mediators, acute airway inflammation and associated late-phase airway obstruction in dual responder primates; however, PAF does not play a significant role in the maintenance of chronic airway inflammation and associated airway hyperresponsiveness in this primate model.

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

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

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Taylor, D. R., and D. C. Cowan. "Assessing airway inflammation." Thorax 65, no. 12 (October 11, 2010): 1031–32. http://dx.doi.org/10.1136/thx.2009.132985.

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

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

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

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

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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 (August 1990): 439–48. http://dx.doi.org/10.1016/s0889-8561(22)00287-9.

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Morianos, Ioannis, and Maria Semitekolou. "Dendritic Cells: Critical Regulators of Allergic Asthma." International Journal of Molecular Sciences 21, no. 21 (October 26, 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 that DCs can also restrain excessive asthmatic responses and thus contribute to the resolution of allergic airway inflammation and the maintenance of pulmonary tolerance. Notably, the transfer of tolerogenic DCs in vivo suppresses Th2 allergic responses and protects or even reverses established allergic airway inflammation. Thus, the identification of novel DC subsets that possess immunoregulatory properties and can efficiently control aberrant asthmatic responses is critical for the re-establishment of tolerance and the amelioration of the asthmatic disease phenotype.

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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 (August 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 inflammatory cells in induced sputum postchallenge. Despite a paucity of eosinophils in the sputum at baseline (<1% of nonsquamous cells), asthmatic subjects showed a substantial EP response with highly heterogeneous constriction and reduced capacity to maximally dilate airways. The LP was associated with substantial airway inflammation in all subjects. However, five subjects showed only mild LP constriction, whereas four showed more marked LP constriction characterized by heterogeneous constriction similar to EP. Bronchoconstriction during LP was fully alleviated by administration of a bronchodilator. These findings, together with the impaired bronchodilatory response during a DI, indicate a physiological abnormality in asthma at the smooth muscle level and indicate that airway inflammation in asthma is associated with a highly nonuniform pattern of constriction. These data support the hypothesis that variability in responsiveness among asthmatic subjects derives from intrinsic differences in smooth muscle response to inflammation.

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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 (May 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 integrity, subepithelial fibrosis, goblet cell hyperplasia/metaplasia, smooth muscle hypertrophy/hyperplasia, and enhanced vascularity. These alterations are hypothesized to contribute to airway hyperresponsiveness, airway obstruction, airflow limitation, and progressive decline of lung function in asthmatic individuals. Consequently, targeting inflammation alone does not suffice to provide optimal clinical benefits. Here we review asthmatic airway remodeling, focusing on airway epithelium, which is critical to maintaining a healthy respiratory system, and is the primary defense against inhaled irritants. In asthma, airway epithelium is both a mediator and target of inflammation, manifesting remodeling and resulting obstruction among its downstream effects. We also highlight the potential benefits of therapeutically targeting airway structural alterations. Since pathological tissue remodeling is likewise observed in other injury- and inflammation-prone tissues and organs, our discussion may have implications beyond asthma and lung disease.

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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 (May 1, 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 allergic airway inflammation using Derp house dust mite (HDM)-induced model of asthma. Our results revealed that the intranasal administration of nonpsychoactive CB2 agonists was highly effective at attenuating allergic airway inflammatory responses. Specifically, CB2 agonists caused a marked inhibition in the accumulation of CD4+ T cells and eosinophils into the airways and the level of Th2 cytokine production in the lungs of mice immunized and challenged with HDM. Moreover, treatment with CB2 agonists ameliorated HDM-induced AHR and mucus production. CB2 receptors were highly expressed by antigen-presenting cells in the airways during allergic inflammation. Collectively, these results demonstrate that CB2 activation leads to suppression of allergen-induced airway inflammation and AHR and may provide a novel approach for the treatment for lung inflammatory diseases such as asthma.

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Dulek, Daniel E., Dawn C. Newcomb, Kasia Goleniewska, Jaqueline Cephus, Weisong Zhou, Sara Reiss, Shinji Toki, 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 (June 23, 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 expression were induced by ovalbumin sensitization and challenge prior to acute lung infection withK. pneumoniae. We hypothesized that preexisting allergic airway inflammation decreases lung IL-17A expression and airway neutrophil recruitment in response to acuteK. pneumoniaeinfection and thereby increases the lungK. pneumoniaeburden. As hypothesized, we found that allergic airway inflammation decreased the number ofK. pneumoniae-induced airway neutrophils and lung IL-17A, IL-17F, and IL-22 expression. Despite the marked reduction in postinfection airway neutrophilia and lung expression of Th17 cytokines, allergic airway inflammation significantly decreased the lungK. pneumoniaeburden and postinfection mortality. We showed that the decreased lungK. pneumoniaeburden was independent of IL-4, IL-5, and IL-17A and partially dependent on IL-13 and STAT6. Additionally, we demonstrated that the decreased lungK. pneumoniaeburden associated with allergic airway inflammation was both neutrophil and CCL8 dependent. These findings suggest a novel role for CCL8 in lung antibacterial immunity againstK. pneumoniaeand suggest new mechanisms of orchestrating lung antibacterial immunity.

