scholarly journals Acute and chronic bovine pulmonary edema and emphysema in Uruguay

2018 ◽  
Vol 38 (10) ◽  
pp. 1929-1934
Author(s):  
Ricardo A. Costa ◽  
Carlos Schild ◽  
Caroline S. Silveira ◽  
Melissa Macías-Rioseco ◽  
Santiago Mirazo ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Wall Thickening ◽  
Alveolar Wall ◽  
Dictyocaulus Viviparus ◽  
Eosinophilic Infiltrate ◽  
Pleural Surface ◽  
Type Ii Pneumocytes ◽  
Respiratory Noises ◽  
Subcutaneous Edema ◽  
Cut Surface

ABSTRACT: An outbreak of pulmonary edema and emphysema with acute and chronic cases is reported in a farm in Uruguay. In a herd of 40 Hereford steers, 20 died. The deaths began four days after a change of paddock, from an old pasture of Avena sativa to a lush growing pasture of the same grass. Acutely affected animals showed severe dyspnea, sialorrhea, cough, and subcutaneous edema, and died within 72 hours. Chronically affected steers showed dyspnea, respiratory noises, weight loss, and intolerance to exercise. The deaths began four days after the change of paddock. Ten days after the first death, the steers were withdrawn from the pasture, but continued dying throughout the following 40 days. Twenty animals died and six were necropsied. Grossly, the lungs were diffusely armed and glistening, with reddish and crepitant cut surface, and presented alveolar septae sharply distended by edema and emphysema. There was subpleural emphysema with air blebs distributed across the pleural surface. Presence of Dictyocaulus viviparus was observed in three steers. In some animals, the trachea was diffusely reddish with presence of pink foam; in some others, there was bloody liquid in the tracheal lumen. Histologic examination showed severe diffuse alveolar and interstitial emphysema, hyaline membranes adhered to the alveolar wall, thickening of the interlobular septae with proliferation of type II pneumocytes, and moderate-to-severe multifocal histiocytic, neutrophilic and eosinophilic infiltrate. In the trachea, there was submucosal hemorrhage and moderate multifocal eosinophilic and lymphocytic infiltrate. The steers with chronic signs presented similar lung lesions, but multifocal pulmonary fibrosis and cardiac dilatation were also observed. The diagnosis of acute bovine pulmonary emphysema and edema (ABPE) was based on the occurrence of the disease after introduction of the herd in a lush green pasture, on the characteristic gross and histologic lesions, and on the absence of other toxic or infectious agents causing similar lesions. Cattle raisers should be alert to the risks of occurrence of this disease after the introduction of the herds into paddocks with green and lush pastures.

scholarly journals Endogenous Hydrogen Sulfide Is an Important Factor in Maintaining Arterial Oxygen Saturation

2021 ◽  
Vol 12 ◽  
Author(s):  
Yan Huang ◽  
Gang Wang ◽  
Zhan Zhou ◽  
Zhengshan Tang ◽  
Ningning Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Wall Thickening ◽  
Alveolar Wall ◽  
Leukocyte Infiltration ◽  
Wild Type ◽  
Interstitial Edema ◽  
And Oxidative Stress

