Mesothelial cell modulation of pleural repair: Thrombin stimulated mesothelial cells release prostaglandin E2

Hott, Jeffery W.; Godbey, Steven W.; Antony, Veena B.

doi:10.1016/0952-3278(94)90005-1

Cited by 13 publications

(9 citation statements)

References 24 publications

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“…On the whole, the chemosensitivity to lactic acid of the parietal pleura seems to prevail. This is not surprising because the bacterial synthesis of lactic acid is present in most of pleural effusions (27,29), and its synthesis may also originate from the pleural inflammatory mesothelial cells (16,23). Thus the present observations of modest respiratory effects elicited by pleural inflammation compared with the marked inhibitory action of mechanical pleural stimulation agree with clinical observations that mostly associate pleuritic symptoms to mechanical stimulation of the pleural cavity.…”

Section: Discussionsupporting

confidence: 81%

Respiratory and circulatory effects of parietal pleural afferent stimulation in rabbits

Jammes

Delpierre²

2006

Journal of Applied Physiology

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Jammes, Yves, and Stéphane Delpierre. Respiratory and circulatory effects of parietal pleural afferent stimulation in rabbits. J Appl Physiol 100: 1539 -1546, 2006; doi:10.1152/japplphysiol.01422.2005. -Respiratory symptoms accompanying pleural diseases combine dyspnea, tachypnea, rapid shallow breathing, and sometimes hypotension. There are no experimental data on the changes in respiratory and circulatory functions elicited by the activation of pleural afferents. After removal of all muscles covering the 5th to 10th intercostal spaces, we investigated in paralyzed, vagotomized rabbits the changes in phrenic discharge, transpulmonary pressure, and systemic arterial pressure in response to an outwardly directed force exerted on the parietal pleura or the local application of solutions containing lactic acid or inflammatory mediators. Mechanical stimulation of the pleura induced an immediate decrease in both integrated phrenic discharge and arterial blood pressure, the responses being positively correlated with the magnitude of force applied on the pleura. No accompanying changes in ventilatory timing, transpulmonary pressure, or heart rate were measured. Lactic acid solution also elicited an inhibition of phrenic activity and a fall in blood pressure. Section of the internal intercostal nerves supplying the stimulated intercostal spaces totally abolished the responses to mechanical stimulation or lactic acid. An inflammatory mixture elicited only modest respiratory and circulatory effects. We concluded that an acute mechanical distension of the parietal pleura as well as its chemical stimulation by lactic acid elicit a marked inhibition of phrenic motoneurons combined to a reduction of the sympathetic outflow to the circulatory system. pleura; sensory innervation; phrenic activity; circulatory control IN A PREVIOUS STUDY IN RABBITS, we identified afferents in internal intercostal nerves that were activated by mechanical and/or chemical stimulation of the thoracic pleura (19). The nerve responses were attributed to the selective activation of pleural afferents because they existed after complete removal of all muscles covering the studied intercostal spaces. Because the conduction velocity of these afferents ranged between 0.5 and 14 m/s, we deduced that they belonged to the group III (thin myelinated) and IV (unmyelinated) fibers. Most units (97%) were activated by mechanical stimulation of the pleura (local positive pressure range ϭ 4.5 to 8.5 cmH 2 O), and we found a linear relationship between the discharge rate of afferents and the force applied to the thoracic wall. However, only 29% of this nerve population was purely mechanosensitive. The other units also responded to lactic acid and/or inflammatory mediators and were considered multimodal receptors. The response to lactic acid was roughly proportional to its concentration.Pleural diseases cause pain, dyspnea, tachypnea, and rapid shallow breathing, and sometimes hypotension, which only occurs under specific circumstances, e.g., tension pneumothorax, over...