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Alqarni, Saleh A., Abdulwahab Bineid, Sheikh F. Ahmad, Naif O. Al-Harbi, Faleh Alqahtani, Khalid E. Ibrahim, Nemat Ali, and Ahmed Nadeem. "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 (August 25, 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 airway inflammation. Therefore, this investigative study was designed to determine the role of LCK in a cockroach extract (CE)-induced airway inflammation murine model of allergic asthma. Further, the effect of a pharmacological LCK inhibitor, A-770041, on allergic airway inflammation and key intracellular pathways in CD4+ T cells was assessed. Our data exhibit that there is an activation of LCK during allergic airway inflammation as depicted by increased p-LCK levels in CD4+ T cells. Activated LCK is involved in the activation of ITK, PLC-γ, GATA3, NFkB, and NFATc1. Activated LCK is also involved in the upregulation of Th2 related cytokines, such as IL-4/IL-5/IL-13 and oxidative stress, and the downregulation of Treg cells. Furthermore, utilization of LCK inhibitor causes the reduction in p-LCK, PLC-γ, GATA3, and NFATc1 as well as Th2 cytokines and oxidative stress. LCK inhibitor causes upregulation of Treg cells in allergic mice. LCK inhibitor also caused a reduction in CE-induced airway inflammation and mucus secretion. Therefore, the inhibition of LCK signaling could be a fruitful approach to adjust allergic airway inflammation through the attuning of Th2/Treg immune responses. This study could lead to the design of newer treatment options for better management of allergic inflammation in asthma.

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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 (February 12, 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 remodeling, airway inflammation, and airway hyperresponsiveness (AHR) were assessed. Relaxin expression was significantly reduced in the airways of mice with AAD compared with controls. Recombinant relaxin treatment in a mouse model of AAD reversed collagen deposition and epithelial thickening, and significantly improved AHR (all P &lt; 0.05 vs. vehicle control), but did not influence airway inflammation or goblet cell hyperplasia. Relaxin treatment was associated with increased matrix metalloproteinase-2 levels, suggesting a possible mechanism for its antifibrotic effects. Endogenous relaxin expression is decreased in murine AAD, whereas exogenous relaxin represents a novel treatment capable of reversing established airway remodeling and AHR.

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Yanagisawa, Haruhiko, Mitsuo Hashimoto, Shunsuke Minagawa, Naoki Takasaka, Royce Ma, Catherine Moermans, Saburo Ito, 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 (January 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 for IL-17A in airway fibrosis was demonstrated using mice deficient in the IL-17 receptor A ( il17ra). Il17ra-deficient mice were protected from both airway inflammation and fibrosis in two different models of airway fibrosis that employ COPD-relevant stimuli. In these models, CD4+ Th17 are a major source of IL-17A with other expressing cell types including γδ T cells, type 3 innate lymphoid cells, polymorphonuclear cells, and CD8+ T cells. Antibody neutralization of IL-17RA or IL-17A confirmed that IL-17A was the relevant pathogenic IL-17 isoform and IL-17RA was the relevant receptor in airway inflammation and fibrosis. These results demonstrate that the IL-17A/IL-17 RA axis is crucial to murine airway fibrosis. These findings suggest that IL-17 might be targeted to prevent the progression of airway fibrosis in COPD.

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Ribeiro, Carla M. P., and Martina Gentzsch. "Impact of Airway Inflammation on the Efficacy of CFTR Modulators." Cells 10, no. 11 (November 22, 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 therapies with two correctors and one potentiator indicate improved outcomes. Enhanced F508del rescue by CFTR modulators is achieved by exposing F508del/F508del primary cultures of human bronchial epithelia to relevant inflammatory stimuli, i.e., supernatant from mucopurulent material or bronchoalveolar lavage fluid from human cystic fibrosis airways. Inflammation enhances the biochemical and functional rescue of F508del by double or triple CFTR modulator therapy and overcomes abrogation of CFTR correction by chronic VX-770 treatment in vitro. Furthermore, the impact of inflammation on clinical outcomes linked to CFTR rescue has been recently suggested. This review discusses these data and possible mechanisms for airway inflammation-enhanced F508del rescue. Expanding the understanding of how airway inflammation improves CFTR rescue may benefit cystic fibrosis patients.

