Cytopathology of Viral Diseases

Cheville, N. F.; Lehmkuhl, Howard D.

doi:10.1002/9780813810379.ch13

Cited by 29 publications

(48 citation statements)

References 222 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The stimulus for this lesion may be damage to the preexisting epithelium due to exposure to ROS or a direct stimulation of the cells that produce certain enzymes. Clara cells are rich in catabolic enzymes, especially those of the pulmonary cytochrome P450 family (Cheville, 1994;Tritscher et al, 2000). CYP1A1 is induced by dioxins and its levels were increased in lung samples from treated animals in this study (data not shown).…”

Section: Immunohistochemical Staining For Gstpimentioning

confidence: 71%

“…Scattered among these are rounder, more cuboidal cells, the type II alveolar epithelial cells. When type I cells are damaged, the repair process of the lung is usually one of proliferation of type II alveolar epithelial cells (Cheville, 1994). In chronic toxicity and carcinogenicity studies in rodents, this proliferation of type II cells is often diagnosed as alveolar epithelial hyperplasia (AEH).…”

Section: Immunohistochemical Staining For Gstpimentioning

confidence: 99%

See 1 more Smart Citation

Characterization of Bronchiolar Metaplasia of the Alveolar Epithelium in Female Sprague—Dawley Rats Exposed to 3,3',4,4',5-Pentachlorobiphenyl (PCB126)

et al. 2004

View full text Add to dashboard Cite

To test the dioxin toxic equivalency factor methodology, the National Toxicology Program conducted a series of 2-year rat bioassays of dioxin-like compounds. Following gavage exposure of female Harlan Sprague-Dawley rats to 2,3 ,4,4 ,5-pentachlorobiphenyl (PCB126), pulmonary alveolar epithelium at the junction of terminal bronchioles and along alveolar ducts was replaced by cuboidal to columnar ciliated cells. Scattered among these were cells exhibiting characteristics consistent with those of Clara cells; they lacked cilia and had a smooth apical surface that protruded into the alveolar space. This lesion was not typical of alveolar epithelial hyperplasia seen in rodent lungs; therefore, studies were done to characterize the lesion. Results of periodic acid-Schiff (PAS) staining, alcian blue (AB) staining, and GSTPi immunohistochemical staining of the lesions seen in treated rats were more similar to normal bronchiolar epithelium than normal alveolar epithelium or alveolar epithelial hyperplasia. These findings, along with the morphology of the cells, provide evidence that this lesion is closer in character to bronchiolar epithelium than alveolar type I or alveolar type II epithelium, and as a result, was called bronchiolar metaplasia.

show abstract

Section: Immunohistochemical Staining For Gstpimentioning

confidence: 71%

Section: Immunohistochemical Staining For Gstpimentioning

confidence: 99%

Characterization of Bronchiolar Metaplasia of the Alveolar Epithelium in Female Sprague—Dawley Rats Exposed to 3,3',4,4',5-Pentachlorobiphenyl (PCB126)

et al. 2004

View full text Add to dashboard Cite

show abstract

“…The distribution of the ECM in the alveolar septa was analyzed subjectively and categorized as either ''concentric'' (surrounding the capillary endothelium and widening the distance between the capillary and alveolar epithelium) or ''eccentric'' (widening the interstitium but displacing the capillary so that it remains closely apposed to one side of the alveolar epithelium). 3 The amount of trichrome-stained collagen was subjectively evaluated and ranked on a scale of 1-5 with five being the most severe. The same scale was used to score the amount of elastin-Norris, Naydan, and Wilson stained septal tissue.…”

