Changes in count and function of splenic lymphocytes from patients with portal hypertension

Li, Zong-Fang; Zhang, Shu; Lv, Gao-Bo; Huang, Ying; Zhang, Wei; Ren, Shengxiang; Yang, Jun; Dang, Shuangsuo

doi:10.3748/wjg.14.2377

Cited by 23 publications

(14 citation statements)

References 19 publications

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“…Additionally, a patient with splenomegaly may have an impacted immune system, and this should be remembered for the immunosuppressed transplant recipient. 17 The mild elevation of INR seen in our patients with late PVT is also notable because it may reflect underlying coagulation abnormalities, as described previously in noncirrhotic portal hypertension. 18 Even though morbidity was clearly increased in our population, PVT did not compromise overall allograft or patient survival.…”

Section: Discussionsupporting

confidence: 75%

“…Although the median platelet count will typically be adequate for most minor procedures, this type of patient is at increased risk for variceal bleeding from associated portal hypertension and splenic rupture if he or she is involved in contact sports or trauma. Additionally, a patient with splenomegaly may have an impacted immune system, and this should be remembered for the immunosuppressed transplant recipient . The mild elevation of INR seen in our patients with late PVT is also notable because it may reflect underlying coagulation abnormalities, as described previously in noncirrhotic portal hypertension …”

Section: Discussionsupporting

confidence: 58%

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Management and long-term consequences of portal vein thrombosis after liver transplantation in children

et al. 2013

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Portal vein thrombosis (PVT) occurs in 12% of pediatric recipients of liver transplantation (LT). Known complications of PVT include portal hypertension, allograft loss, and mortality. The management of PVT is varied. A single-center, case-control study of pediatric LT recipients with portal vein (PV) changes after LT was performed. Cases were categorized as early PVT (if PVT was detected within 30 days of transplantation) or late PVT (if PVT was detected more than 30 days after transplantation or if early PVT persisted beyond 30 days). Two non-PVT control patients were matched on the basis of the recipient weight, transplant indication, and allograft type to each patient with PVT. Thirty-two of the 415 LT recipients (7.7%) received 37 allografts and developed PVT. In comparison with control patients, a higher proportion of patients with PVT had PVT present before LT (13.3% versus 0%, P 5 0.01). Patients with early PVT usually returned to the operating room, and 9 of 15 patients (60%) had PV flow restored. Patients with late PVT had lower white blood cell (4.9 [1000/lL] versus 6.8 [1000/lL], P < 0.01) and platelet counts (140 [1000/lL] versus 259 [1000/lL], P < 0.01), an elevated international normalized ratio (1.2 versus 1.0, P < 0.001), and more gastrointestinal bleeding (25% versus 8.3%, P 5 0.03) compared to controls. Patients with PVT were also less frequently at the expected grade level (52% versus 88%, P < 0.001). The patient survival rates were 84%, 78%, and 78% and 91%, 84%, and 79% for cases and controls at 1, 5, and 10 years, respectively. The allograft survival rates were 90%, 80%, and 80% for cases and 94%, 89%, and 87% for controls at 1, 5, and 10 years, respectively. In conclusion, patients with early and late PVT had preserved allograft function, and there was no impact on mortality. Patients diagnosed with early PVT often underwent operative interventions with successful restoration of flow. Patients diagnosed with late PVT experienced variceal bleeding, and some required portosystemic shunting procedures. Academic delays were also more common. In late PVT, the clinical presentation dictates care because the optimal management algorithm has not yet been determined. Multi-institutional studies are needed to confirm these findings and improve patient outcomes.

