Novel Circulating and Tissue Monocytes as Well as Macrophages in Pancreatitis and Recovery

Manohar, Murli; Jones, Elaina K.; Rubin, Samuel J.; Subrahmanyam, Priyanka B.; Swaminathan, Gayathri; Mikhail, David; Bai, Lawrence; Singh, Gulshan; Yi, Wei; Sharma, Vishal; Siebert, Janet; Maecker, Holden T.; Husain, Sohail Z.; Park, Walter G.; Pandol, Stephen J.; Habtezion, Aida

doi:10.1053/j.gastro.2021.08.033

Cited by 37 publications

(20 citation statements)

References 43 publications

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“… 20 Moreover, Usp25 knockdown has been shown to generate proinflammatory effects in Kupffer cells. 48 Taken together, these studies indicate that increasing Usp25 activity may counter inflammatory responses in AP.…”

Section: Discussionmentioning

confidence: 77%

USP25 Deficiency Exacerbates Acute Pancreatitis via Up-Regulating TBK1–NF-κB Signaling in Macrophages

Liu

Luo

et al. 2022

Cellular and Molecular Gastroenterology and Hepatology

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Section: Discussionmentioning

confidence: 77%

USP25 Deficiency Exacerbates Acute Pancreatitis via Up-Regulating TBK1–NF-κB Signaling in Macrophages

Liu

Luo

et al. 2022

Cellular and Molecular Gastroenterology and Hepatology

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“…62 Macrophages appear to be a negative factor in the progression of pancreatitis because of excessive recruitment and release of proinflammatory factors. 63,64 As in Figure 3, Liangfang Zhang's group used autologous macrophage membrane to coating PLGA nanoparticles, supplemented with phospholipase A2 (PLA2) attractant (Melittin) and inhibitor (MJ-33), and prepared a kind of "Lure-and-Kill" macrophage-like nanoparticles (MΦ-NP(L&K)). 65 The MΦ-NP(L&K) can significantly reduce the expression levels of serum markers (including PLA2, IL-6, TNF-α, IL-1β) in the MAP mouse model, relieve the edema of pancreatic tissue, and reduce the number of necrotic pancreatic acinar cells.…”

Section: Cell Membrane Camouflaged Nanoparticlesmentioning

confidence: 99%

A Mini-Review of Diagnostic and Therapeutic Nano-Tools for Pancreatitis

Zhang¹,

Li²,

Yang³

et al. 2022

IJN

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Pancreatitis is an inflammatory reaction of pancreatic tissue digestion, edema, bleeding and even necrosis caused by activation of pancreatin due to various causes. In particular, patients with severe acute pancreatitis (SAP) often suffer from secondary infection, peritonitis and shock, and have a high mortality rate. Chronic pancreatitis (CP) can cause permanent damage to the pancreas. Due to the innate characteristics, structure and location of the pancreas, there is no effective treatment, only relief of symptoms. Especially, AP is an unpredictable and potentially fatal disease, and the timely diagnosis and treatment remains a major challenge. With the rapid development of nanomedicine technology, many potential tools can be used to address this problem. In this review, we have introduced the pathophysiological processes of pancreatitis to understanding its etiology and severity. Most importantly, the current progress in the diagnosis and treatment tools of pancreatitis based on nanomedicine is summarized and prospected.

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“…In mice with CER-AP, the number of circulating monocytes peaked at 12 h and pancreatic monocytes at 24 h, both returning to baseline during the recovery phase (by 168 h) ( 64 ). Following NaTC-AP and in PDL-AP in rats, monocyte numbers in peripheral blood were significantly elevated from 30 min and 6 h respectively ( 65 , 66 ).…”

Section: Monocytes In Apmentioning

confidence: 99%

“…Following NaTC-AP and in PDL-AP in rats, monocyte numbers in peripheral blood were significantly elevated from 30 min and 6 h respectively ( 65 , 66 ). An increased frequency of monocytes was observed both in circulation and in the pancreas at 72 h in mice with CDE-AP but this was not statistically significant in circulation ( 64 ). In a similar manner, peripheral monocytes were elevated in AP patients on admission, especially those who had more severe clinical phenotype ( 67 – 69 ).…”

Section: Monocytes In Apmentioning

confidence: 99%

Circulating monocytes in acute pancreatitis

et al. 2022

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Acute pancreatitis is a common gastrointestinal disease characterized by inflammation of the exocrine pancreas and manifesting itself through acute onset of abdominal pain. It is frequently associated with organ failure, pancreatic necrosis, and death. Mounting evidence describes monocytes - phagocytic, antigen presenting, and regulatory cells of the innate immune system - as key contributors and regulators of the inflammatory response and subsequent organ failure in acute pancreatitis. This review highlights the recent advances of dynamic change of numbers, phenotypes, and functions of circulating monocytes as well as their underling regulatory mechanisms with a special focus on the role of lipid modulation during acute pancreatitis.

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Novel Circulating and Tissue Monocytes as Well as Macrophages in Pancreatitis and Recovery

Cited by 37 publications

References 43 publications

USP25 Deficiency Exacerbates Acute Pancreatitis via Up-Regulating TBK1–NF-κB Signaling in Macrophages

USP25 Deficiency Exacerbates Acute Pancreatitis via Up-Regulating TBK1–NF-κB Signaling in Macrophages

A Mini-Review of Diagnostic and Therapeutic Nano-Tools for Pancreatitis

Circulating monocytes in acute pancreatitis

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