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Shevchenko, Marina A., Ekaterina A. Servuli, Dina E. Murova, Julia D. Vavilova, Elena L. Bolkhovitina, Ekaterina N. Chursanova, and Alexander M. Sapozhnikov. "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 (November 30, 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 airway inflammation, we investigated the proportions of eosinophils and neutrophils in blood, lungs, and bone marrow over time. Bronchoalveolar lavage (BAL) fluid cytokine (including IL-4) levels and the proportions of bone marrow IL-4Rα (CD124)-expressing neutrophils were estimated. Results: We identified skewing from the neutrophil- to eosinophil-mediated immune response in the blood after five extract applications. At this point, the BAL fluid IL-4 level was not elevated, while IL-12p40 and CXCL1 levels were considerably increased. At the early stage of allergic airway inflammation, the proportions of neutrophils expressing CD124 and circulating neutrophils expressing CXCR2 (CD182) were significantly increased. Upon inflammation progression, the former remained elevated, but the latter significantly decreased. Conclusions: Thus, in allergic airway inflammation, bone marrow neutrophils become insensible to the attractive chemokine CXCL1 signals and susceptible to IL-4 effects.

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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 (April 15, 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 inflammation. In our mouse model of asthma, OVA aerosol challenge in OVA-sensitized mice leads to CD4-dependent peribronchial and perivascular eosinophilic inflammation, lung Th2 cytokine production, and systemic IgE production. We have used conditional depletion of airway DC by treatment of thymidine kinase-transgenic mice with the antiviral drug ganciclovir to deplete DC during the secondary exposure to OVA. In sensitized thymidine kinase-transgenic mice, a significant decrease in the number of bronchoalveolar CD4 and CD8 T lymphocytes and B lymphocytes was seen after ganciclovir treatment. In addition, Th2 cytokine-associated eosinophilic airway inflammation was almost completely suppressed. These studies demonstrate for the first time that the DC is essential for presenting inhaled Ag to previously primed Th2 cells in the lung, leading to chronic eosinophilic airway inflammation. Altering the function of airway DC may therefore be an important target for new anti-asthma therapy.

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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 (March 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 internal stimuli, leading to the influx of Ca2+. Functional TRPA1 channels have been identified in neuronal and non-neuronal tissues of the lung, including ASM. In the airways, these channels can regulate the release of mediators that are markers of airway inflammation in asthma and COPD. For, example, TRPA1 controls cigarette-smoke-induced inflammatory mediator release and Ca2+ mobilization in vitro and in vivo, a response tied to disease pathology in COPD. Recent work has revealed that pharmacological or genetic inhibition of TRPA1 inhibits the allergen-induced airway inflammation in vitro and airway hyper-responsiveness (AHR) in vivo. Collectively, it appears that TRPA1 channels may be determinants of ASM contractility and local inflammation control, positioning them as part of novel mechanisms that control (patho)physiological function of airways and ASM.

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Hanania, N. "Airway inflammation in asthma: current and future targets and therapies." Breathe 6, no. 3 (March 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 of persistent disease, but not all patients achieve asthma control even when these agents are used in high doses and in combination with other medications, such as a long-acting β2-agonist (LABA) or a leukotriene modifier. Such patients may require additional therapy. As information about asthma pathophysiology and inflammatory phenotypes continues to accumulate, and additional anti-inflammatory options become available, it may be possible to target anti-inflammatory therapy to various aspects of the disease and consequently to improve treatment of patients who respond inadequately to standard ICS-based therapy. Several novel anti-inflammatory therapies are at different stages of clinical development. This article will provide an overview of current and future approaches targeting airway inflammation in asthma.

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Almolki, Abdelhamid, Camille Taillé, Gillian F. Martin, Peter J. Jose, Christine Zedda, Marc Conti, Jerome Megret, Dominique Henin, Michel Aubier, and Jorge Boczkowski. "Heme oxygenase attenuates allergen-induced airway inflammation and hyperreactivity in guinea pigs." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 1 (July 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), and airway responsiveness to histamine in ovalbumin (OVA)-sensitized and multiple aerosol OVA or saline-challenged guinea pigs (6 challenges, once daily, OVA group and control group, respectively). Airway inflammation, mucus secretion, oxidative stress, and responsiveness were significantly increased in the OVA group compared with the control group. HO upregulation by repeated administrations of hemin (50 mg/kg ip) significantly decreased airway responsiveness in control animals and airway inflammation, mucus secretion, oxidative stress, and responsiveness in OVA animals. These effects were reversed by the concomitant administration of the HO inhibitor tin protoporphyrin-IX (50 μmol/kg ip). Repeated administrations of tin protoporphyrin-IX alone significantly increased airway responsiveness in control animals but did not modify airway inflammation, mucus secretion, oxidative stress, and responsiveness in OVA animals. These results suggest that upregulation of the HO pathway has a significant protective effect against airway inflammation, mucus hypersecretion, oxidative stress, and hyperresponsiveness in a model of allergic asthma in guinea pigs.