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Section: Discussionsupporting

confidence: 75%

Section: Discussionsupporting

confidence: 58%

Management and long-term consequences of portal vein thrombosis after liver transplantation in children

et al. 2013

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“…Generally, the pool of naïve Th cells depends on the proliferation and apoptosis of these cells and their differentiation into effector memory Th cells [38]. In splenic WP, naïve T cells undergo activation and differentiate into effector memory T cells, which can penetrate inflamed tissues to clear them from pathogens [39]. In our study, the normalization of the WP areas of cirrhotic spleen was accompanied by the restoration of the percentage of effector memory T cells among splenic Th cells.…”

Section: Discussionsupporting

confidence: 55%

Propranolol Suppresses the T-Helper Cell Depletion-Related Immune Dysfunction in Cirrhotic Mice

Tsai,

Hsu,

Huang

et al. 2020

Cells

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Bacterial translocation (BT) and splenomegaly contribute to cirrhosis-associated immune dysfunction (CAID) including T cell depletion, infection, and chronic inflammation. β-blockers have been reported to decrease BT and improve splenomegaly. This study explores the modulation of β1 and β2 adrenergic receptors (ADRB1/ADRB2) by propranolol treatment on the peripheral and splenic immune dysfunction of cirrhotic mice. In vivo experiments were performed in bile duct ligation (BDL)- and thioacetamide (TAA)-cirrhotic mice receiving two weeks of propranolol treatment. Acute effects of propranolol were evaluated in T-helper (Th) cells isolated from spleen of cirrhotic mice. Over-expression of β1 and β2 adrenergic receptors (ADRB1/ADRB2) in spleen and T lymphocytes was associated with high peripheral/splenic lipopolysaccharide binding protein levels. Moreover, a decrease in Th cells percentage, increase in Treg subset, and cytokines were accompanied by increased apoptosis, proliferation, and reduced white pulp hyperplasia in cirrhotic mice, which were counteracted by propranolol treatment. The Th-cell depletion, systemic inflammation, BT, and infection were improved by chronic propranolol treatment. Acute propranolol treatment inhibited apoptosis, Treg-conditioned differentiation, and promoted Th2-conditioned differentiation through ADRB-cyclic adenosine monophosphate (cAMP) signals in cirrhotic mice. In conclusion, suppression of ADRB1 and ADRB2 expressions in spleen and splenic T lymphocytes by acute and chronic propranolol treatment ameliorate systemic and splenic immune dysfunction in cirrhosis.

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“…T and B lymphocyte proliferation are response due to antigen or mitogen stimulation. The proliferation ability was indicated the important role of lymphocytes in the immune system function [20]. produce IL-4 and IL-5.…”

Section: Resultsmentioning

confidence: 99%

Mus musculus (Linnaeus, 1758) Immune Responses Caused by Escherichia coli (Migula, 1895) Infection

Mitasari¹,

Gofur²,

Listyorini³

2017

KLS

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Escherichia coli (Migula, 1895) is a negative gram bacteria which have an ability to cause some deseases, such as meningitis, urinary tract infection and digestive tract infection. Lipopolysaccharide (LPS) in its cell wall induces immune responses in many ways. The objective of this study was to investigate the effect of E. coli infection on lymphocyte numbers and spleen weight in mice [Mus musculus (Linnaeus, 1758)]. Twenty five male mice were grouped into negative control, positive control group treated with PBS, and three experimental groups injected intraperitonially with E. coli 1.5 × 10 3 cfu/mL,1.5 × 10 5 cfu/mL or 1.5 × 10 7 cfu/mL respectively. About 5 d after the injection, the spleen were collected. Spleen were weighed using digital balance, number of lymphocyte were counted using hemocytometer. E. coli infection significantly increase both weight of the spleen and number lymphocyte.In conclusion, mice responded to E. coli infection by increasing the number of its lymphocyte.

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Changes in count and function of splenic lymphocytes from patients with portal hypertension

Abstract: (3) with the significant increase in the weight of the PH spleen (832.6 ± 278.2 g vs 211.7 ± 85.6 g, P < 0.01), the total quantity of lymphocytes (absolute quantity) increased significantly [(0.685 ± 0.072

Cited by 23 publications

References 19 publications

Management and long-term consequences of portal vein thrombosis after liver transplantation in children

Management and long-term consequences of portal vein thrombosis after liver transplantation in children

Propranolol Suppresses the T-Helper Cell Depletion-Related Immune Dysfunction in Cirrhotic Mice

Mus musculus (Linnaeus, 1758) Immune Responses Caused by Escherichia coli (Migula, 1895) Infection

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