Kupffer cell numbers during human development

Cope, E. M. W.; Dilly, Susan

doi:10.1111/j.1365-2249.1990.tb05360.x

Cited by 8 publications

(3 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The liver is exposed to exogenous agents that reach the fetus either directly from the placenta (via the umbilical vein) or from the amniotic fluid, which is swallowed and resorbed in the intestine (via the portal vessels). Kupffer cells are macrophages lining the hepatic sinusoids, which are capable of recognition and phagocytosis of a wide range of bacteria as well as immune complexes [ 173 ]. Kupffer cells are able to produce cytokines (IL-6, IL-1β, TNF-α) [ 174 , 175 ], which can modify fetal hematopoiesis.…”

Section: Evidence Of Multi-systemic Involvement In Firsmentioning

confidence: 99%

The fetal inflammatory response syndrome: the origins of a concept, pathophysiology, diagnosis, and obstetrical implications

Jung

Romero

Yeo

et al. 2020

Seminars in Fetal and Neonatal Medicine

139

112

View full text Add to dashboard Cite

Section: Evidence Of Multi-systemic Involvement In Firsmentioning

confidence: 99%

The fetal inflammatory response syndrome: the origins of a concept, pathophysiology, diagnosis, and obstetrical implications

Jung

Romero

Yeo

et al. 2020

Seminars in Fetal and Neonatal Medicine

139

112

View full text Add to dashboard Cite

“…4B,E). 27,[32][33][34][35] The number of MAC387þ cells was significantly elevated in AALF compared with pathological control liver tissue (median, 95 cells/10 hpf [IQR, 50-182] versus median, 20 cells/10 hpf [IQR, [20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35]; P ¼ 0.001; n ¼ 8 AALF patients, n ¼ 8 pathological controls).…”

Section: Patientmentioning

confidence: 99%

Source and characterization of hepatic macrophages in acetaminophen-induced acute liver failure in humans

et al. 2012

View full text Add to dashboard Cite

Acetaminophen‐induced acute liver failure (AALF) is associated with innate immunity activation, which contributes to the severity of hepatic injury and clinical outcome. A marked increase in hepatic macrophages (h‐mϕ) is observed in experimental models of AALF, but controversy exists regarding their role, implicating h‐mϕ in both aggravation and resolution of liver injury. The role of h‐mϕ in human AALF is virtually unexplored. We sought to investigate the role of chemokine (C‐C motif) ligand 2 (CCL2) in the recruitment of circulating monocytes to the inflamed liver and to determine how the h‐mϕ infiltrate and liver microenvironment may contribute to tissue repair versus inflammation in AALF. We evaluated circulating monocytes, their chemokine (C‐C motif) receptor 2 (CCR2) expression, and serum CCL2 levels in patients with AALF. Cell subsets and numbers of circulation‐derived (MAC387+) or resident proliferating (CD68/Ki67+) h‐mϕ in hepatic immune infiltrates were determined by immunohistochemistry. Inflammatory cytokine levels were determined in whole and laser microdissected liver tissue by proteome array. In AALF, circulating monocytes were depleted, with the lowest levels observed in patients with adverse outcomes. CCL2 levels were high in AALF serum and hepatic tissue, and circulating monocyte subsets expressed CCR2, suggesting CCL2‐dependent hepatic monocyte recruitment. Significant numbers of both MAC387+ and CD68+ h‐mϕ were found in AALF compared with control liver tissue with a high proportion expressing the proliferation marker Ki67. Levels of CCL2, CCL3, interleukin (IL)‐6, IL‐10, and transforming growth factor‐β1 were significantly elevated in AALF liver tissue relative to chronic liver disease controls. Conclusion: In AALF, the h‐mϕ population is expanded in areas of necrosis, both through proliferation of resident cells and CCL2‐dependent recruitment of circulating monocytes. The presence of h‐mϕ within an anti‐inflammatory/regenerative microenvironment indicates that they are implicated in resolution of inflammation/tissue repair processes during AALF. (HEPATOLOGY 2012)

show abstract

“…During this period, cells similar to the Kupffer cells are observed between the hepatocyte cords (32). Kupffer cells, which are few in the early intrauterine period, increase during pregnancy and almost reach the levels of an adult in the neonatal period (33).…”

Section: Liver Developmentmentioning

confidence: 99%

Development of Liver and Pancreas

Eşrefoğlu¹,

Taşlıdere²,

Çetin³

2016

Bezmialem Science

View full text Add to dashboard Cite

The parenchyma of the liver and pancreas is derived from the endoderm, whereas the stroma is derived from the mesoderm. Both of them are derived from the endoderm of the foregut as the esophagus, stomach, and a part of duodenum. At the 3 rd -4 th of development, the liver, gallbladder and bile ducts become diverticulum hepaticum that is derived from the caudal portion of the foregut. There were inductive effects of septum transversum and cardiac mesoderm for the development of liver diverticulum. The pancreas arise from the endoderm of the foregut. The pancreas is derived from the fusion of the ventral and dorsal pancreas bulbs, which arise from the endoderm of the duodenum. The inductive effects of the notochord and dorsal aorta play a role in the development of the pancreas. In this manuscript, we attempted to review the morphological and functional development of the liver and pancreas with the aid of pictures obtained from various stages of prenatal and postnatal development in the organs of rats.

show abstract

Kupffer cell numbers during human development

Cited by 8 publications

References 10 publications

The fetal inflammatory response syndrome: the origins of a concept, pathophysiology, diagnosis, and obstetrical implications

The fetal inflammatory response syndrome: the origins of a concept, pathophysiology, diagnosis, and obstetrical implications

Source and characterization of hepatic macrophages in acetaminophen-induced acute liver failure in humans

Development of Liver and Pancreas

Contact Info

Product

Resources

About