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

Kroegel, Claus; Antony, Veena B.

doi:10.1183/09031936.97.10102411

Cited by 187 publications

(142 citation statements)

References 68 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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“…Given the above-mentioned studies and the fact that carrageenan-induced pleural inflammation is a well-established model of acute lung injury [48,53,54], it is tempting to speculate that adenosine and inosine acting through adenosine A 2B receptors increase the endothelial barrier protection, reducing the loss of fluid to pleural cavity, consequently reducing pleural exudation.…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory effects of purine nucleosides, adenosine and inosine, in a mouse model of pleurisy: evidence for the role of adenosine A2 receptors

Lapa

Silva

Cabrini

et al. 2012

Purinergic Signalling

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Adenosine and its metabolite, inosine, have been described as molecules that participate in regulation of inflammatory response. The aim of this study was to investigate the effect of adenosine and inosine in a mouse model of carrageenan-induced pleurisy as well as the participation of adenosine receptors in this response. Injection of carrageenan into the pleural cavity induced an acute inflammatory response characterized by leukocyte migration, pleural exudation, and increased release of interleukin-1β and tumor necrosis factor-α in pleural exudates. The treatment with adenosine (0.3-100 mg/kg, i.p.) and inosine (0.1-300 mg/ kg, i.p.) 30 min before carrageenan injection reduced significantly all these parameters analyzed. Our results also demonstrated that A 2A and A 2B receptors seem to mediate the adenosine and inosine effects observed, since pretreatment with selective antagonists of adenosine A 2A (ZM241385) and A 2B (alloxazine) receptors, reverted the inhibitory effects of adenosine and inosine in pleural inflammation. The involvement of A 2 receptors was reinforced with adenosine receptor agonist CGS21680 treatment, since its anti-inflammatory effects were reversed completely and partially with ZM241385 and alloxazine injection, respectively. Moreover, the combined treatment with subeffective dose of adenosine (0.3 mg/kg) and inosine (1.0 mg/kg) induced a synergistic anti-inflammatory effect. Thus, based on these findings, we propose that inosine contributes with adenosine to exert anti-inflammatory effects in pleural inflammation, reinforcing the notion that endogenous nucleosides play an important role in controlling inflammatory diseases. This effect is likely mediated by the activation of adenosine A 2 subtype receptors and inhibition of production or release of pro-inflammatory cytokines.

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“…These discrepancies are probably due to the fact that different models and parameters of mAbs were used in these different studies for assessing the outcome of infection [17]. As one of the most frequent types of PF, TP develops when M. tuberculosis releases antigenic proteins into the pleural space and involves the migration of immune cells to the site of disease [18,19]. Therefore, TP is a suitable model for understanding the localized and systemic characteristics of B cells that are observed during M. tuberculosis infection.…”

Section: Discussionmentioning

confidence: 99%

B lymphocytes that migrate to tuberculous pleural fluid via the SDF‐1/CXCR4 axis actively respond to antigens specific for Mycobacterium tuberculosis

Feng

Liu

et al. 2011

Eur J Immunol

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B-cell biology has been largely uncharacterized in the field of tuberculosis (TB). In this study, we investigated the immunophenotypical and functional characteristics of B cells obtained from the pleural fluid (PF) and peripheral blood of patients with tuberculous pleuritis (TP). Our results indicated that the total numbers of B cells, CD271 memory B cells and plasmablasts were clearly lower in the PF than in peripheral blood. Furthermore, we found significantly higher expression of CXCR4 on B cells in the PF, and a chemotaxis assay showed that B cells in the PF were more responsive to stromal cell-derived factor-1 (SDF-1) than B cells from peripheral blood. In addition, SDF-1 levels in PF were remarkably high compared with SDF-1 levels in plasma, suggesting that the SDF-1/CXCR4 axis might facilitate the migration of circulating B cells into tuberculous pleural space. Importantly, we observed that significantly more antibodies were produced by B cells in the PF following stimulation with BCG, early secretory antigenic target (ESAT-6)/culture filtrate protein-10 (CFP-10) or ESAT-6 protein.Collectively, these data demonstrate that Mycobacterium tuberculosis-specific B cells exist at local sites of infection in TP patients and this localization might influence the immune response to M. tuberculosis. Key words: B cells . Chemokine receptors . Immune responses . Tuberculous pleuritis Supporting Information available onlineIntroduction Tuberculosis (TB), one of the oldest infectious diseases associated with humans, is a chronic disease caused by infection with Mycobacterium tuberculosis [1,2]. The incidence of TB has increased during the past 20 years for reasons such as insufficient prevention efforts, incorrectly prescribed medication, the emergence of drug-resistant strains of M. tuberculosis and the prevalence of human immunodeficiency virus (HIV) infection [3,4]. Traditionally, the immune response against M. tuberculosis infection is dominated by cell-mediated immunity (CMI), which relies primarily on CD4 1 and CD8 1 T cells. Therefore, many studies have been conducted in an attempt to augment cellular immunity, with an aim to develop new vaccine candidates against TB [5][6][7]. In contrast to these investigations, the contribution of B cells and humoral immunity in the TB field remains largely unexamined and elusive. Fewer efforts to promote an effective humoral response against M. tuberculosis have been made compared with those devised to elicit a cellular response [8]. However, it is worth noting that any successful, novel vaccine strategy against TB will have to properly invoke both humoral and cellular immunity, given that these responses are the two critical arms of adaptive immunity and always collaborate to repel infectious pathogens [9]. Numerous murine studies have shown that B cells and antibodies have pleiotropic activities and display previously underappreciated roles during M. tuberculosis infection [10][11][12]. In contrast to the murine studies, there are limited data regarding any phenotypic and...

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

Abstract: The understanding of these processes and the sequence of events leading to pleural loculation, pleural adhesion or repair are likely to provide the basis for early therapeutic intervention and reduce pleural-associated morbidity.

Cited by 187 publications

References 68 publications

Respiratory and circulatory effects of parietal pleural afferent stimulation in rabbits

Respiratory and circulatory effects of parietal pleural afferent stimulation in rabbits

Anti-inflammatory effects of purine nucleosides, adenosine and inosine, in a mouse model of pleurisy: evidence for the role of adenosine A2 receptors

B lymphocytes that migrate to tuberculous pleural fluid via the SDF‐1/CXCR4 axis actively respond to antigens specific for Mycobacterium tuberculosis

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