Acute Immunologic Pulmonary Alveolitis

Johnson, Kent J.; Ward, Peter A.

doi:10.1172/jci107770

Cited by 195 publications

(125 citation statements)

References 15 publications

(14 reference statements)

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“…Vascular permeability was quantitated by the degree of extravasation of '"I-labeled murine serum albumin (MSA). This method is similar to assays that have proved to be useful in measures of lung and dermal inflammation (16,17). 1Z51-labeled MSA was injected intravenously (4 pCi per mouse) and, after 1 hour, the accumulation of radiolabel in the knee joints was measured using the device described for 9 y m T~ measurement.…”

Section: Methodsmentioning

confidence: 99%

An experimental model for hydrogen peroxide–induced tissue damage. Effects of a single inflammatory mediator on (peri)articular tissues

Schalkwijk

Berg

Putte

et al. 1986

Arthritis & Rheumatism

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Hydrogen peroxide is receiving increasing attention as a mediator of tissue damage during inflammation. To evaluate its destructive potential in vivo, we devised a model in which hydrogen peroxide is, initially, the sole mediator of tissue damage. Glucose oxidase, which was made cationic to obtain good retention in tissue, was injected intraarticularly in mouse knee joints. This enzyme produces hydrogen peroxide, using endogenous glucose as a substrate. The local production of hydrogen peroxide induced drastic vascular damage, as measured by 99mTc uptake and leakage of 125I‐albumin. The chondrocyte proteoglycan synthesis was severely inhibited, as measured by 35SO4 incorporation. Histologic examination showed impressive inflammatory and degenerative changes, including periarticular infiltration, chondrocyte death, subchondral erosions, and muscle necrosis. Intraarticular administration of catalase could inhibit these vascular effects and cartilage damage. Systemic administration of ebselen, a synthetic glutathione peroxidase‐like compound, provided partial protection. Indomethacin and piroxicam were not effective in the acute phase. We think this model is useful both for testing drugs that are purported to act as scavengers of hydrogen peroxide and for studying chronic destructive processes.

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Section: Methodsmentioning

confidence: 99%

An experimental model for hydrogen peroxide–induced tissue damage. Effects of a single inflammatory mediator on (peri)articular tissues

Schalkwijk

Berg

Putte

et al. 1986

Arthritis & Rheumatism

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“…[1][2][3][4][5][6][7][8][9][10][11] Although inflammation is a natural host response to infection and injury, excessive or unresolved inflammatory processes can play a role in cell injury and tissue remodeling with severe pathological consequences. For example, leukocytes such as neutrophils, eosinophils, and monocytes have been implicated as mediators of lung and vascular injury, [12][13][14][15][16][17] although the extent to which inflammatory cells and mediators directly cause lung cell injury or modulate development of fibrosis remains controversial.…”

mentioning

confidence: 99%

Direct Leukocyte Migration across Pulmonary Arterioles and Venules into the Perivascular Interstitium of Murine Lungs during Bleomycin Injury and Repair

Wang

Kachel

Cesta

et al. 2011

The American Journal of Pathology

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During acute lung injury and repair, leukocytes are thought to enter the lung primarily across alveolar capillaries and postcapillary venules. We hypothesized that leukocytes also migrate across pulmonary arterioles and venules, which serve as alternative sites for leukocyte influx into the lung during acute lung injury and repair. Lung sections from C57BL/6J mice up to 14 days after intratracheal bleomycin (3.33 U/kg) or saline instillation were assessed by light, fluorescence, confocal, and transmission electron microscopy for evidence of inflammatory cell sequestration and transmigration at these sites. After bleomycin treatment, large numbers of leukocytes (including neutrophils, eosinophils, and monocytes) were present in the vascular lumina and in perivascular interstitia of pulmonary arterioles and venules, as well as within the vascular walls. Leukocytes were observed within well-defined pathways in arteriolar walls and much less structured pathways in venular walls, apparently in the process of transmigration. Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were expressed at sites of leukocyte interaction with the luminal surface, especially in arterioles. Leukocytes appeared to exit from the vessels near collagen fibers into the perivascular interstitium. Results indicate that leukocytes can directly migrate across arteriolar and venular walls into the perivascular interstitium, which may represent an important but under-recognized pathway for leukocyte influx into the lung during injury and repair.

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“…Details of the techniques are given elsewhere (2). In some experiments, the permeability changes were determined by the intravenous injection of 20 ,tg homologous rat IgG isolated from normal rat serum and labeled with 125I (11). A given sample of 1251_ IgG containing 105 cpm was injected intravenously together with the BSA into each animal.…”

Section: Methodsmentioning

confidence: 99%

“…The degree of permeability in 2-h Arthus reactions was expressed as the amount of radioactivity (determined by gamma ray emission in a crystal scintillation counter) in a 25-mm skin site. These procedures have been described in detail in a recent publication (11). Vascular damage in the 4-h reaction sites was determined by measurements of diameters of hemorrhage.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Suppression of immune complex-induced inflammation by the chemotactic factor inactivator.

Johnson¹,

Anderson²,

Ward³

1977

J. Clin. Invest.

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Acute Immunologic Pulmonary Alveolitis

Abstract: A B S T R A C

Cited by 195 publications

References 15 publications

An experimental model for hydrogen peroxide–induced tissue damage. Effects of a single inflammatory mediator on (peri)articular tissues

An experimental model for hydrogen peroxide–induced tissue damage. Effects of a single inflammatory mediator on (peri)articular tissues

Direct Leukocyte Migration across Pulmonary Arterioles and Venules into the Perivascular Interstitium of Murine Lungs during Bleomycin Injury and Repair

Suppression of immune complex-induced inflammation by the chemotactic factor inactivator.

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