The histology of experimental pleural injury with tetracycline, empyema, and carrageenan

Strange, Charlie; Tomlinson, James R.; Wilson, Clay; Harley, Russell A.; Miller, K. Scott; Sahn, Steven A.

doi:10.1016/0014-4800(89)90020-8

Cited by 58 publications

(31 citation statements)

References 36 publications

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“…Mesothelial cells undergo significant morphologic changes during the repair process, adopting a "reactive" cuboidal morphology shortly after serosal injury (8). With normal repair, they revert to a squamous morphology and no significant functional impairment results.…”

Section: Introductionmentioning

confidence: 99%

“…With normal repair, they revert to a squamous morphology and no significant functional impairment results. When severe mesothelial cell injury occurs, the likelihood of fibrosis and its pathophysiologic consequences increases (8). It has been demonstrated that mesothelial cells have the capacity to directly participate in fibrin deposition and fibrinolysis (9-1 1 ).…”

Section: Introductionmentioning

confidence: 99%

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Metalloproteinases and tissue inhibitor of metalloproteinases in mesothelial cells. Cellular differentiation influences expression.

Marshall¹,

Santana²,

Xu³

et al. 1993

J. Clin. Invest.

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Mesothelial cells play a critical role in the remodeling process that follows serosal injury. Although mesothelial cells are known to synthesize a variety of extracellular matrix components including types I, III, and IV collagens, their potential to participate in matrix degradation has not been explored. We now report that human pleural and peritoneal mesothelial cells express interstitial collagenase, 72-and 92-kD gelatinases (type IV collagenases), and the counterregulatory tissue inhibitor of metalloproteinases (TIMP). Our initial characterization of the mesothelial cell metalloenzymes and TIMP has revealed: (a) they are likely identical to corresponding molecules secreted by other human cells; (b) they are secreted rather than stored in an intracellular pool; (c) a primary site of regulation occurs at a pretranslational level; (d) phorbol myristate acetate, via activation of protein kinase C, upregulates expression of collagenase, 92-kD gelatinase, and TIMP, but has no effect on expression of 72-kD gelatinase; and (e) lipopolysaccharide fails to upregulate the biosynthesis of either metalloproteinases or TIMP. Of particular interest is the observation that the state of cellular differentiation has a striking influence on the expression of metalloenzymes and TIMP, such that epithelioid cells display a more matrix-degradative phenotype (increased 92-kD gelatinase and decreased TIMP) than their fibroblastoid counterparts. We speculate that mesothelial cells directly participate in the extracellular matrix turnover that follows serosal injury via elaboration of metalloproteinases and TIMP. Additionally, the reactive cuboidal mesothelium which is characteristic of the early response to serosal injury may manifest a matrix-degradative phenotype favoring normal repair rather than fibrosis. (J. Clin. Invest. 1993. 91:1792-1799

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Metalloproteinases and tissue inhibitor of metalloproteinases in mesothelial cells. Cellular differentiation influences expression.

Marshall¹,

Santana²,

Xu³

et al. 1993

J. Clin. Invest.

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“…A number of drugs and physical agents, such as tetracycline, minocycline, Corynebacterium parvum, talc, bleomycin, nitrogen mustard, doxorubicin, quinacrine, and radioactive colloid gold, have been employed in order to decrease or prevent fluid accumulation in the pleural cavity (for review see [71,72]). Although the mechanisms underlying drug-induced pleural symphysis are not well understood and may differ depending on the sclerosing agent used, increasing evidence suggests that an inflammatory reaction may play an important role.…”

Section: Pleurodesismentioning

confidence: 99%

Immunobiology of pleural inflammation: potential implications for pathogenesis, diagnosis and therapy

Kroegel¹,

Antony²

1997

Eur Respir J

186

132

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“…The drugs carrageenan and tetracycline prompt dramatic increase in PlMs (e.g. Sahn and Potts, 1978;Ackerman et al, 1980;Strange et al, 1989;Baumann et al, 1993) by recruiting monocytes from the peripheral circulation (Antony et al, 1985). In vivo experiments have demonstrated tumoricidal- (Basic et al, 1979;Nagashima et al, 1987), phagocytic- (Meuret et al, 1980;Zlotnik et al, 1982;Zlotnik and Crowle, 1982), and antimicrobial activities of the PlMs (Meuret et al, 1980;Hammerstrom, 1980;Zlotnik and Crowle, 1982).…”