The gasotransmitter H2S is involved in various physiological and pathophysiological processes. The aim of this study was to investigate the physiological functions of H2S in the lungs. In the model of mouse with genetic deficiency in a H2S natural synthesis enzyme cystathionine-γ-lyase (CSE), we found that arterial oxygen saturation (SaO2) was decreased compared with wild type mice. Hypoxyprobe test showed that mild hypoxia occurred in the tissues of heart, lungs and kidneys in Cse-/- mice. H2S donor GYY4137 treatment increased SaO2 and ameliorated hypoxia state in cardiac and renal tissues. Further, we revealed that lung blood perfusion and airway responsiveness were not linked to reduced SaO2 level. Lung injury was found in Cse-/- mice as evidenced by alveolar wall thickening, diffuse interstitial edema and leukocyte infiltration in pulmonary tissues. IL-8, IL-1β, and TNF-α levels were markedly increased and oxidative stress levels were also significantly higher with increased levels of the pro-oxidative biomarker, MDA, decreased levels of the anti-oxidative biomarkers, T-AOC and GSH/GSSG, and reduced superoxide dismutase (SOD) activity in lung tissues of Cse-/- mice compared with those of wild type mice. GYY4137 treatment ameliorated lung injury and suppressed inflammatory state and oxidative stress in lung tissues of Cse-/- mice. A decrease in SaO2 was found in normal mice under hypoxia. These mice displayed lung injury as evidenced by alveolar wall thickening, interstitial edema and leukocyte infiltration. Increased levels of inflammatory cytokines and oxidative stress were also found in lung tissues of the mice with hypoxia insult. GYY4137 treatment increased SaO2 and ameliorated lung injury, inflammation and oxidative stress. Our data indicate that endogenous H2S is an important factor in maintaining normal SaO2 by preventing oxidative stress and inflammation in the lungs.

scholarly journals Exposure to Atmospheric Ultrafine Particles Induces Severe Lung Inflammatory Response and Tissue Remodeling in Mice

2019 ◽  
Vol 16 (7) ◽  
pp. 1210 ◽  
Author(s):  
Yara Saleh ◽  
Sébastien Antherieu ◽  
Romain Dusautoir ◽  
Laurent Y. Alleman ◽  
Jules Sotty ◽  
...  
Keyword(s):  
Ultrafine Particles ◽  
Chronic Exposure ◽  
Time Course ◽  
Fine Particles ◽  
Respiratory Health ◽  
Wall Thickening ◽  
Alveolar Wall ◽  
Similar Chemical ◽  
Time Course Experiment ◽  
Severe Lung

Exposure to particulate matter (PM) is leading to various respiratory health outcomes. Compared to coarse and fine particles, less is known about the effects of chronic exposure to ultrafine particles, despite their higher number and reactivity. In the present study, we performed a time-course experiment in mice to better analyze the lung impact of atmospheric ultrafine particles, with regard to the effects induced by fine particles collected on the same site. Trace element and PAH analysis demonstrated the almost similar chemical composition of both particle fractions. Mice were exposed intranasally to FF or UFP according to acute (10, 50 or 100 µg of PM) and repeated (10 µg of PM 3 times a week during 1 or 3 months) exposure protocols. More particle-laden macrophages and even greater chronic inflammation were observed in the UFP-exposed mice lungs. Histological analyses revealed that about 50% of lung tissues were damaged in mice exposed to UFP for three months versus only 35% in FF-exposed mice. These injuries were characterized by alveolar wall thickening, macrophage infiltrations, and cystic lesions. Taken together, these results strongly motivate the update of current regulations regarding ambient PM concentrations to include UFP and limit their emission.

Unusual inflammatory and fibrogenic pulmonary responses to single-walled carbon nanotubes in mice

2005 ◽  
Vol 289 (5) ◽  
pp. L698-L708 ◽  
Author(s):  
Anna A. Shvedova ◽  
Elena R. Kisin ◽  
Robert Mercer ◽  
Ashley R. Murray ◽  
Victor J. Johnson ◽  
...  
Keyword(s):  
Carbon Nanotubes ◽  
Single Walled Carbon Nanotubes ◽  
Wall Thickening ◽  
Raw 264.7 ◽  
Alveolar Wall ◽  
Raw 264.7 Macrophages ◽  
Single Walled Carbon ◽  
Tnf Α ◽  
Walled Carbon Nanotubes ◽  
Tgf Β1

