Morphometric Evaluation of Ultrastructural Changes in Type II Alveolar Cells of Rat Lung Produced by Bromhexine

Respiration ◽  
1971 ◽  
Vol 28 (5) ◽  
pp. 438-456 ◽  
Author(s):  
J. Gil ◽  
U. Thurnheer
Keyword(s):  
Ultrastructural Changes ◽  
Type Ii ◽  
Rat Lung ◽  
Alveolar Cells ◽  
Type Ii Alveolar Cells ◽  
Morphometric Evaluation

Differentiating Type i and Type ii Alveolar Cells in Rat Lung by OsO4NaI Staining

1970 ◽  
Vol 45 (5) ◽  
pp. 215-219 ◽  
Author(s):  
William F. McNary ◽  
Al-Walid El-Bermani
Keyword(s):  
Type I ◽  
Type Ii ◽  
Rat Lung ◽  
Alveolar Cells ◽  
Type Ii Alveolar Cells

scholarly journals Bradykinin Stimulates Type II Alveolar Cells to Release Neutrophil and Monocyte Chemotactic Activity and Inflammatory Cytokines

1998 ◽  
Vol 153 (6) ◽  
pp. 1885-1893 ◽  
Author(s):  
Sekiya Koyama ◽  
Etsuro Sato ◽  
Hiroshi Nomura ◽  
Keishi Kubo ◽  
Masakazu Miura ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Chemotactic Activity ◽  
Type Ii ◽  
Alveolar Cells ◽  
Type Ii Alveolar Cells

PM2.5-induced lung inflammation in mice: Differences of inflammatory response in macrophages and type II alveolar cells

2017 ◽  
Vol 37 (10) ◽  
pp. 1203-1218 ◽  
Author(s):  
Miao He ◽  
Takamichi Ichinose ◽  
Seiichi Yoshida ◽  
Tomohiro Ito ◽  
Cuiying He ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Lung Inflammation ◽  
Type Ii ◽  
Alveolar Cells ◽  
Type Ii Alveolar Cells

scholarly journals CD8+ T Cell–mediated Injury In Vivo Progresses in the Absence of Effector T Cells

2001 ◽  
Vol 194 (12) ◽  
pp. 1835-1846 ◽  
Author(s):  
Barbara A. Small ◽  
Sarah A. Dressel ◽  
Christopher W. Lawrence ◽  
Donald R. Drake ◽  
Mark H. Stoler ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Tissue Injury ◽  
Cd8 T Cell ◽  
Effector T Cells ◽  
Type Ii ◽  
Pulmonary Injury ◽  
Alveolar Cells ◽  
Type Ii Alveolar Cells

Tissue injury is a common sequela of acute virus infection localized to a specific organ such as the lung. Tissue injury is an immediate consequence of infection with lytic viruses. It can also result from the direct destruction of infected cells by effector CD8+ T lymphocytes and indirectly through the action of the T cell–derived proinflammatory cytokines and recruited inflammatory cells on infected and uninfected tissue. We have examined CD8+ T cell–mediated pulmonary injury in a transgenic model in which adoptively transferred, virus-specific cytotoxic T lymphocytes (CTLs) produce lethal, progressive pulmonary injury in recipient mice expressing the viral target transgene exclusively in the lungs. We have found that over the 4–5 day course of the development of lethal pulmonary injury, the effector CTLs, while necessary for the induction of injury, are present only transiently (24–48 h) in the lung. We provide evidence that the target of the antiviral CD8+ T cells, the transgene expressing type II alveolar cells, are not immediately destroyed by the effector T cells. Rather, after T cell–target interaction, the type II alveolar cells are stimulated to produce the chemokine monocyte chemoattractant protein 1. These results reinforce the concept that, in vivo, the cellular targets of specific CTLs may participate directly in the development of progressive tissue injury by activating in response to interaction with the T cells and producing proinflammatory mediators without sustained in vivo activation of CD8+ T cell effectors.

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