2002
DOI: 10.1046/j.1440-1843.2002.00362.x
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Interleukin‐1β and tumour necrosis factor‐α increase microvascular leakage in the guinea pig trachea

Abstract: Pro-inflammatory cytokines, TNFalpha and IL-1beta are able to induce significant microvascular leakage in the guinea pig trachea.

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Cited by 9 publications
(7 citation statements)
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“…The hypothesis that the function of h-IAP1 is to prevent virus-induced apoptosis is further supported by the early time point of upregulation of h-IAP1 at 12 h after D2V infection in HUVECs (Table 4). Similar modulation of apoptosis is seen in other viral systems (42,56,58). Activation of the myxovirus pathway during D2V infection in endothelial cells may be an important antiviral response.…”
Section: Discussionsupporting
confidence: 63%
“…The hypothesis that the function of h-IAP1 is to prevent virus-induced apoptosis is further supported by the early time point of upregulation of h-IAP1 at 12 h after D2V infection in HUVECs (Table 4). Similar modulation of apoptosis is seen in other viral systems (42,56,58). Activation of the myxovirus pathway during D2V infection in endothelial cells may be an important antiviral response.…”
Section: Discussionsupporting
confidence: 63%
“…It is interesting to note that asthma is in many ways a disease analogous to atherosclerosis in that both diseases are characterized by chronic inflammation and involve increased smooth muscle hyperplasia and hypertrophy, proinflammatory gene expression, lesion development, extracellular matrix remodeling, and infiltration of inflammatory leukocytes. Analogous to atherosclerotic lesions, the airways of asthmatic patients display endothelial and microvascular damage, which is thought to expose the lung to blood plasma and its constituents including lipoprotein particles such as LDL (34). Thus the asthmatic airway may be subject to a similar inflammatory microenvironment as vascular cells following endothelial damage.…”
Section: Discussionmentioning
confidence: 99%
“…cysteinyl leukotrienes, histamine, bradykinin, 5‐HT and cytokines) are capable of inducing this effect when released in response to an inflammatory insult in the airway, where they can act upon the endothelium of post‐capillary venules to open these intercellular gaps. This effect causes plasma to ‘leak’ out into extravascular sites because of hydrostatic pressure gradients (Olivenstein et al , ; Reynolds et al , ; Greiff et al , ). This phenomenon is a very distinctive feature of acute inflammation but is also observed in more chronic diseases such as asthma (Laitinen et al , ; Li and Wilson, ; Innes et al , ; Khor et al , ) and COPD (Hill et al , ; Minakata et al , ; Bessa et al , ).…”
Section: Introductionmentioning
confidence: 99%
“…However, the effect of PGE 2 and the EP receptors on airway MVL has not been extensively investigated. To investigate this, Evans Blue dye was used as a marker of MVL, a method that has been used for decades to quantify vascular permeability in various tissues and a variety of species (Miles and Miles, ; Evans et al , ; Rogers et al , ; Baluk et al , ; Reynolds et al , ; Xie et al , ; Zhuang et al , ). First, we established the responses to PGE 2 in both mouse and guinea pig airways.…”
Section: Introductionmentioning
confidence: 99%