Deep vein thrombosis (DVT) is

We immunohistochemically examined neutrophils and macrophages in venous thrombi, which developed in the ligation of the inferior vena cava (IVC). Myeloperoxidase (MPO)-positive neutrophils and F4/80-positive macrophages were detected in the whole course of thrombi after IVC ligation. Morphometrically, the number of neutrophils was greatest at 1 day after IVC ligation and, thereafter, gradually decreased with an increase of the post-ligation interval. In contrast, the number of macrophages peaked at 7 days after ligation. The number of intrathrombus neutrophils was significantly higher than that of intrathrombus macrophages at 1 and 3 days, and the average ratios of neutrophils to macrophages (N/M ratios) were 6.8 +/- 1.1 (4.8-9.0) and 2.5 +/- 0.4 (1.7-4.2) at 1 and 3 days, respectively. After more than 5 days, all samples had N/M ratios of <2.0 (0.2-1.4). These observations suggest that an N/M ratio of >2.0 indicates a thrombus age of 1-3 days. To differentiate between 1- and 3-day-old thrombi, an N/M ratio markedly exceeding 5.0 strongly indicates an age of 1 day. Furthermore, an N/M ratio of 1.0 or less probably indicates an age of more than 5 days. The present study demonstrated that the immunohistochemical detection of intrathrombus neutrophils and macrophages was suitable to determine the age of venous thrombi.

TNF-Rp55-KO mice exhibited impaired alkali-induced CNV through reduced intracorneal infiltrating macrophage VEGF and iNOS expression.

The potential role of macrophages in pulmonary fibrosis (PF) prompted us to evaluate the roles of CX3CR1, a chemokine receptor abundantly expressed in macrophages during bleomycin (BLM)-induced PF. Intratracheal BLM injection induced infiltration of leukocytes such as macrophages into the lungs, which eventually resulted in fibrosis. CX3CR1 expression was mainly detected in the majority of macrophages and in a small portion of α-smooth muscle actin-positive cells in the lungs, while CX3CL1 was expressed in macrophages. BLM-induced fibrotic changes in the lungs were reduced without any changes in the number of leukocytes in Cx3cr1 −/− mice, as compared with those in the wild-type (WT) mice. However, intrapulmonary CX3CR1+ macrophages displayed pro-fibrotic M2 phenotypes; lack of CX3CR1 skewed their phenotypes toward M1 in BLM-challenged lungs. Moreover, fibrocytes expressed CX3CR1, and were increased in BLM-challenged WT lungs. The number of intrapulmonary fibrocytes was decreased in Cx3cr1 −/− mice. Thus, locally-produced CX3CL1 can promote PF development primarily by attracting CX3CR1-expressing M2 macrophages and fibrocytes into the lungs.

No abstract