Single-walled carbon nanotubes (SWCNT) are new materials of emerging technological importance. As SWCNT are introduced into the life cycle of commercial products, their effects on human health and environment should be addressed. We demonstrated that pharyngeal aspiration of SWCNT elicited unusual pulmonary effects in C57BL/6 mice that combined a robust but acute inflammation with early onset yet progressive fibrosis and granulomas. A dose-dependent increase in the protein, LDH, and γ-glutamyl transferase activities in bronchoalveolar lavage were found along with accumulation of 4-hydroxynonenal (oxidative biomarker) and depletion of glutathione in lungs. An early neutrophils accumulation ( day 1), followed by lymphocyte ( day 3) and macrophage ( day 7) influx, was accompanied by early elevation of proinflammatory cytokines (TNF-α, IL-1β; day 1) followed by fibrogenic transforming growth factor (TGF)-β1 (peaked on day 7). A rapid progressive fibrosis found in mice exhibited two distinct morphologies: 1) SWCNT-induced granulomas mainly associated with hypertrophied epithelial cells surrounding SWCNT aggregates and 2) diffuse interstitial fibrosis and alveolar wall thickening likely associated with dispersed SWCNT. In vitro exposure of murine RAW 264.7 macrophages to SWCNT triggered TGF-β1 production similarly to zymosan but generated less TNF-α and IL-1β. SWCNT did not cause superoxide or NO·production, active SWCNT engulfment, or apoptosis in RAW 264.7 macrophages. Functional respiratory deficiencies and decreased bacterial clearance ( Listeria monocytogenes) were found in mice treated with SWCNT. Equal doses of ultrafine carbon black particles or fine crystalline silica (SiO2) did not induce granulomas or alveolar wall thickening and caused a significantly weaker pulmonary inflammation and damage.

scholarly journals An alteration of the gut-liver axis drives pulmonary inflammation after intoxication and burn injury in mice

2014 ◽  
Vol 307 (7) ◽  
pp. G711-G718 ◽  
Author(s):  
Michael M. Chen ◽  
Anita Zahs ◽  
Mary M. Brown ◽  
Luis Ramirez ◽  
Jerrold R. Turner ◽  
...  
Keyword(s):  
Bacterial Translocation ◽  
Burn Injury ◽  
Pulmonary Inflammation ◽  
Bacterial Load ◽  
Total Body Surface Area ◽  
Alcohol Exposure ◽  
Hepatic Damage ◽  
Wall Thickening ◽  
Alveolar Wall ◽  
Gut Barrier Function

Approximately half of all adult burn patients are intoxicated at the time of their injury and have worse clinical outcomes than those without prior alcohol exposure. This study tested the hypothesis that intoxication alters the gut-liver axis, leading to increased pulmonary inflammation mediated by burn-induced IL-6 in the liver. C57BL/6 mice were given 1.2 g/kg ethanol 30 min prior to a 15% total body surface area burn. To restore gut barrier function, the specific myosin light chain kinase inhibitor membrane-permeant inhibitor of kinase (PIK), which we have demonstrated to reduce bacterial translocation from the gut, was administered 30 min after injury. Limiting bacterial translocation with PIK attenuated hepatic damage as measured by a 47% reduction in serum alanine aminotransferase ( P < 0.05), as well as a 33% reduction in hepatic IL-6 mRNA expression ( P < 0.05), compared with intoxicated and burn-injured mice without PIK. This mitigation of hepatic damage was associated with a 49% decline in pulmonary neutrophil infiltration ( P < 0.05) and decreased alveolar wall thickening compared with matched controls. These results were reproduced by prophylactic reduction of the bacterial load in the intestines with oral antibiotics before intoxication and burn injury. Overall, these data suggest that the gut-liver axis is deranged when intoxication precedes burn injury and that limiting bacterial translocation in this setting attenuates hepatic damage and pulmonary inflammation.

scholarly journals Acute and 30-day oral toxicity studies of a novel coccidiostat – ethanamizuril

