Allergic Airway Inflammation Initiates Long-Term Vascular Remodeling of the Pulmonary Circulation

Rydell‐Törmänen, Kristina; Uller, Lena; Erjefält, Jonas

doi:10.1159/000199721

Cited by 17 publications

(18 citation statements)

References 49 publications

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“…[75][76][77][78][79] Particulate 75 and soluble [76][77][78][79] antigens can elicit this remodeling response. Our own work 76 has shown that this remodeling response is dependent on the presence of CD4+ T cells and Th2 cytokines (interleukin: IL-4, IL-13), mediators known for their critical role in asthma.…”

Section: Pulmonary Arterial Remodeling Triggered By Immune Responses mentioning

confidence: 99%

Perspective: Ambient Air Pollution: Inflammatory Response and Effects on the Lung's Vasculature

et al. 2014

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Particulates from air pollution are implicated in causing or exacerbating respiratory and systemic cardiovascular diseases and are thought to be among the leading causes of morbidity and mortality. However, the contribution of ambient particulate matter to diseases affecting the pulmonary circulation, the right heart, and especially pulmonary hypertension is much less documented. Our own work and that of other groups has demonstrated that prolonged exposure to antigens via the airways can cause severe pulmonary arterial remodeling. In addition, vascular changes have been well documented in a typical disease of the airways, asthma. These experimental and clinical findings link responses in the airways with responses in the lung's vasculature. It follows that particulate air pollution could cause, or exacerbate, diseases in the pulmonary circulation and associated pulmonary hypertension. This perspective details the literature for support of this concept. Data regarding the health effects of particulate matter from air pollution on the lung's vasculature, with emphasis on the lung's inflammatory responses to particulate matter deposition and pulmonary hypertension, are discussed. A deeper understanding of the health implications of exposure to ambient particulate matter will improve our knowledge of how to improve the management of lung diseases, including diseases of the pulmonary circulation. As man-made ambient particulate air pollution is typically linked to economic growth, a better understanding of the health effects of exposure to particulate air pollution is expected to integrate the global goal of achieving healthy living for all.

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Section: Pulmonary Arterial Remodeling Triggered By Immune Responses mentioning

confidence: 99%

Perspective: Ambient Air Pollution: Inflammatory Response and Effects on the Lung's Vasculature

et al. 2014

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“…Interestingly, the capillaries of the lower airways are not usually fenestrated in the healthy lung [75], but this phenomenon has been observed in asthmatics [76]. Moreover, vascular remodelling, characterized by a thickening of the VSMC layer, EC proliferation and perivascular fibrosis, has been observed in the bronchi of mice subjected to respiratory ovalbumin (OVA) [77] and chronic house dust mite [78] exposure.…”

Section: Pericytes In Asthmamentioning

confidence: 99%

Pericytes in Chronic Lung Disease

Rowley¹,

Johnson²

2014

Int Arch Allergy Immunol

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Pericytes are mesenchymal cells embedded within the abluminal surface of the endothelium of microvessels such as capillaries, pre-capillary arterioles, post-capillary and collecting venules, where they maintain microvascular homeostasis and participate in angiogenesis. In addition to their roles in supporting the vasculature and facilitating leukocyte extravasation, pericytes have been recently investigated as a subpopulation of mesenchymal stem cells (MSCs) due to their capacity to differentiate into numerous cell types including the classic MSC triad, i.e. osteocytes, chondrocytes and adipocytes. Other studies in models of fibrotic inflammatory disease of the lung have demonstrated a vital role of pericytes in myofibroblast activation, collagen deposition and microvascular remodelling, which are hallmark features of chronic lung diseases such as asthma, chronic obstructive pulmonary disorder, pulmonary fibrosis and pulmonary hypertension. Further studies into the mechanisms of the pericyte-to-myofibroblast transition and migration to fibrotic foci will hopefully clarify the role of these cells in chronic lung disease and confirm the importance of pericytes in human fibrotic pulmonary disease.

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“…These changes include sub-epithelial fibrosis, increase of airway smooth muscle mass and excessive mucus secretion from hyperplastic goblet cells [24]. Allergic airway inflammation can evoke similar long-term structural alterations as those seen in pulmonary blood vessels [25]. Airway remodeling is also due, at least in part, to an excess of extracellular matrix deposition in the airway wall, which leads to sub-epithelial collagen deposition [26].…”

Section: Infiltration Of Blood-born Inflammatory Cellsmentioning

confidence: 99%

Inhaled KMUP-1 Prevents Allergic Pulmonary Vascular Inflammation and Remodeling via NO and Suppressed MMP-9 and ICAM-1/VCAM-1

Liu¹,

Hsieh²,

Wu³

et al. 2012

IADT

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Allergic Airway Inflammation Initiates Long-Term Vascular Remodeling of the Pulmonary Circulation

Cited by 17 publications

References 49 publications

Perspective: Ambient Air Pollution: Inflammatory Response and Effects on the Lung's Vasculature

Perspective: Ambient Air Pollution: Inflammatory Response and Effects on the Lung's Vasculature

Pericytes in Chronic Lung Disease

Inhaled KMUP-1 Prevents Allergic Pulmonary Vascular Inflammation and Remodeling via NO and Suppressed MMP-9 and ICAM-1/VCAM-1

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