Reply to Koh: Signaling dynamics of DNA damage response invoked by combination therapy are dose-dependent

Warren, Nicholas J.H.; Eastman, Alan

doi:10.1074/jbc.rl119.007419

Cited by 1 publication

(2 citation statements)

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“…The second wave comes from infiltrating granulocytes and monocytes that elevate proinflammatory cytokine and chemokine production. Except for inflammatory cytokine secretion and oxidative stress induction, neutrophils release their DNA, histone proteins, high mobility group box 1, and granule components into the pancreas to form neutrophil extracellular traps (NETs), which facilitate inflammation by duct occlusion and trypsin activation [ 14 , 19 ]. In parallel, NF- κ B and STAT3 pathways become activated in monocytes.…”

Section: Discussionmentioning

confidence: 99%

“…Mice with Induced Acute Pancreatitis. As previously described [5,14,15], the pancreatitis damage was assessed in the aspects of inflammation as evidenced by infiltrated inflammatory cells, acinar cell vacuolization and necrosis, and edema in the pancreas. The overall total severity score was 14.7 for no injection, 16.6 for wt BMC injection, and 22.6 for db/db BMC injection (p = 0:001 for db/db BMC injection vs. no injection; p = 0:002 for db/db BMC vs. wt BMC) (Figure 3(a)).…”

Section: The Effect Of Bmc Injection On Histological Changes Inmentioning

confidence: 99%

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Diabetic Bone Marrow Cell Injection Accelerated Acute Pancreatitis Progression

Luo

Yan

Zhang

et al. 2021

Journal of Immunology Research

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Acute pancreatitis (AP) is one of the leading causes of hospital admission, 20% of which could progress to the severe type with extensive acinar cell necrosis. Clinical studies have reported that diabetes is an independent risk factor of the incidence of AP and is associated with higher severity than nondiabetic subjects. However, how diabetes participates in AP progression is not well defined. To investigate this question, wild-type (wt) and diabetic db/db mice at the age of 16 weeks were used in the study. AP was induced in wt recipients by 10 injections of 50 μg/kg caerulein with a 1 h interval. One hour after the last caerulein injection, bone marrow cells (BMC) isolated from wt and db/db mice were injected intraperitoneally into the recipients ( 1 × 10 7 cells/recipient). The recipients with no BMC injection served as controls. Thirteen hours after BMC injection, serum lipase activity was 1.8- and 1.3-folds higher in mice that received db/db BMC, compared with those with no injection and wt BMC injection, respectively ( p ≤ 0.02 for both). By H&E staining, the overall severity score was 14.7 for no cell injection and 16.6 for wt BMC injection and increased to 22.6 for db/db BMC injection ( p ≤ 0.002 for both). In particular, mice with db/db BMC injection developed more acinar cell necrosis and vacuolization than the other groups ( p ≤ 0.03 for both). When sections were stained with an antibody against myeloperoxidase (MPO), the density of MPO+ cells in pancreatitis was 1.9- and 1.6-folds higher than wt BMC and no BMC injection groups, separately ( p ≤ 0.02 for both). Quantified by ELISA, db/db BMC produced more IL-6, GM-CSF, and IL-10 compared with wt BMC ( p ≤ 0.04 for all). In conclusion, BMC of db/db mice produced more inflammatory cytokines. In response to acinar cell injury, diabetic BMC aggravated the inflammation cascade and acinar cell injury, leading to the progression of acute pancreatitis.

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Section: Discussionmentioning

confidence: 99%

Section: The Effect Of Bmc Injection On Histological Changes Inmentioning

confidence: 99%