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Section: Discussionsupporting

confidence: 81%

Respiratory and circulatory effects of parietal pleural afferent stimulation in rabbits

Jammes

Delpierre²

2006

Journal of Applied Physiology

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“…Resolution of inflammation and repair of the serosa without fibrosis requires a downregulation of the inflammatory response, including inhibition of fibroblast proliferation and collagen production. Mesothelial cells are likely to contribute to controlling inflammation both in normal and inflamed tissue because they have cyclo‐oxygenase (COX) activity, 126 expressing COX‐1 and COX‐2 mRNA, 127,128 and metabolize arachidonic acid to release prostaglandins and prostacyclin 127,129–132 . Exposure of mesothelial cells to macrophage‐conditioned medium or the cytokines IL‐1β and TNF‐α resulted in an increase in the levels of both COX‐1 and COX‐2 mRNA, with the greatest increase being seen for COX‐2 127 …”

Section: Inflammationmentioning

confidence: 99%

“…Mesothelial cells are likely to contribute to controlling inflammation both in normal and inflamed tissue because they have cyclo-oxygenase (COX) activity, 126 expressing COX-1 and COX-2 mRNA, 127,128 and metabolize arachidonic acid to release prostaglandins and prostacyclin. 127,[129][130][131][132] Exposure of mesothelial cells to macrophage-conditioned medium or the cytokines IL-1b and TNF-a resulted in an increase in the levels of both COX-1 and COX-2 mRNA, with the greatest increase being seen for COX-2. 127…”

Section: Inflammationmentioning

confidence: 99%

Mesothelial cells: Their structure, function and role in serosal repair

2002

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Mesothelial cells: Their structure, function and role in serosal repair MUTSAERS SE. Respirology 2002; 7: 171-191 The mesothelium is composed of an extensive monolayer of specialized cells (mesothelial cells) that line the body's serous cavities and internal organs. Traditionally, this layer was thought to be a simple tissue with the sole function of providing a slippery, non-adhesive and protective surface to facilitate intracoelomic movement. However, with the gradual accumulation of information about serosal tissues over the years, the mesothelium is now recognized as a dynamic cellular membrane with many important functions. These include transport and movement of fluid and particulate matter across the serosal cavities, leucocyte migration in response to inflammatory mediators, synthesis of pro-inflammatory cytokines, growth factors and extracellular matrix proteins to aid in serosal repair, release of factors to promote both the deposition and clearance of fibrin, and antigen presentation. Furthermore, the secretion of molecules, such as glycosaminoglycans and lubricants, not only protects tissues from abrasion, but also from infection and possibly tumour dissemination. Mesothelium is also unlike other epithelial-like surfaces because healing appears diffusely across the denuded surface, whereas in true epithelia, healing occurs solely at the wound edges as sheets of cells. Although controversial, recent studies have begun to shed light on the mechanisms involved in mesothelial regeneration. In the present review, the current understanding of the structure and function of the mesothelium and the biology of mesothelial cells is discussed, together with recent insights into the mechanisms regulating its repair.

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“…Potent mitogens for fibroblasts include PDGF, FGF, and epithelial growth factor (EGF). Inhibitors of fibroblast growth include prostaglandin E 2 , which can be produced by pleural mesothelial cells [37]. IFN-γ may have either an inhibitory or a stimulatory effect on the growth of pleural fibroblasts.…”

Section: Changes In Pleural Cell Populationsmentioning

confidence: 99%

Pathophysiology of the Pleura

Jantz

Antony²

2008

Respiration

111

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The pleural mesothelial cell is an essential cell in maintaining the normal homeostasis of the pleural space and it is also a central component of the pathophysiologic processes affecting the pleural space. In this review, we will review the defense mechanisms of the pleural mesothelium and changes in pleural physiology as a result of inflammatory, infectious, and malignant conditions with a focus on cytokine and chemokine networks. We will also review the processes involved in the pathogenesis of pleural fibrosis.

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Mesothelial cell modulation of pleural repair: Thrombin stimulated mesothelial cells release prostaglandin E2

Cited by 13 publications

References 24 publications

Respiratory and circulatory effects of parietal pleural afferent stimulation in rabbits

Respiratory and circulatory effects of parietal pleural afferent stimulation in rabbits

Mesothelial cells: Their structure, function and role in serosal repair

Pathophysiology of the Pleura

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