Engulfment of Gram-Positive Bacteria by Pancreatic Stellate Cells in Pancreatic Fibrosis

Morishita, Keiichi; Shimizu, Kyoko; Haruta, Ikuko; Kawamura, Shunji; Kobayashi, Makio; Shiratori, Keiko

doi:10.1097/mpa.0b013e3181d7ace1

Cited by 8 publications

(7 citation statements)

References 34 publications

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“…6 Moreover, products of gram-positive bacteria, such as peptidoglycans and lipoteichoic acid, also cause up-regulation of ECM synthesis in PSCs. 7 In line with these findings, it has been shown that LPSs are required for the development of pancreatic fibrosis caused by alcohol-induced pancreatitis in the rat model. 8 Bacterial DNA is also recognized by TLRs.…”

mentioning

confidence: 78%

“…6 Interestingly, only TLR2 ligands promoted the synthesis of ECM. 7 For this reason, we first evaluated the expression of TLR9 by means of RT-PCR and immunofluorescent cytochemistry. We confirmed that both primary quiescent and passaged PSCs constitutively expressed TLR9 at the messenger RNA (mRNA) level (Fig.…”

Section: Rat Pscs Expressed Tlr9 and Could Endocytose Cpg Odnmentioning

confidence: 99%

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Bacterial DNA Promotes Proliferation of Rat Pancreatic Stellate Cells Thorough Toll-Like Receptor 9

Nakamura¹,

Ito²,

Oono³

et al. 2011

Pancreas

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mentioning

confidence: 78%

Section: Rat Pscs Expressed Tlr9 and Could Endocytose Cpg Odnmentioning

confidence: 99%

Bacterial DNA Promotes Proliferation of Rat Pancreatic Stellate Cells Thorough Toll-Like Receptor 9

Nakamura¹,

Ito²,

Oono³

et al. 2011

Pancreas

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“…There have been reports that stimulation by a component of gram-negative bacilli, such as LPS or flagellin, a component of gram-positive cocci, such as LTA, or stimulation similar to that in viral infection, such as Poly (I : C), has effects similar to stimulation by cytosolic dsDNA. Therefore, common transcriptional factors, such as NF- κ B, are thought to induce expression of inflammatory cytokine and chemokine genes [17, 35, 36]. We previously reported that dsDNA from bacteria such as Escherichia coli has no inflammatory effect [11].…”

Section: Discussionmentioning

confidence: 99%

Cytosolic Double-Stranded DNA as a Damage-Associated Molecular Pattern Induces the Inflammatory Response in Rat Pancreatic Stellate Cells: A Plausible Mechanism for Tissue Injury-Associated Pancreatitis

Nakamura

Ito

Igarashi

et al. 2012

International Journal of Inflammation

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Pancreatitis is an inflammatory disease of unknown causes. There are many triggers causing pancreatitis, such as alcohol, common bile duct stone, virus and congenital or acquired stenosis of main pancreatic duct, which often involve tissue injuries. Pancreatitis often occurs in sterile condition, where the dead/dying pancreatic parenchymal cells and the necrotic tissues derived from self-digested-pancreas were observed. However, the causal relationship between tissue injury and pancreatitis and how tissue injury could induce the inflammation of the pancreas were not elucidated fully until now. This study demonstrates that cytosolic double-stranded DNA increases the expression of several inflammatory genes (cytokines, chemokines, type I interferon, and major histocompatibility complex) in rat pancreatic stellate cells. Furthermore, these increase accompanied the multiple signal molecules genes, such as interferon regulatory factors, nuclear factor-kappa B, low-molecular-weight protein 2, and transporter associated with antigen processing 1. We suggest that this phenomenon is a plausible mechanism that might explain how cell damage of the pancreas or tissue injury triggers acute, chronic, and autoimmune pancreatitis; it is potentially relevant to host immune responses induced during alcohol consumption or other causes.

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“…αSMA ×400 A B and TIMP2 to maintain the balance of extracellular matrix, which is usually disrupted after activation in pancreatitis and PDAC. Several in vitro and in vivo studies suggest that PSCs may have progenitor-like capabilities, possessing ATP-binding cassette G2 (ABCG2) and they transform into insulin-secreting cells upon exposure to the relevant culture medium (40,(43)(44)(45)(46).…”

Section: Sirius Red ×200mentioning

confidence: 99%

Multifunctional role of pancreatic stellate cells in pancreatic cancer

Mekapogu¹,

Pothula²,

Pirola³

et al. 2019

Ann Pancreat Cancer

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Pancreatic ductal adenocarcinoma (PDAC) constitutes 90% of all pancreatic malignancies and is characterised by extensive desmoplasia and early metastasis. The risk factors for PDAC include a family history of the disease, cigarette smoking, chronic pancreatitis, obesity and diabetes mellitus (1,2). PDAC most commonly occurs in the 60 to 80 year age group, and its incidence is 50% higher in men than in women and (1) genetic mutations such as BRCA2, CDKN2A, STK11, PRSS1, SPINK1, CFTR, PALB2 and ATM increase the risk for PDAC (3), patients with chronic pancreatitis have a 15 fold increased risk of developing PDAC (4), cigarette smoking increases the risk of PDAC by 75% even up to 10 years after cessation of smoking and (5) diabetes mellitus increases the risk by 30% up to 20 years after diagnosis (6). Obesity and high body mass index are positively correlated with the risk of developing PDAC (7). One meta-analysis showed a 19% increase in risk of developing PDAC in obese individuals (BMI ≥30 kg/m 2) compared to normal participants (BMI 22 kg/m 2) (8). The genetic mutational landscape of PDAC involves the alteration of 69 genes which affect 12 core signalling pathways (9). Both oncogenes and tumour suppressor genes are mutated of which the major genes involved in PDAC are the oncogene Kristen Rat Sarcoma Virus (KRAS), and three tumour suppressor genes-TP53, CDKN2A and SMAD4. KRAS is the earliest mutation seen in low-grade pancreatic

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Engulfment of Gram-Positive Bacteria by Pancreatic Stellate Cells in Pancreatic Fibrosis

Abstract: The fibrogenic action of PSCs seems to be more strongly associated with activation of the toll-like receptor-dependent pathway than it is with phagocytosis of bacteria by PSCs.

Cited by 8 publications

References 34 publications

Bacterial DNA Promotes Proliferation of Rat Pancreatic Stellate Cells Thorough Toll-Like Receptor 9

Bacterial DNA Promotes Proliferation of Rat Pancreatic Stellate Cells Thorough Toll-Like Receptor 9

Cytosolic Double-Stranded DNA as a Damage-Associated Molecular Pattern Induces the Inflammatory Response in Rat Pancreatic Stellate Cells: A Plausible Mechanism for Tissue Injury-Associated Pancreatitis

Multifunctional role of pancreatic stellate cells in pancreatic cancer

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