2019 ◽  
Vol 8 (5) ◽  
pp. 686-695 ◽  
Author(s):  
Wenlong Xiao ◽  
Xiaoyang Wang ◽  
Chunmei Wang ◽  
Mi Wang ◽  
Chenzhong Fei ◽  
...  
Keyword(s):  
Clinical Signs ◽  
Female Rats ◽  
Male Rats ◽  
Wall Thickening ◽  
High Dose ◽  
Alveolar Wall ◽  
Oral Toxicity ◽  
Male And Female Rats ◽  
Adverse Effect Level ◽  
Ld50 Value

Abstract Ethanamizuril is a novel triazine compound that exhibits remarkable anticoccidial activity. Owing to its pharmacological properties, this study was conducted to evaluate the acute and 30-day oral toxicity of ethanamizuril. In the acute study, ethanamizuril was administered once by oral gavage to mice and rats. The calculated LD50 values for mice and rats were 5776 and 4743 mg per kg b.w, respectively, but the LD50 value for male rats was higher than that of female rats. In the subchronic study, male and female rats were fed with diets supplemented with 0, 20, 60 or 120 mg kg−1 ethanamizuril for 30 days. Treatment related clinical signs of alopecia on the back and neck of the animals were observed in the 60 and 120 mg kg−1 dose groups from the third week of treatment. Significant differences in haematological and biochemical parameters as well as organ-to-body weight ratios were detected between the 60 and 120 mg kg−1 groups. Histopathological observations revealed that 60 and 120 mg kg−1 ethanamizuril could induce focal hepatocellular necrosis and split phase. Slight renal tubule protein casts in the kidneys and alveolar wall thickening in the lungs were also observed in the high dose groups of both genders. The dietary no-observed-adverse-effect level (NOAEL) of ethanamizuril for 30 days was 20 mg kg−1 feed.

THE PULMONARY SYNDROME OF WILSON AND MIKITY

PEDIATRICS ◽  
1965 ◽  
Vol 36 (3) ◽  
pp. 374-384
Author(s):  
Paul R. Swyer ◽  
Maria Delivoria-Papadopoulos ◽  
Henry Levison ◽  
Bernard J. Reilly ◽  
John U. Balis
Keyword(s):  
Work Of Breathing ◽  
Respiratory Acidosis ◽  
Minute Volume ◽  
Lung Mechanics ◽  
Arterial Oxygen ◽  
Wall Thickening ◽  
Alveolar Wall ◽  
Electron Microscopic ◽  
Elastic Resistance ◽  
Immature Lung

Eight examples of the Wilson-Mikity Syndrome are reported, 2 of whom died at 127 and 145 days of age respectively. The radiology of the condition is relatively specific and gives strong grounds for suspicion of the diagnosis when taken in the clinical context. Gross, histological, and electron microscopic examinations reveal areas of normality, emphysema, and immaturity. The electron microscope additionally shows areas where the alveolar wall thickening is due to the presence of smooth muscle, reticulin, and collagen. The most likely etiology is a disorder in postnatal alveolar development related to premature birth and functional use of an immature lung. There are changes in lung mechanics with decreased compliance and increased non-elastic resistance to airflow mainly in expiration. The mechanical work of breathing is increased. There is a respiratory acidosis in spite of an increased minute volume. Arterial oxygen desaturation is common, increased by crying and only partially relieved by oxygen. Large R → L shunts have been demonstrated which are probably intrapulmonary.

Smoking-Related “Interstitial” Lung Disease

2014 ◽  
Vol 139 (8) ◽  
pp. 974-977 ◽  
Author(s):  
Teri J. Franks ◽  
Jeffrey R. Galvin
Keyword(s):  
Lung Injury ◽  
Cigarette Smoke ◽  
Cigarette Smoke Exposure ◽  
Wall Thickening ◽  
Alveolar Wall ◽  
Cigarette Smokers ◽  
Pulmonary Langerhans Cell Histiocytosis ◽  
Airway Injury ◽  
Wide Range ◽  
Arteriolar Wall