Section: Light Microscopic Evaluationmentioning

confidence: 99%

“…Histologically, however, the interstitium of the alveolar septa is defined as the space between the alveolar epithelial cells and the capillaries. 3,13 A variety of alterations in injury and repair in interstitial pneumonia may lead to a common progression toward interstitial fibrosis. 4 The process of fibrosis in the alveolar parenchyma often has an insidious onset and uncertain etiology.…”

mentioning

confidence: 99%

Interstitial Lung Disease in West Highland White Terriers

2005

View full text Add to dashboard Cite

Abstract. Progressive respiratory failure and pulmonary fibrosis in West Highland White Terriers (WHWT) is an apparently genetic disorder of unknown pathogenesis. This study characterizes the light microscopic, ultrastructural, and immunohistochemical features of affected WHWT in comparison with lesions in usual interstitial pneumonia (UIP) of humans. Lesions in WHWT were confined to the expansion of the interstitial space of alveolar septa by extracellular matrix (ECM) determined to be mixtures of type-I and -III collagens. Features of UIP such as intra-alveolar fibroblastic foci, subpleural distribution, and honeycombing were not observed in six WHWT. Comparison with normal dogs showed no apparent increase in septal myofibroblasts. Ultrastructually, the ECM in alveolar septa consisted of large aggregates of periodic collagen filaments underlying alveolar capillaries that were surrounded by thick bands of amorphous to fine fibrillar matrix. This study suggests that chronic pulmonary disease of WHWT is a result of aberrant collagen regulation.

show abstract

“…The objectives of this selected topic review were 2-fold: (1) to describe the components of virus-induced lesions at both the cellular and organhsue level and to point out the contributions of both the inflammatory and immune response to the histogenesis of these lesions; and (2) to emphasize the subtle and long-term effects of viral infections upon various physiological functions and the similarities of action between viruses and chemicals using immunomodulation as the model system.…”

Section: Discussionmentioning

confidence: 99%

Immunity, Viral Pathology and Assessment of Immune Dysfunction in Virology and Toxicology

Krakowka

1987

Toxicol Pathol

View full text Add to dashboard Cite

General patterns of tissue injury are recognized as characteristic for certain groups of viruses and certain types of host/virus interactions. Acute viral infections, limited in time and space, tend to be accompanied by florid but brief virus replication cycles in tissues and lesions or signs of disease are largely attributable to the cytolytic effects of the virus on host cells. Chronic or persistent viral diseases tend to have low (or difficult to detect) levels of infectious virus on tissues and the lesions tend to be dominated by inflammation, antiviral immune responses and/or host tissue proliferation. At the cellular level, 3 general categories of response to viral infection are recognized: acute cellular swelling with eventual cytolysis, persistent infection, and transformation (neoplastic) infection. Acute cellular swelling may be accompanied by syncytial giant cell formation and/or viral inclusion bodies. Cells persistently infected with viruses though morphologically normal, are increasingly recognized as functionally deficient and may eventually display degenerative change. Transformation to neoplastic growth can be both benign or malignant in cellular expression. In vivo, the initial neutrophilic inflammatory response to virus-induced cellular necrosis is transient and is rapidly superseded by virus-specific inflammation mediated by both humoral and cellular factors and supplemented by the numerous inflammation amplification pathways. Vasculitis, a common but frequently unappreciated event, may produce nonspecific tissue damage via hemorrhage and ischemia in addition to providing a mechanism for egress of inflammatory factors into the areas of virus-induced cellular damage. During the healing phase, repair by substitution (e.g., fibrosis and scarring) or by proliferation of uninfected replacement cells may dominate sites of viral infection. Functional effects of viruses upon infected hosts are more common than is ordinarily appreciated and, in general, tend to involve control networks such as the nervous, endocrine and immune systems. In this regard, the similarities of mechanisms and effects of the actions of viruses and chemicals on lymphoid tissue are striking. The net systemic effects of these agents may well be enhanced susceptibility to infectious disease, altered responses to toxic agents, and greater sensitivity to chemically-mediated neoplastic transformation.

show abstract

Cytopathology of Viral Diseases

Cited by 29 publications

References 222 publications

Characterization of Bronchiolar Metaplasia of the Alveolar Epithelium in Female Sprague—Dawley Rats Exposed to 3,3',4,4',5-Pentachlorobiphenyl (PCB126)

Characterization of Bronchiolar Metaplasia of the Alveolar Epithelium in Female Sprague—Dawley Rats Exposed to 3,3',4,4',5-Pentachlorobiphenyl (PCB126)

Interstitial Lung Disease in West Highland White Terriers

Immunity, Viral Pathology and Assessment of Immune Dysfunction in Virology and Toxicology

Contact Info

Product

Resources

About