Pathogenic role of antigen-antibody complexes
Gabriel Virella in Medical Immunology, 2019
The clinical expression of IC disease depends on the target organs where the deposition of IC predominates: The kidney is very frequently affected (SLE, mixed cryoglobulinemia, chronic infections, poststreptococcal glomerulonephritis, purpura hypergammaglobulinemia, serum sickness, etc.), usually with glomerulonephritis as the prevailing feature.The joints are predominantly affected in rheumatoid arthritis.The skin is affected in cases of serum sickness, mixed cryoglobulinemia, purpura, and vasculitis.The large vessels are affected by the subendothelial formation of antigen-antibody complexes containing oxidized LDL and the corresponding antibodies, leading to the development or progression of atherosclerosis.The lungs are affected in extrinsic alveolitis.
Altered Regulation of Fibrinolysis in Scleroderma and Potential for Thrombolytic Therapy
Pia Glas-Greenwalt in Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
Lung involvement occurs in approximately 75% of patients.31 However, progressive lung disease leading to respiratory failure is surprisingly uncommon.32-34 A pattern of restrictive ventilatory defects and a reduced diffusing capacity for carbon monoxide is the most common finding.35-37 Early in the course of lung disease, an inflammatory component is present.38-40 This may be manifest as an alveolitis with large numbers of macrophages, lymphocytes, neutrophils, and eosinophils in bronchoalveolar aspirates.39-43 At autopsy, diffuse alveolar, interstitial, and pleural fibrosis are commonly observed. Pulmonary hypertension of varying severity brought on by gradual obliteration of the pulmonary vascular bed is typically observed in patients with widespread skin involvement.1 By comparison, approximately 5% of patients with the limited form of cutaneous disease develop severe pulmonary arterial hypertension with cor pulmonale that typically occurs in the relative absence of pulmonary fibrosis.1,44 This form of pulmonary disease is characterized by subintimal proliferative changes and medial hypertrophy of small pulmonary arteries.45
Pulmonary Fibrosis: Human and Experimental Disease
Marcos Rojkind in Connective Tissue in Health and Disease, 2017
As previously mentioned, the characteristics of alveolitis depend on the disease or group of diseases analyzed, and there may be remarkable differences among them. However, all of them share two basic features: the increase in the number of inflammatory and immune effector cells within the alveolar structures as well as shifts in the relative proportions of these cells. In order to simplify this problem, Crystal et al.3 have classified the inflammation into two types: lymphocyte alveolitis and neutrophil alveolitis. The former type is characterized by an increase of lymphocytes in lung tissue and bronchoalveolar lavage (BAL), and is generally found in granulomatous diseases such as sarcoidosis and HP. The latter type is dominated by the macrophage, but its most remarkable feature is the chronic presence of neutrophils, as occurs in IPF and asbestosis. However, it has been reported that eosinophils are frequently increased in some neutrophil alveolitis,9,19 and I believe that perhaps granulocyte alveolitis is a more appropriate term. Unfortunately, only a few ILD are well characterized, and this concept may not be representative of them all.
Pulmonary toxicity and gene expression changes in response to whole-body inhalation exposure to multi-walled carbon nanotubes in rats
Published in Inhalation Toxicology, 2022
Tina M. Sager, Christina M. Umbright, Gul Mehnaz Mustafa, Jenny R. Roberts, Marlene S. Orandle, Jared L. Cumpston, Walter G. McKinney, Theresa Boots, Michael L. Kashon, Pius Joseph
The 45 (mg/m3)h cumulative dose group of rats had minimal histological changes, i.e., small areas of focal alveolitis and airway epithelial hyperplasia in less than 25% of the MWCNT-7 exposed rats (Figure 3(B)). No granulomatous lesions were detected in this group of rats. Intra-alveolar macrophages were elevated in all exposed rats but at a much less prominent level compared with the higher dose groups of rats. Small focal areas of alveolitis with slightly increased cellularity and alveolar thickness was seen sporadically in some of the control, air exposed rats which is considered as background lesions (Figure 3(A)). The lung histology of the rats exposed to the lowest, 22.5 (mg/m3)h cumulative dose of MWCNT-7, was similar to that of the control, air exposed rats (micrograph not presented).
Protective and anti-inflammatory effect of selenium nano-particles against bleomycin-induced pulmonary injury in male rats
Published in Drug and Chemical Toxicology, 2021
Rana Shahabi, Ali Anissian, Seyed Ali Javadmoosavi, Farinaz Nasirinezhad
The right lung fixed for one week in 10% (w/v) buffered formaldehyde solution at room temperature; the tissue was dried in graded ethanol and fixed in paraffin. The paraffin-embedded tissues were cut to 4-μm thicknesses with a microtome. Stained with hematoxylin and eosin (H&E) for evaluation of histopathological changes, and Masson’s trichrome staining was performed to identify the density of the accumulated collagen fibers. All slides were examined by a certified histologist (blinded manner) using an LX400 light microscope (LaboMed, Fremont, CA) at 400 magnifications. The degree of alveolitis and inflammation was reviewed by the method suggested by Szapiel et al. (1979) (Table 2). A total of 10 fields in each slide and 10 slides in each rat were examined. The mean score of all fields in each section was considered as the inflammatory score.
High-dose immunosuppression to prevent death after paraquat self-poisoning – a randomised controlled trial
Published in Clinical Toxicology, 2018
Indika Gawarammana, Nicholas A. Buckley, Fahim Mohamed, Kamal Naser, K. Jeganathan, P. L. Ariyananada, Klintean Wunnapuk, Timothy A. Dobbins, John A. Tomenson, Martin F. Wilks, Michael Eddleston, Andrew H. Dawson
In contrast, a recent review of pathophysiological mechanisms in paraquat poisoning found neither animal models nor plausible pathophysiological explanation for why high dose immunosuppression would be effective in paraquat poisoning in humans [9]. Paraquat rapidly generates reactive oxygen species which causes cellular damage via lipid peroxidation, activation of nuclear factor kappa B, mitochondrial damage and apoptosis in many organs. This leads to rapid deterioration of renal and liver function and development of acute alveolitis. Cyclophosphamide and methylprednisolone have not been shown to have beneficial effects in scavenging free radicals during the acute stage. Nor were these treatments alone (without dexamethasone) associated with better outcomes in the large nationwide study from Taiwan [25].
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