Context Emphysema, respiratory bronchiolitis, desquamative interstitial pneumonia, pulmonary Langerhans' cell histiocytosis, small-airway injury including submucosal and adventitial fibrosis, increased bronchus-associated lymphoid tissue, and small artery/arteriolar wall thickening are recognized histologic findings in cigarette smokers. It has only recently been acknowledged that the range of lung injury from cigarette smoke is wider than generally accepted, in particular, there is increasing recognition that fibrosis of alveolar walls occurs in smokers. Objectives To review the literature that describes the range of histologic findings in cigarette smokers and that links cigarette smoke exposure to the development of alveolar wall fibrosis. Data Sources Relevant peer-reviewed literature indexed in PubMed (National Library of Medicine) form the basis of this review. Conclusions Smokers demonstrate a wide range of lung injury at biopsy that defies simple placement within single categories, and the current categories do not adequately take into account the importance of alveolar wall and airway fibrosis.

scholarly journals Desquamative Interstitial Pneumonitis in a Healthy Non-Smoker: A Rare Diagnosis

2014 ◽  
Vol 21 (2) ◽  
pp. 86-88 ◽  
Author(s):  
Ryan R Kroll ◽  
Diane A Flood ◽  
John Srigley
Keyword(s):  
Interstitial Pneumonitis ◽  
Potato Chip ◽  
Rare Condition ◽  
Respiratory Illness ◽  
Smoking History ◽  
Tissue Sampling ◽  
Eosinophilic Infiltrate ◽  
Type Ii Pneumocytes ◽  
Rare Diagnosis ◽  
Alveolar Septa

This article reports a rare condition first described in 1965 and is most commonly associated with smoking and certain occupations. Onset of nonspecific symptoms is typically insidious and, while bloodwork and imaging may be valuable, tissue sampling is required for diagnosis. Desquamative interstitial pneumonitis most commonly affects tobacco smokers in their fourth or fifth decades of life; this article, however, describes the condition in a 27-year-old who worked in a potato chip factory.Desquamative interstitial pneumonitis is an interstitial lung disease most commonly associated with smoking. It causes respiratory symptoms including indolent cough and dyspnea. Characteristic findings on computed tomography include bilateral ground-glass opacities, septal thickening and preserved structure. Diagnosis is made by tissue sampling, which classically demonstrates alveolar macrophages, and thickened alveolar septa with an eosinophilic infiltrate lined with hyperplastic type II pneumocytes. Treatment is immune suppression with steroids or other agents, and avoiding the causal agent. The case reported describes a 27-year-old woman with no smoking history who worked in a potato chip factory, presenting with cough, dyspnea and dizziness. The patient had characteristic findings on imaging and was diagnosed via biopsy with desquamative interstitial pneumonitis. She improved clinically with reduced exposure and steroid therapy. While food production workers are at risk for respiratory illness, there are no reported cases of desquamative interstitial pneumonitis in this setting.

scholarly journals Genetic variability of T cell responses in hypersensitivity pneumonitis identified using the BXD genetic reference panel

2020 ◽  
Vol 318 (4) ◽  
pp. L631-L643 ◽  
Author(s):  
Jin Wang ◽  
Tae Won Yoon ◽  
Robert Read ◽  
Ae-Kyung Yi ◽  
Robert W. Williams ◽  
...  
Keyword(s):  
T Cells ◽  
Genetic Variability ◽  
Hypersensitivity Pneumonitis ◽  
Significant Risk ◽  
Wall Thickening ◽  
Alveolar Wall ◽  
Mesenchymal Transition ◽  
Risk Of Death ◽  
Exposed Population ◽  
Lymphoid Aggregates

