Pulmonary Alveolar Epithelial Changes in Response to Freund's Adjuvant

Faulkner, Charles S.; Esterly,; John, R. W. Govan

doi:10.21236/ad0868356

Cited by 15 publications

(22 citation statements)

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“…First, the pro- (24,25). The intravenous administration of Freund's adjuvant to rabbits resulted in Type II cells that contained larger and more numerous lamellar bodies (39). Likewise, the lungs of rats exposed to cigarette smoke for 25 days contained hypertrophic lype II cells with increased numbers of lamellar bodies (40).…”

Section: The Type 11 Cellmentioning

confidence: 99%

Hypertrophy and Hyperplasia of Alveolar Type II Cells in Response to Silica and Other Pulmonary Toxicants

Miller¹,

Hook²

1990

Environmental Health Perspectives

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Section: The Type 11 Cellmentioning

confidence: 99%

Hypertrophy and Hyperplasia of Alveolar Type II Cells in Response to Silica and Other Pulmonary Toxicants

Miller¹,

Hook²

1990

Environmental Health Perspectives

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“…A prominent feature of the pulmonary response to intravenous complete Freund's adjuvant in the rabbit is the proliferation of type-I1 pneumonocytes [8,15,281. Alveolar epithelial hyperplasia was seen in bovine lungs beginning about 72 hours post-adjuvant injection.…”

Section: Discussionmentioning

confidence: 99%

“…Granuloma formation is a characteristic feature of the pulmonary response to intravenous complete Freund's adjuvant in the calf and other species [8,15,20,28,29,36,391. In this study, granuloma formation occurred by seven days post-adjuvant injection and remained prominent for the remainder of the 30-day observation interval.…”

Section: Discussionmentioning

confidence: 99%

“…After fixation, 15 samples of lung tissue were trimmed for embedding according to a predetermined sampling procedure. Two tissue samples (one dorsal and one ventral) were taken from standardized areas of each lobe, except that only one sample was taken from the accessory lobe.…”

Section: Specimen Preparationmentioning

confidence: 99%

“…The pulmonary response to intravenous complete Freund's adjuvant has been detailed in various species [5,8,11,15,16,19,20,28,29,36,391. It is characterized by a pronounced acute inflammatory reaction and limited mononuclear cell infiltration of the pulmonary interstitium and meets the criteria of uniformity and reproducibility.…”

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confidence: 99%

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The Bovine Pulmonary Inflammatory Response: Adjuvant Pneumonitis in Calves

Lay

Slauson

1982

Vet Pathol

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Abstract. Twenty one-to two-month-old Holstein, Angus, or Holstein-Angus crossbred calves were given intravenous complete Freund's adjuvant and their lungs were examined at 24 hours to 30 days post-injection. Two calves given intravenous saline served as normal controls. The evolving pulmonary inflammatory response was characterized initially by multifocal vasculitis and acute multifocal exudative pneumonitis which progressed to a granulomatous interstitial pneumonitis by seven days post-injection. Discrete granulomas characterized the lesions in the lungs and lymph nodes at 30 days post-injection, and granulomas also were seen in liver, kidney, and spleen. Clinically, the calves were tachypneic and pyrexic during the first week post-injection. Four calves developed acute pulmonary edema and died during, or shortly after, administration of the adjuvant. This model of experimental pneumonia in calves is similar to complete Freund's adjuvant-induced experimental pneumonia in other species. It is reproducible and predictable in its course of development and resolution, and provides a useful model for studying basic mechanisms of pulmonary inflammatory injury and repair in the bovine lung.In comparison to other domestic species, cattle seem particularly susceptible to inflammatory pulmonary disease, possibly as a consequence of multiple factors including anatomic peculiarities and functional differences in pulmonary defense mechanisms [41]. In order to study the basic mechanisms involved in the development and resolution of acute inflammatory lesions in the bovine lung and their impact on pulmonary clearance mechanisms, it is necessary to utilize a uniformly reproducible, controllable and, ideally, noninfectious experimental model of pulmonary injury.Various infectious agents including Pasteurellu sp. [ 17, 181, parainfluenza virus type 3 [9], infectious bovine rhinotracheitis virus [22], and bovine respiratory syncytial virus [27], have been used to induce experimental pneumonia in cattle and calves. The use of these agents, however, necessitates isolation facilities and special precautions in handling of animals and tissues, and the disease produced by such agents often is difficult to reproduce uniformly.A variety of noninfectious agents including 3-methylindole [lo], L-tryptophan [ 13, 371, 4-ipomeanol [ 14, 32, 451 and the "perilla ketone" [25, 461 as well as NO2 gas [ 121 506

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Pulmonary sarcoidosis: A clinico‐pathological study

Judd

Finnegan

Curran

1975

The Journal of Pathology

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The light and electron microscopic changes in biopsy tissue from the lung of a 30-year-old housewife severeley incapacitated by diffuse pulmonary sarcoidosis with pulmonary hypertension are presented. The lung tissue was distorted by numerous granulomas in the interstitial tissues and within alveoli. Many pulmonary blood vessels including arteries were damaged by the granulomas. The ultrastructural features of the epithelioid cells were found to be distinctive and probably specific. The giant cells which accompanied the epithelioid cells contained two types of inclusion body: one appeared to be related to the Schaumann body but the nature and origin of the second type was not clear. Many of the granulomas were surrounded by avascular fibrous tissue which contained, in addition to mature fibroblasts, myofibroblasts and a primitive form of cell that appeared to be a fibroblast precursor. It was conjectured that the myofibroblasts, through their contractile powers, might increase the distortion of the lung architecture and thereby the patient's disability. The alveolar walls were thickened by a diffuse infiltrate of macrophages and epithelioid cells but there was no excess of collagen and elastic fibres. The evidence suggested that the epithelioid cells developed from macrophages. From the cellular nature of the diffuse infiltration of the alveolar walls and the absence of fibrosis it seemed that the disease was still at an early and active stage, a conclusion strengthened by the fact that treatment with corticosteroids led to marked and sustained clinical improvement.

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Pulmonary Alveolar Epithelial Changes in Response to Freund's Adjuvant

Cited by 15 publications

References 1 publication

Hypertrophy and Hyperplasia of Alveolar Type II Cells in Response to Silica and Other Pulmonary Toxicants

Hypertrophy and Hyperplasia of Alveolar Type II Cells in Response to Silica and Other Pulmonary Toxicants

The Bovine Pulmonary Inflammatory Response: Adjuvant Pneumonitis in Calves

Pulmonary sarcoidosis: A clinico‐pathological study

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