Interstitial lung diseases of the interstitial-proliferative type

The term of "chronic interstitial pneumonia" had been more accurately redefined by Liebow and, subsequently, by Otto and had been subdivided by different pathomorphological phenomena. The interstitial-proliferative type is of particular interest, in this context. Reported in this paper is the bioptic histopathological pattern of 15 patients with interstitial lung disease of the interstitial-proliferative type, with these findings being correlated to clinical symptoms. A distinction is made between an independent form in its own right and a histologically identical interstitial phenomenon accompanying other pulmonary diseases, primarily in concomitance with lung cancer, and recordable also from postmortem investigations. Interstitial-proliferative inflammations are adequately controllable by antibiotics.     

Interstitial lung diseases: Imaging contribution to diagnosis and elementary radiological lesions

Interstitial pneumonias comprise a heterogeneous group of disorders in which a multidisciplinary approach is important for accuracy in diagnosis; indeed, one might say, even mandatory. The team of collaborators should include radiologists, because high resolution computed tomography (HRCT) of the thorax is the first, and most of times, the only imaging examination to be prescribed after chest X-ray. Elementary lesions of the interstitium can be accurately described with HRCT, inasmuch as lung windowing with sharp filtering in this technique reproduces the microscopic features of the lung. Guidance of bronchoalveolar lavage and biopsy procedures is also possible with HRCT.     

Interstitial lung disease in systemic autoimmune rheumatic diseases: a comprehensive review

Background: Interstitial lung diseases (ILDs) are among the most serious complications associated with systemic rheumatic diseases, and lead to significant morbidity and mortality; they may also be the first manifestation of connective tissue diseases (CTDs). The aim of this narrative review is to summarise the data concerning the pathogenesis of CTD/ILD and its distinguishing features in different rheumatic diseseas.

Areas covered: The pathogenesis, clinical aspects and treatment of ILD associated with rheumatic systemic diseases and CTDs were reviewed by searching the PubMed, Medline, and Cochrane Library databases for papers published between 1995 and February 2017 using combinations of words or terms. Articles not written in English were excluded.

Expert commentary: The management of CTD–ILD is challenging because of the lack of robust data regarding the treatments used, the heterogeneity of the diseases themselves, and the scarcity of well-defined outcome measures. Treatment decisions are often made clinically on the basis of functional, radiographic progression, and exacerbating factors such as age and the burden of comorbidities. Given the complexities of diagnosis and the paucity of treatment trials, the management of CTD patients with ILD requires multidisciplinary collaboration between rheumatologists and pulmonologists in CTD-ILD clinics.     

Interstitial matrix and transendothelial fluxes in normal lung

Pulmonary gas exchange critically depends upon the hydration state and the thinness of the interstitial tissue layer within the alveolo-capillary barrier. In the interstitium, fluid freely moving within the fibrous extracellular matrix equilibrates with water chemically interacting with hyaluronic acid and proteoglycans, the non-fibrillar components of the matrix. The integrity of the macromolecular assembly of the tissue matrix is required in all processes involved in establishing and maintaining the adequate interstitial tissue fluid volume, by providing: (a) a stiff three dimensional fibrous scaffold, functioning as an efficient safety factor to oppose fluid filtration into the tissue and preventing tissue fluid accumulation; (b) a restrictive perivascular and interstitial sieve with respect to plasma proteins; (c) a mechanical support to initial lymphatics. Therefore, disturbances of the deposition and/or turnover of the matrix and/or of its three dimensional architecture and composition are invariably accompanied by profound changes of the steady state tissue fluid dynamics, eventually evolving towards severe lung disease.     

Interstitial lung disease: Elementary lesions and diagnosis

An effective approach to the diagnosis of interstitial lung diseases requires a standardized method of evaluation with a structured analysis, beginning with scanning microscopy and proceeding to a more detailed assessment. This article is structured around the histologic patterns defined by Leslie that facilitate this process. They include acute injury, fibrosis, cellular infiltrates, airspace filling, formation of nodules, and minimal changes. Illustrations of all of these patterns are provided, together with a discussion of the disease entities that manifest them.     

Interstitial lung disease--the new synergy between radiology and pathology

In the last 30 years, high-resolution computed tomography (HRCT) has been the major advance in diagnosis of diffuse parenchymal lung disease (DPLD). We review the diagnostic accuracy of HRCT and discuss how the gold standard in diagnosis of DPLD has shifted from histopathological diagnosis in isolation to a multidisciplinary approach. This latter process is now accepted as providing the highest levels of diagnostic accuracy in patients with DPLD and lung biopsy is primarily reserved for cases with atypical clinical or radiological presentations.     

Interstitial fluid pressure in the isolated perfused rabbit lung

WIIG, H., OPDAHL, H., NICOLAYSEN, A. & NICOLAYSEN, G. 1985. Interstitial fluid pressure in the isolated perfused rabbit lung. Acta Physiol Scand 125 , 601–607. Received 10 March 1985, accepted 9 May 1985. ISSN 0001–6772. Department of Physiology, University of Bergen and Institute of Physiology, University of Oslo, Norway. Interstitial fluid pressure was measured in nine isolated perfused rabbit lungs with the servonull micropipette method. Bevelled glass micropipettes, with tip diameter 2–6 μm (o.d.) were inserted 2–6 mm into the left lung. At alveolar pressures of 3 to 5 cm H₂O we found mean interstitial fluid pressures of 1.0 (SD 1.0) and 1.6 (SD 1.0) cm H₂O relative to pleural pressure in the upper (n = 19) and lower (n = 21) lobes respectively. The vertical distance between the measuring sites in the upper and lower lobes was about 3 cm. Net filtration caused by elevated left atrial pressure caused practically no change in interstitial fluid pressure. Increased alveolar pressure either increased or decreased interstitial fluid pressure. The measured pressures probably represent interstitial fluid pressure in alveolar junctions or in the interstitium around small pulmonary arteries or veins. We conclude that interstitial fluid pressure in these sites is between alveolar and pleural pressure, and that it is only moderately affected by changes in alveolar pressure. The interstitial compliance appears to be high and there seem to be little or no vertical gradients in interstitial fluid pressure within the lung.     