Hypersensitivity pneumonitis (HP) is an interstitial lung disease that may progress to fibrosis and significant risk of death. HP develops following repeated exposures to inhaled environmental antigens; however, only a fraction of the exposed population develops the disease, suggesting that host genetics contribute to disease susceptibility. We used the BXD family of mice with the Saccharopolyspora rectivirgula (SR) model of HP to investigate the role of genetics in susceptibility to HP. The BXD family is derived from a B6 mother and a D2 father and has been used to map susceptibility loci to numerous diseases. B6, D2, and BXD progeny strains were exposed to SR for 3 wk, and the development of HP was monitored. The B6 and D2 strains developed alveolitis; however, the cellular composition was neutrophilic in the D2 strain and more lymphocytic in the B6 strain. Hematoxylin-eosin staining of lung sections revealed lymphoid aggregates in B6 lungs, whereas D2 lungs exhibited a neutrophilic infiltration. Twenty-eight BXD strains of mice were tested, and the results reveal significant heritable variation for numbers of CD4+ or CD8+ T cells in the air spaces. There was significant genetic variability for lymphoid aggregates and alveolar wall thickening. We mapped a significant quantitative trait locus (QTL) on chromosome 18 for CD8+CD69+ T cells that includes cadherin 2 ( Cdh2), an excellent candidate gene associated with epithelial-mesenchymal transition, which is upregulated in lungs of strains with HP. These results demonstrate that the BXD family is a valuable and translationally relevant model to identify genes contributing to HP and to devise early and effective interventions.

scholarly journals First evidence of Klebsiella pneumoniae infection in Aceh cattle: Pathomorphology and antigenic distribution in the lungs

2021 ◽  
Vol 14 (4) ◽  
pp. 1007-1013
Author(s):  
Darniati Darniati ◽  
Surachmi Setiyaningsih ◽  
Dewi Ratih Agungpriyono ◽  
Ekowati Handharyani
Keyword(s):  
Klebsiella Pneumoniae ◽  
Chronic Infection ◽  
Interstitial Fibrosis ◽  
Acute Infection ◽  
Bovine Mastitis ◽  
Foodborne Pathogen ◽  
Wall Thickening ◽  
Alveolar Wall ◽  
Chronic Infections ◽  
Bronchial Dilatation

Background and Aim: Klebsiella pneumoniae is an emerging zoonotic and foodborne pathogen worldwide. Hypervirulent K. pneumoniae (hvKp) was reported as the causative agent of bovine mastitis. This is the first study in Indonesia that has been conducted to determine the capsular serotype of K. pneumoniae, pulmonary gross pathology and histopathology, and distribution of hvKp in the lungs of Aceh cattle. Materials and Methods: The presence of K. pneumoniae in Aceh cattle was investigated in two slaughterhouses in Banda Aceh and Aceh Besar, Indonesia. Lung tissues with gross pathological lesions were collected from 15 cattle presenting with depression, dehydration, or cachexia. The confirmation and capsular serotyping of K. pneumoniae isolates were performed using polymerase chain reaction. The tissues were stained with hematoxylin-eosin and immunohistochemistry to observe the histopathological lesions and the distribution of the hvKp antigens. Results: The pneumonic lesions identified in the lungs of Aceh cattle included hyperemia, hemorrhage, consolidation, and atelectasis. K. pneumoniae was isolated in all 15 lung tissues with pathological pneumonic lesions. Two patterns of infection were observed histopathologically. Acute infection was characterized by hyperemia, inflammatory cell infiltration, hemorrhage, bronchiolar epithelium hyperplasia, bronchial and bronchiolar obstruction with purulent exudates, edema, and atelectasis. On the other hand, chronic infection was defined by macrophage infiltration, emphysema, bronchial dilatation, pleural fibrosis, and alveolar wall thickening by interstitial fibrosis. Immunohistochemical staining using monospecific antisera induced by the hvKp isolate confirmed the presence of K. pneumoniae-specific antigens in the acute infection, predominantly in the bronchiolar, vascular, and alveolar areas. In contrast, generally diffuse infiltrates were found in the pleura and interstitial alveolar areas in chronic infection. Conclusion: hvKp can be detected in the lungs of Aceh cattle, representing acute and chronic infections. The distribution of Klebsiella antigens in the lung tissue was consistent with the histopathological findings.

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