Section: Pleural Macrophages (Plms)mentioning

confidence: 99%

Cellular Defences of the Lung: Comparative Perspectives

Maina¹

2012

Respiratory Diseases

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'Our lungs are highly complex organs that are exquisitely specialized for gas exchange and host defense.' Rawlins (2010) 1. Introduction General considerationsThe most important function of the lung is to acquire molecular oxygen and eliminate carbon dioxide. Except probably for the gastrointestinal system, no other organ in the body interacts with the external environment as constantly and as intimately as the respiratory system. For example, during a 24 hour period, at rest, the human lung is ventilated ~25,000 times with ~20,000 L of air (e.g. Burri, 1985; Brain, 1996), it has a respiratory surface area (RSA) of ~140 m 2 (about the size of a tennis court) which is located in the acini that lie no more than 40 to 50 cm from the external environment (air) (e.g. Weibel, 1984), and the thickness of the blood-gas (tissue) barrier (BGB) (harmonic mean thickness, ht) is 0.62 μm, a value about one-fiftieth of the thickness of a foolscap paper or that of a human head hair (Gehr et al., 1978(Gehr et al., , 1990a. By weight, each day, more than 20 kg of air enters and leaves the human body, a load that far exceeds that of food and water ingested during the same time period (Brain, 1996). Depending on the level of air pollution, different types and quantities of foreign particulates and microbial pathogens are inhaled. While large RSA and thin BGB increase gas exchange, the concomitant downside to these structural properties is that they make the lung a leading portal of entry and therefore attack by pathogenic micro-organisms, damage by allergens and particulates, and injury by noxious gases (e.g. Brain, , 1992Lambrecht et al. 2001;Garn et al., 2006). The inhaled particulates are deposited on the epithelial lining of the conducting airways and that of the peripheral air spaces where they are retained for various durations before they are removed or destroyed (e.g. Geiser et al., 1988; Gehr et al., 1990 a, b). Brain (1996) observed that 'the lung is unique in that the marriage between environment and lung disease is profound. The respiratory system threfore forms a huge challenge to the body's immune integrity (e.g. von Garnier and Nicod, 2009 , 1993;Schwartz, 1994;Brunekreef et al., 1995;Ware, 2000;Pope, 2000;Nemmar et al., 2002;Pope et al., 2002;Suwa et al., 2002;Schulz et al., 2005;Kaufman, 2010;Brook et al., 2010; van den Hooven et al., 2011;Kampfrath et al., 2011 gc.ca/ccdpc-cpcmc/crdmrc/facts_gen_e.html). According to the Canadian Lung Association (CLA), the economic burden of respiratory disease in the Country is ~3 billion ($US) dollars (http://www.bukisa.com/articles/455926_lung-health-occupational-healthincidence#ixzz1I4jwMvBX). Based on net changes in gross domestic product (GDP) growth forecasts, the estimated annual cost of SARS (Sudden Avian Respiratory Syndrome) in Asia exceeds 10 billion dollars ($US) (Lee and McKibbin, 2003;Fan, 2003;McKibbin and Sidorenko, 2006) and according to the World Bank's estimates, an influenza pandemic may result in a loss (expenditure) of 800 billion dollars ($US) (Brahm...

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The histology of experimental pleural injury with tetracycline, empyema, and carrageenan

Cited by 58 publications

References 36 publications

Metalloproteinases and tissue inhibitor of metalloproteinases in mesothelial cells. Cellular differentiation influences expression.

Metalloproteinases and tissue inhibitor of metalloproteinases in mesothelial cells. Cellular differentiation influences expression.

Immunobiology of pleural inflammation: potential implications for pathogenesis, diagnosis and therapy

Cellular Defences of the Lung: Comparative Perspectives

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