Immunocytes and Activated Stellate Cells in Pancreatic Fibrogenesis

Jaskiewicz, K; Nałecz, A; Rzepko, Robert; Śledziński, Zbigniew

doi:10.1097/00006676-200304000-00006

Cited by 27 publications

(17 citation statements)

References 16 publications

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“…Although the mechanisms accounting for the transition from acute to chronic pancreatitis are unknown, there are studies providing descriptions of the nature of the chronic inflammation [82][83][84][85][86][87][88][89] . In general, these studies demonstrate that the majority of the inflammatory cells in chronic pancreatitis tissue are macrophages and T lymphocytes.…”

Section: Inflammation In Alcoholic Pancreatitismentioning

confidence: 99%

Pathobiology of Alcoholic Pancreatitis

Pandol¹,

Raraty

2007

Pancreatology

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Section: Inflammation In Alcoholic Pancreatitismentioning

confidence: 99%

Pathobiology of Alcoholic Pancreatitis

Pandol¹,

Raraty

2007

Pancreatology

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“…7,9,20 In fact, the ECM influences the growth, differentiation, survival, and motility of cells by providing a physical scaffold and by acting as a reservoir for soluble mitogens. 11,12,21,22 Therefore, the dynamic microenvironment promotes tumor growth and invasion.…”

mentioning

confidence: 99%

α-Smooth Muscle Actin Expressing Stroma Promotes an Aggressive Tumor Biology in Pancreatic Ductal Adenocarcinoma

et al. 2010

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OBJECTIVES: Pancreatic ductal adenocarcinoma (PDAC) is often characterized by a prominent desmoplastic stroma that is induced partially by alpha-smooth muscle actin (SMA)-expressing activated pancreatic stellate cells (PSCs). This study aimed to investigate the significance of alpha-SMA expression in PDAC and the correlation between alpha-SMA mRNA levels and the patient prognosis. METHODS: We obtained formalin-fixed, paraffin-embedded tissue samples from 109 patients with PDAC, who underwent pancreatectomy at our institution from 1992 to 2007. We measured alpha-SMA mRNA levels by quantitative real-time reverse transcription-polymerase chain reaction and investigated the association of alpha-SMA mRNA expression with clinicopathologic parameters and survival time. We also assessed the influence of activated PSCs on malignant behaviors of pancreatic cancer cells using in vitro experiments. RESULTS: alpha-SMA immunoreactivity was detected exclusively in the stroma of PDAC. The group with high alpha-SMA expression showed a significantly shorter survival, as shown by univariate analysis (P = 0.005) and multivariate analysis (P < 0.0001). alpha-SMA-expressing activated PSCs enhanced the invasiveness, proliferation, and colony formation of pancreatic cancer cells. CONCLUSIONS: Quantitative analysis of alpha-SMA mRNA expression using formalin-fixed, paraffin-embedded tissue samples was useful to predict the prognosis of patients with PDAC. Activated PSCs may regulate the malignant behavior of pancreatic cancer cells.

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“…Leukocytes are considered to play a crucial role in the inflammatory process of chronic pancreatitis (5,10,12,17,18). On the other hand, PSCs as the main producers of the ECM have been essentially implicated in pancreatic fibrosis, a characteristic pathomorphological symptom of the disease.…”

Section: Discussionmentioning

confidence: 99%

“…Total cell RNA was isolated using the RNeasy kit according to the manufacturer's instructions. Total RNA (1 g) was reverse transcribed into cDNA using oligo(dT) [12][13][14][15][16][17][18] primer and Superscript II. To correct for variations in different preparations, the cDNA samples were adjusted to equal the input cDNA concentrations, based on their hypoxanthine phosphoribosyl transferase or ␤-actin content as housekeeping genes.…”

Section: Rna Isolation and Rt-pcrmentioning

confidence: 99%

Inhibition of lymphocyte apoptosis by pancreatic stellate cells: impact of interleukin-15

Sparmann¹,

Glass²,

Brock³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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There is growing evidence that pancreatic stellate cells (PSCs) produce cytokines and take part in the regulation of inflammatory processes in the pancreas. IL-15 inhibits apoptosis of various cell populations. This study was performed to investigate whether PSCs produce IL-15 and thereby can affect lymphocytes. Primary PSCs were isolated from the rat pancreas using density gradient centrifugation. mRNA expression of IL-15 was demonstrated by RT-PCR, and IL-15 protein was analyzed by immunoblotting. Lymphocytes obtained from rat mesenterial lymph nodes were cocultured with in vitro activated PSCs. Apoptosis has been quantified by the binding of annexin V-FITC with a flow cytometer. Proliferation was monitored using [3H]thymidine incorporation. PSCs express two splice variants of IL-15. The protein was detectable only in cell lysates but not in the cell culture supernatant. Cocultivation of lymphocytes with PSCs and IL-15 inhibited spontaneous lymphocyte apoptosis, and this effect was reduced by an anti-IL-15 antibody. Lymphocytes induced vice versa the proliferation and collagen production of PSCs. The inhibition of spontaneous lymphocyte apoptosis in cocultures with PSCs was at least partially mediated by cell-bound IL-15. This effect and the stimulation of PSCs by lymphocytes may lead to a circulus vitiosus, resulting in the persistence of inflammatory processes and the development of fibrosis during chronic pancreatitis.

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Immunocytes and Activated Stellate Cells in Pancreatic Fibrogenesis

Abstract: Results of this work show that a significant number of IP cases might have an autoimmune etiology. There was a positive correlation between activated stellate cell marker expression and the degree of fibrosis.

Cited by 27 publications

References 16 publications

Pathobiology of Alcoholic Pancreatitis

Pathobiology of Alcoholic Pancreatitis

α-Smooth Muscle Actin Expressing Stroma Promotes an Aggressive Tumor Biology in Pancreatic Ductal Adenocarcinoma

Inhibition of lymphocyte apoptosis by pancreatic stellate cells: impact of interleukin-15

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