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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 (January 23, 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. Experimental models have shown that direct instillation of these factors to airways epithelia cause damage with a consequential inflammatory response. The pathophysiology of these responses is gradually being dissected, with better understanding of acute gastric aspiration injury, a major cause of acute lung injury, providing opportunities for therapeutic intervention and potentially, ultimately, improved understanding of the chronic airway response to aspiration. Ultimately, clarification of the inflammatory pathways which are related to micro-aspirationviapepsin and bile acid salts may eventually progress to pharmacological intervention and surgical studies to assess the clinical benefits of such therapies in driving symptom improvement or reducing disease progression.

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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 (November 1, 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 animals did not show an increase in smooth muscle cell (SMC) number in the left main bronchus, suggesting that short-lived inflammatory mechanisms caused the acute AHR. In contrast, 7 days after the last aerosol challenge, there was a modest increase in SMC number, but no AHR to ACh. Addition of FCS to the chronic OA challenge protocol had no effect on the degree of inflammation but resulted in a marked increase in both SMC number and a persistent (7-day) AHR. These results raise the possibility that increases in airway SMC number rather than, or in addition to, chronic inflammation contribute to the persistent AHR detected in this model.

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Henderson, W. R., D. B. Lewis, R. K. Albert, Y. Zhang, W. J. Lamm, G. K. Chiang, F. Jones, et al. "The importance of leukotrienes in airway inflammation in a mouse model of asthma." Journal of Experimental Medicine 184, no. 4 (October 1, 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 eosinophils, and bronchial hyperreactivity to methacholine. Specific inhibitors of 5-lipoxygenase and 5-lipoxygenase-activating protein (FLAP) blocked airway mucus release and infiltration by eosinophils indicating a key role for leukotrienes in these features of allergic pulmonary inflammation. The role of leukotrienes or eosinophils in mediating airway hyperresponsiveness to aeroallergen could not be established, however, in this murine model.

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van Rijt, Leonie S., Steffen Jung, Alex KleinJan, Nanda Vos, Monique Willart, Catherine Duez, Henk C. Hoogsteden, and Bart N. Lambrecht. "In vivo depletion of lung CD11c+ dendritic cells during allergen challenge abrogates the characteristic features of asthma." Journal of Experimental Medicine 201, no. 6 (March 21, 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. Airway administration of DT depleted CD11c+ DCs and alveolar macrophages and abolished the characteristic features of asthma, including eosinophilic inflammation, goblet cell hyperplasia, and bronchial hyperreactivity. In the absence of CD11c+ cells, endogenous or adoptively transferred CD4+ Th2 cells did not produce interleukin (IL)-4, IL-5, and IL-13 in response to OVA aerosol. In CD11c-depleted mice, eosinophilic inflammation and Th2 cytokine secretion were restored by adoptive transfer of CD11c+ DCs, but not alveolar macrophages. These findings identify lung DCs as key proinflammatory cells that are necessary and sufficient for Th2 cell stimulation during ongoing airway inflammation.

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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 (August 1, 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 an in vivo model based on the maturation of human fetal CF and non-CF small airways in severe combined immunodeficiency mice. We show that uninfected mature CF small airway grafts, but not matched non-CF controls, undergo time-dependent neutrophil-mediated inflammation, leading to progressive lung tissue destruction. This model of mature human small airways provides the first clear-cut evidence that, in CF, inflammation may arise at least partly from a primary defect in the regulation of neutrophil recruitment, independently of infection.

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Szczepankiewicz, Dawid, Wojciech Langwiński, Paweł Kołodziejski, Ewa Pruszyńska-Oszmałek, Maciej Sassek, Joanna Nowakowska, Agata Chmurzyńska, Krzysztof W. Nowak, and Aleksandra Szczepankiewicz. "Allergic Inflammation Alters microRNA Expression Profile in Adipose Tissue in the Rat." Genes 11, no. 9 (September 2, 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. The eosinophil count and the total IgE level were determined to confirm the induction of allergic inflammation. MiRNA expression profiling was done using the next-generation sequencing with validation by qPCR. We found that allergic airway inflammation significantly increased fat in adipose tissue, glucose concentration, and the gene expression of adipose tissue-derived proinflammatory peptides (leptin, TNFα). In miRNA-seq analysis, we showed significant differences in the expression of 36 mature miRNAs, three precursors, and two miRNA families in adipose tissue of allergic rats. Two miRNAs—miRNA-151-5p and miRNA-423-3p—showed significantly increased expression in qPCR in adipose tissue and lungs of sensitized animals. Allergic airway inflammation affects fat tissue and alters miRNA expression profile in adipose tissue in the rat.

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

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Journal articles on the topic 'Airway inflammation'

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