ライフサイエンスコーパス: hepatic macrophage

1 ar proinflammatory phenotypic alterations in hepatic macrophages.

2 egulating inflammatory signaling pathways in hepatic macrophages.

3 r production of osteopontin by NKT cells and hepatic macrophages.

4 he absence of C3a receptor, C5a receptor, or hepatic macrophages.

5 es) in activation of IkappaB kinase (IKK) in hepatic macrophages.

6 eciprocally modulated by ethanol and HA35 in hepatic macrophages.

7 ptake and destruction of RBCs by splenic and hepatic macrophages.

8 in monocytes and Kupffer cells, the resident hepatic macrophages.

9 and IFN-alpha/beta produced by LCMV-infected hepatic macrophages.

10 In mice, administration of CSF1-Fc promoted hepatic macrophage accumulation via proliferation of res

11 Treatment of hepatic macrophages after chronic ethanol feeding with s

12 creased ROS associated with CD11b+F4/80+Gr1+ hepatic macrophage aggregation, resulting in transformin

13 trated that prednisolone treatment inhibited hepatic macrophage and neutrophil infiltration in CCl4 -

14 ion analyses, we identified 2 populations of hepatic macrophages and 2 populations of monocytes.

15 ol feeding for 4 days increased apoptosis of hepatic macrophages and activated complement in both wil

16 Products of hepatic macrophages and lymphocytes are acknowledged reg

17 ion of classical and alternatively activated hepatic macrophages and natural killer T cells, in the a

18 d the proinflammatory activation of cultured hepatic macrophages and partially blocked liver injury f

19 pendent manner in both adult mouse and human hepatic macrophages and plays an integral role in facili

20 required for iron-induced IKK activation in hepatic macrophages and TAK1, PI3K, and p21ras physicall

21 ated malondialdehyde-LDL (MDA-LDL) uptake by hepatic macrophages and was associated with excess colla

22 main CCR8-expressing cells in the liver were hepatic macrophages, and CCR8 was functionally necessary

23 the efflux of recycled iron from splenic and hepatic macrophages, and the release of iron from storag

24 Circulating monocytes and hepatic macrophages are central mediators of inflammator

25 Despite the fact that resident hepatic macrophages are known to contribute to early alc

26 acetaminophen-induced injury, with resident hepatic macrophage as the main effector cells.

27 athways of fibrogenesis; (5) re-emergence of hepatic macrophages as determinants of matrix degradatio

28 Hepatic macrophage beta(2) integrin binding to beta-N-ac

29 d no induction of HSC activation pathways by hepatic macrophages but a profound activation of the NF-

30 recognition of mouse and human platelets by hepatic macrophage complement type 3 (CR3) receptors.

31 TM) accumulation is reduced by ~40%, whereas hepatic macrophage content is decreased by ~80%.

32 The level of ISG immunostaining in hepatic macrophages correlated inversely with that of he

33 In wild-type hepatic macrophages, deoxycholic acid induced the associ

34 y-associated liver disease demonstrates that hepatic macrophage dysfunction occurs in obesity and sug

35 We show for the first time that hepatic macrophages enhance myofibroblast survival in a

36 These observations indicate that splenic and hepatic macrophages export iron during S. Typhimurium in

37 pendent outcome of HBV and demonstrated that hepatic macrophages facilitate lymphoid organization and

38 aining liposomes deplete mice of splenic and hepatic macrophages for 5-7 days.

39 Tollip expression was decreased in hepatic macrophages from ethanol-fed rats, but treatment

40 ed HRG is a critical endogenous modulator of hepatic macrophage functionality and investigated its im

41 A marked increase in hepatic macrophages (h-mphi) is observed in experimental

42 ssion in biliary epithelial cells and within hepatic macrophages (h-mpsi) in areas of necrosis.

43 In particular, the critical role of hepatic macrophages has been highlighted and the priming

44 Proinflammatory M1 activation of hepatic macrophages (HM) is critical in pathogenesis of

45 ctivation of M1 phenotypes in isolated mouse hepatic macrophages (HMacs) and in a murine macrophage c

46 it endotoxin-induced NF-kappaB activation in hepatic macrophages (HMs), suggesting a role for the int

47 murine macrophage cell line and rat primary hepatic macrophages (HMs).

48 tellate cells (HSCs), endothelial cells, and hepatic macrophages; however, its role in liver fibrosis

49 or, as well as in wild-type mice depleted of hepatic macrophages; however, there was no increase in h

50 dings underscore the potential importance of hepatic macrophages in regulating both stellate cell bio

51 O treatment determined a strong reduction in hepatic macrophage infiltration and reduced hepatic mRNA

52 nifested further with extramedullary tumors, hepatic macrophage infiltration, and metabolic reprogram

53 f CXCL10 reduced FFC-induced proinflammatory hepatic macrophage infiltration, while natural killer ce

54 Specifically, levels of pulmonary and hepatic macrophage inflammatory protein 1alpha (MIP-1alp

55 nduced septic shock, we demonstrate that the hepatic macrophage is the primary source of elevated cir

56 TLR4 signaling in hepatic macrophages is increased after chronic ethanol f

57 Depletion of hepatic macrophages led to CD8(+) T cell activation and

58 butions not only of hepatocytes, but also of hepatic macrophages, liver-associated lymphocytes, sinus

59 ver transplantation reveal increased CD68(+) hepatic macrophage numbers with massive infiltrates of p

60 studies, we analyzed the effects of blocking hepatic macrophages on expression of beta2 integrins and

61 ulture media of isolated HCs (P < 0.001) and hepatic macrophages (P < 0.001), with HCs being the pred

62 of infiltrating monocytes into cells with a hepatic macrophage phenotype.

63 determined the cellular sources of SLPI and hepatic macrophage phenotype.

64 Although it is well established that hepatic macrophages play a crucial role in the developme

65 CCR8 critically mediates hepatic macrophage recruitment upon injury, which subseq

66 independent of PAR2 drives CD11b(+)CD11c(+) hepatic macrophage recruitment, and TF-PAR2 signaling co

67 Accordingly, AnxA1 addition to isolated hepatic macrophages reduced galectin-3 expression.

68 However, recruited hepatic macrophages (RHMs) were recently shown to repres

69 der lipotoxic conditions, palmitate inhibits hepatic macrophage secretion of IGFBP-3, thereby releasi

70 s of different inflammatory cells, including hepatic macrophages, T and B lymphocytes, natural killer

71 nous hemoglobin increased the sensitivity of hepatic macrophages to subsequent stimulation by LPS.

72 The contribution of hepatic macrophages to these events has been largely ove

73 s molecular factor promoting polarization of hepatic macrophages toward the M1 phenotype, thereby pro

74 In homeostatic conditions, hepatic macrophages were overall reduced and preferentia

75 t of CD8(+) T cell responses was mediated by hepatic macrophages, which were predisposed by maternal