Smoking-related interstitial lung diseases

In pulmonary pathology, a wide spectrum of morphological changes is related to the consequences of smoking, and recognizing them on surgical specimens and on small transbronchial biopsies represents a challenge for the pathologist. Respiratory bronchiolitis, also referred to as smoker's bronchiolitis, is a common histologic feature found in the lung tissue of cigarette smokers. When identified as the sole histopathologic finding in the clinical setting of symptomatic interstitial lung disease, a diagnosis of respiratory bronchiolitis-interstitial lung disease is made. Since smoking is recognized to cause a variety of histologic patterns encompassing respiratory bronchiolitis, respiratory bronchiolitis-interstitial lung disease, desquamative interstitial pneumonia and pulmonary Langerhans cell hystiocytosis, smoking-related interstitial lung disease may be a useful concept to keep in mind for the pathologists. The relationship of smoking with each of these entities has been largely established on the basis of epidemiologic evidence. Although they have been retained as distinct and separate conditions in various classifications of interstitial lung diseases, these entities share a number of clinical, radiologic, and pathologic features suggesting that they represent a spectrum of patterns of interstitial lung disease occurring in predisposed individuals who smoke. Evaluation of histologic features, particularly in surgical lung biopsy samples, is important in making the distinction between these disorders. However, even after tissue biopsy, it may sometimes be difficult to clearly separate these entities. Recently, respiratory bronchiolitis-interstitial lung disease with fibrosis has been described and postulated that this is a smoking-related condition distinct from fibrotic non-specific interstitial pneumonia.     

MicroRNA与肺部疾病

MicroRNA(miRNA)在生物的发育、疾病的发生和发展过程中扮演着重要角色,以其在生命活动中起到的调控作用而备受关注.大量研究证实miRNA与包括肺的生长发育、肺内炎性反应、肺癌、肺纤维化等在内的肺部疾病的发生和发展及转归有着密切的关联.MiRNA芯片技术是一种有效地、高通量地获取miRNA表达的手段,已经成功地...     

Interstitial and free lung cells in acute inflammation in the guinea-pig

Different cell types were studied in bronchoalveolar lavage fluid (BAL) and solid lung tissue of guineapigs. Whereas alveolar macrophages (AM) and eosinophils predominated in BAL, the proportion of AM and lymphocytes was highest in the lung tissue. After an inhalation exposure to LPS, the number of neutrophils increased rapidly in the lung tissue reaching a maximum after 4 hours, and more slowly in the airways reaching a maximum after 24 hours. This suggests that other mechanisms than secretion of chemotatic factors from AM, shown to be active up to 4 hours after exposure, are responsible for the later phase of the neutrophil invasion into the airways. Passive migration or other mediators may be involved.     

Clinical proteomics in lung diseases

Proteomics is a relatively new approach for understanding the pathology and pathogenesis of various diseases. It has also been used for characterizing the modifications in protein expression during the development of interstitial lung diseases, in lung tumors, or following exposure to exogenous stress signals. We compared the protein composition of primary human lung fibroblasts derived from patients with lung fibrosis and control fibroblasts of unaffected lung tissues. We found a predominant modulation in proteins related to the cytoskeleton, including decreased expression of vimentin and lamin A/C, and increased expression of moesin. Furthermore, we observed lower levels of components of the antioxidative system, such as omega class glutathione S-transferase and an up-regulation of an intracellular chloride channel. In fibroblasts obtained from fibrotic lungs, the expression of a major histocompatibility complex class I C was decreased, and so was the expression of tripeptidyl-peptidase-I-precursor, a collagen-degrading exopeptidase. Our results and the studies reviewed in this paper represent just the beginning of detailed studies that should unravel the relevance and the functional consequences of differential protein expressions in the diseased lung.     

NOD蛋白与肺部疾病

天然免疫系统通过识别模式识别受体(patternrecognition receptors,PRR)介导的病原相关分子模式(pathogen-associated molecular patterns,PAMP)是抗微生物宿主防御的第1道防线,在机体感染早期发挥重要的保护性作用。在近来的研究中证实除Toll样受体(toll-like receptors,TLRs)     

Redox-based therapeutics for lung diseases

Because oxidative stress is such a common factor of lung diseases, we cannot help asking why so many diseases are caused by the same oxidative stress. It is likely to be a consequence of diversity in sources and location of oxidative stress, and concomitant factors. The aim of this forum is to characterize the disease-specific involvement of oxidative stress and to make use of it for therapeutics. It is also of note that oxidative-stress biomarkers are useful tools for disease management. Exhaled nitric oxide has been established as a marker of bronchial asthma in clinical practice. By using recent noninvasive techniques, such as exhaled breath condensate, other markers of lipid peroxidation or antioxidants are now under evaluation. Antioxidant therapy, as represented by N-acetylcysteine, has widely been tested as a treatment for lung disorders, but it has had limited success in clinical practice. The clinical outcome might be improved by combination therapy or better patient selection. Novel antioxidant drugs are also under investigation. Molecular targeted therapy against redox-sensitive signaling pathways could be an alternative therapeutic approach. Moreover, disease-specific pathways have been identified whose regulation could be more efficient and less toxic than regulating universal pathways.