Asthma: A Dynamic Disease of Inflammation and Repair

Holgate, Stephen T.

doi:10.1002/9780470515334.ch2

Cited by 40 publications

(16 citation statements)

References 80 publications

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“…Hormones and neuropeptides released into the circulation when individuals experience stress are thought to be involved in regulating both immune-mediated and neurogenic inflammatory processes [3]. Dysregulation of normal homeostatic neural, endocrine, and immunologic mechanisms can occur in the face of chronic stress, leading to chronic hyperarousal or hyporesponsiveness that may impact disease expression [4][5][6][7]. This discussion updates a previous review [3] providing further insights into potential mechanisms linking stress to atopic disorders.…”

Section: Introductionmentioning

confidence: 77%

The impact of stress on the development and expression of atopy

Wright¹,

Cohen²,

Cohen³

2005

Current Opinion in Allergy and Clinical Immunology

304

220

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Section: Introductionmentioning

confidence: 77%

The impact of stress on the development and expression of atopy

Wright¹,

Cohen²,

Cohen³

2005

Current Opinion in Allergy and Clinical Immunology

304

220

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“…Oxidation at the C-3 position produces the flavonols kaempferol (12) and quercitrin (13). A double bond at C-2, formed through dehydration, produces flavones such as chrysin (14), apigenin (15) and rutin (16) as well as isoflavones such as genistin (41), genistein (42) daidzin (43), and daidzein (44). The action of reductases on flavonols produces flavan-3-ols such as catechin (46), epicatechin (47), and epigallocatechin gallate (48), and the colorful anthocyanidins, such as apigenidin (49) and cyanidin (50).…”

Section: Chemistry and Occurrence Of Flavonoidsmentioning

confidence: 99%

“…Several inflammatory mediators are released during injury such as histamine, prostaglandins, thromboxanes and leukotrienes, as well as cytokines and nitric oxide [42,43]. Nitric oxide (NO) is produced when the amino acid L-arginine is converted in L-citrulline by nitric oxide synthase [44] using NG-hydroxyl-L-arginine as an intermediate [38].…”

Section: General Aspects and The Role Of Flavonoids In The Inflammationmentioning

confidence: 99%

“…Soy isoflavones containing high levels of genistein (42) (over 40%) and other derivatives, such as daidzein (44) and daidzin (43), were used in a murine model of allergic asthma. The oral administration of increase doses of soy isoflavones significantly attenuated OVA-induced AHR in response to intravenous methacholine and also reduced the eosinophils count in lung.…”

Section: Asthmamentioning

confidence: 99%

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Structure-Activity Association of Flavonoids in Lung Diseases

et al. 2014

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Flavonoids are polyphenolic compounds classified into flavonols, flavones, flavanones, isoflavones, catechins, anthocyanidins, and chalcones according to their chemical structures. They are abundantly found in Nature and over 8,000 flavonoids have from different sources, mainly plant materials, have been described. Recently reports have shown the valuable effects of flavonoids as antiviral, anti-allergic, antiplatelet, antitumor, antioxidant, and anti-inflammatory agents and interest in these compounds has been increasing since they can be helpful to human health. Several mechanisms of action are involved in the biological properties of flavonoids such as free radical scavenging, transition metal ion chelation, activation of survival genes and signaling pathways, regulation of mitochondrial function and modulation of inflammatory responses. The anti-inflammatory effects of flavonoids have been described in a number of studies in the literature, but not frequently associated to respiratory disease. Thus, this review aims to discuss the effects of different flavonoids in the control of lung inflammation in some disorders such as asthma, lung emphysema and acute respiratory distress syndrome and the possible mechanisms of action, as well as establish some structure-activity relationships between this biological potential and chemical profile of these compounds.

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“…CD44 is a cellular adhesion receptor that is upregulated following tissue injury and implicated in many chronic inflammatory diseases (Holgate, 1997;Mikecz et al, 1995;Jain et al, 1996;Puré and Cuff, 2001). As a principal receptor for hyaluronan (HA), CD44 participates in the activation of leukocytes and parenchymal cells in areas of inflammation, suggesting a role for CD44 in tissue remodeling and fibrosis (Aruffo et al, 1990;Foster et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Fibroblast migration is mediated by CD44-dependent TGFβ activation

Acharya

Majumdar

Jacob

et al. 2008

Journal of Cell Science

139

105

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CD44 contributes to inflammation and fibrosis in response to injury. As fibroblast recruitment is critical to wound healing, we compared cytoskeletal architecture and migration of wild-type (CD44WT) and CD44-deficient (CD44KO) fibroblasts. CD44KO fibroblasts exhibited fewer stress fibers and focal adhesion complexes, and their migration was characterized by increased velocity but loss of directionality, compared with CD44WT fibroblasts. Mechanistically, we demonstrate that CD44WT cells generated more active TGFβ than CD44KO cells and that CD44 promotes the activation of TGFβ via an MMP-dependent mechanism. Reconstitution of CD44 expression completely rescued the phenotype of CD44KO cells whereas exposure of CD44KO cells to exogenous active TGFβ rescued the defect in stress fibers and migrational velocity, but was not sufficient to restore directionality of migration. These results resolve the TGFβ-mediated and TGFβ-independent effects of CD44 on fibroblast migration and suggest that CD44 may be critical for the recruitment of fibroblasts to sites of injury and the function of fibroblasts in tissue remodeling and fibrosis.

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Asthma: A Dynamic Disease of Inflammation and Repair

Cited by 40 publications

References 80 publications

The impact of stress on the development and expression of atopy

The impact of stress on the development and expression of atopy

Structure-Activity Association of Flavonoids in Lung Diseases

Fibroblast migration is mediated by CD44-dependent TGFβ activation

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