Nonsteroidal Anti-Inflammatory Drugs Alter the Human Mesothelial Pleural Permeability via Ion Cellular Transportation by Inhibiting Prostaglandin Synthesis

Kouritas, Vasileios; Zisis, Charalambos; Bellenis, Ion; Gourgoulianis, Konstantinos; Molyvdas, Paschalis-Adam; Hatzoglou, Chrissi

doi:10.1159/000336837

Cited by 8 publications

(8 citation statements)

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“…Although these studies did not include a mapping of the expression in pleura as shown e.g., on functional level (Kouritas et al, 2008), they might become important for the understanding of pathophysiological regulatory mechanisms of transcellular pleural transport, shown for histamine and prostaglandins, recently (Kouritas et al, 2011, 2012). …”

Section: Transport and Barrier Mechanisms In Pleura Mesotheliummentioning

confidence: 99%

Tight junction physiology of pleural mesothelium

Markov

Amasheh

2014

Front. Physiol.

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Pleura consists of visceral and parietal cell layers, producing a fluid, which is necessary for lubrication of the pleural space. Function of both mesothelial cell layers is necessary for the regulation of a constant pleural fluid volume and composition to facilitate lung movement during breathing. Recent studies have demonstrated that pleural mesothelial cells show a distinct expression pattern of tight junction proteins which are known to ubiquitously determine paracellular permeability. Most tight junction proteins provide a sealing function to epithelia, but some have been shown to have a paracellular channel function or ambiguous properties. Here we provide an in-depth review of the current knowledge concerning specific functional contribution of these proteins determining transport and barrier function of pleural mesothelium.

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Section: Transport and Barrier Mechanisms In Pleura Mesotheliummentioning

confidence: 99%

Tight junction physiology of pleural mesothelium

Markov

Amasheh

2014

Front. Physiol.

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“…Decreases in production of prostaglandins play a critical role in subsequently decreasing the permeability of the pleura, leading to increased pleural fluid and reduction in clearance of pathogens 11, 14, 23 . NSAIDs might also paradoxically increase inflammatory response within the lungs, as indicated by greater white blood cell migration, in particular, neutrophils 13, 14 . It is also possible that the use of NSAIDs can decrease severity of symptoms of respiratory infection, thereby delaying hospitalization and proper treatment 3, 12 …”

Section: Discussionmentioning

confidence: 99%

“…Observational studies have indicated an increased risk of pneumonia complications associated with NSAIDs in this patient population 3–12 . It has also been hypothesized that NSAIDs, like ibuprofen, can induce proinflammatory cascades that may increase inflammatory response within the lungs, as indicated by greater white blood cell migration, particularly neutrophils 13, 14 …”

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confidence: 98%

Non‐steroidal Anti‐inflammatory Drugs and the Risk of Pneumonia Complications: A Systematic Review

et al. 2020

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There have been concerns regarding the safety of nonsteroidal antiinflammatory drugs (NSAIDs) in patients with respiratory infections. However, to date, the quality of the evidence has not been systematically assessed. The purpose of this systematic review was to evaluate the role of NSAIDs on pneumonia complications. OVID MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, Database of Abstracts of Reviews of Effects, and Google Scholar were searched. Studies that examined pneumonia complications in patients who had taken NSAIDs before onset of symptoms were identified. Quality assessment was conducted using the Risk of Bias in Non‐randomized Studies – of Interventions (ROBINS‐I) assessment tool, which was adapted to include biases that were pertinent to this question. The search strategy identified 1721 potential studies through the 5 primary databases and searching reference lists. Of these, 10 studies met the inclusion criteria, including 5 nested case‐control studies, 2 population‐based case‐control studies, and 3 cohort studies. In total, 59,724 adults were included from 4 of the studies (range = 57–59,250) and 1217 children from 5 studies (range = 148–540). All studies demonstrated a positive association; in adults (odds ratio/risk ratio range = 1.8–8.1) and children (odds ratio/risk ratio range = 1.9–6.8). Studies were limited by moderate or serious risk of confounding bias, exposure misclassification, and protopathic biases and sparse data bias. The results of this review demonstrate that published studies on the effect of NSAIDs use and risk of pneumonia complications are subject to a number of biases. These results should not be extrapolated as evidence of harm for NSAIDs, including ibuprofen, in respiratory ailments but highlight the need for more methodologically robust studies to evaluate this potential relationship.

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“…NSAIDs were shown to hinder pleural permeability ex vivo, by inhibiting prostaglandin synthesis and eventually blocking the epithelial sodium channel ENaC and the Na þ / K þÀ ATPase activity normally operating in the pleura [30]. In vivo experiments also demonstrated that NSAIDs limited the absorption of provoked hydrothoraces, by reducing the acute and late absorption rate and thus the volume of the hydrothorax eventually absorbed [29,31]. Additionally, NSAIDs induced increased white cell migration within the pleural cavity with a higher percentage of neutrophils present, indicating the initiation of an inflammatory response in the remaining hydrothorax [29,31].…”

Section: Discussionmentioning

confidence: 99%

“…In vivo experiments also demonstrated that NSAIDs limited the absorption of provoked hydrothoraces, by reducing the acute and late absorption rate and thus the volume of the hydrothorax eventually absorbed [29,31]. Additionally, NSAIDs induced increased white cell migration within the pleural cavity with a higher percentage of neutrophils present, indicating the initiation of an inflammatory response in the remaining hydrothorax [29,31]. It is highly likely that NSAIDs have a similar effect in parapneumonic effusions; their effects on ENaC and Na þ ÀK þ ATPase decrease the absorption rate of the pleural fluid and pathogen clearance allowing potential pathogens to lead to complicated pleural effusion [32].…”

Section: Discussionmentioning

confidence: 99%