Ultrastructural and cytochemical evaluation of sepsis-induced changes in the rat pulmonary intravascular mononuclear phagocytes
acid-phosphatase; Anatomy & Morphology; Blood; cells; coagulation; differentiation; endotoxin; expression; host defence; human macrophage; lung uptake; monocytes; mononuclear phagocyte system; surface-coat
Sepsis stimulates an increase in the number and activity of mononuclear phagocytes in systemic host-defence organs. The present study was conducted to define the ultrastructural and cytochemical characteristics of the mononuclear phagocytes that sequester in the lung microvasculature of septic rats, Fourteen rats were challenged with a single intraperitoneal injection of saline (0.5 ml/100 g), E. coli (2 x 10(7)/100 g) or glucan (4 mg/100 g), and euthanased 2, 4, or 7 d later. The lungs were inflation fixed and processed for transmission electron microscopy. Cellular morphology was used to identify the intravascular mononuclear phagocytes and acid phosphatase (AcPase) expression was monitored as an index of cellular differentiation and activation. Control rats contained a limited number of monocytes in the pulmonary vasculature. In contrast, large numbers of activated mononuclear phagocytes were seen in the microvasculature within 48 h of treatment with either microbial product. The recruited pulmonary intravascular mononuclear phagocytes (PIMP) exhibited AcPase-reactive Golgi complexes, accumulation of secretory vesicles and other features of cell activation consistent with enhanced biosynthetic activity. Subsequent electron microscopy, conducted 4 and 7 d posttreatment, suggested that a progressive decline in the number and activity of PIMPs then occurred. In order to quantify the sepsis-induced accumulation of AcPase-positive PIMP, the experimental challenges were repeated in 11 rats and, 48 h later, tissue samples were evaluated by light microscopy for tartrate-insensitive acid phosphatase. Control rats exhibited 0.148 +/- 0.107 AcPase-positive PIMP/alveoli. E. coli and glucan challenged animals exhibited significant (P < 0.01) increases in AcPase-positive mononuclear phagocytes, with 0.782+/-0.073 and 0.636+/-0.170 PIMP/alveoli respectively, The results demonstrate that focal sepsis stimulates a significant, but transient, recruitment of activated mononuclear phagocytes into the rat pulmonary microvasculature.
Singh B; Doane K J; Niehaus G D
Journal of Anatomy
1998
1998-01
Journal Article
<a href="http://doi.org/10.1046/j.1469-7580.1998.19210013.x" target="_blank" rel="noreferrer noopener">10.1046/j.1469-7580.1998.19210013.x</a>
Suppression Of Pulmonary Metastases Of Rat Mammary-cancer By Recombinant Urokinase Plasminogen-activator Inhibitor
adenocarcinomas; breast; cells; colon; extracellular-matrix degradation; invasion; membrane; model; monocytes; receptor-bound urokinase; Surgery
Evans D M; Lin P L
American Surgeon
1995
1995-08
Journal Article or Conference Abstract Publication
n/a
Plaque-associated myeloid cells derive from resident microglia in an Alzheimer's disease model
accumulation; distinct; dynamics; fate; macrophages; monocytes; pathology; reveals; system; turnover
Alzheimer's disease (AD) is accompanied by a robust inflammatory response mediated by plaque-associated myeloid cells of the brain. These cells exhibit altered gene expression profiles and serve as a barrier, preventing neuritic dystrophy. The origin of these cells has been controversial and is of therapeutic importance. Here, we genetically labeled different myeloid populations and unequivocally demonstrated that plaque-associated myeloid cells in the AD brain are derived exclusively from resident microglia, with no contribution from circulating peripheral monocytes.
Reed-Geaghan Erin G; Croxford Andrew L; Becher Burkhard; Landreth Gary E
Journal of Experimental Medicine
2020
2020-04
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
journalArticle
<a href="http://doi.org/10.1084/jem.20191374" target="_blank" rel="noreferrer noopener">10.1084/jem.20191374</a>