Lymphocyte subsets and cellular immunity in patients with chronic pancreatitis

Ockenga, J.; Kemper, A.; Jacobs, Ramon E. A.; Manns, MP

doi:10.1016/s0016-5085(98)81974-4

Cited by 7 publications

(7 citation statements)

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“…The pattern of circulating lymphocyte subsets in patients with CP, a disease characterized by a progressive destruction of the exocrine and endocrine pancreas, was not different from that of CS, with the exception of CD4 + lymphocytes, which were found to be increased in these patients. This finding was opposite to that of patients with PC and in agreement with previous results of the literature, [28][29][30] supporting the hypothesis that an alteration of the immune system is a key element in the Progression in stage of PC was also found to significantly affect circulating lymphocytes, which were reduced in stage IV patients. Because nutritional status has been shown to influence the immune status of patients with malignancies, 31,32 we verified whether the reduction of circulating lymphocytes in PC is a direct consequence of the tumor or an epiphenomenon.…”

Section: Discussionsupporting

confidence: 86%

Decreased Total Lymphocyte Counts in Pancreatic Cancer: An Index of Adverse Outcome

Fogar

Sperti²,

Basso³

et al. 2006

Pancreas

228

169

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Section: Discussionsupporting

confidence: 86%

Decreased Total Lymphocyte Counts in Pancreatic Cancer: An Index of Adverse Outcome

Fogar

Sperti²,

Basso³

et al. 2006

Pancreas

228

169

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“…PBMC of CP patients have been shown to acquire certain phenotypic and functional changes (10, 11), some of them correlating with the most prominent clinical symptom of CP, pain (32). Although neurogenic inflammation and inflammatory pain have been implicated in the pathogenesis of acute pancreatitis and CP (5,22,29), the full spectrum of neuroimmune interactions remains to be better elucidated.…”

Section: Discussionmentioning

confidence: 99%

Altered anti-inflammatory response of mononuclear cells to neuropeptide PACAP is associated with deregulation of NF-κB in chronic pancreatitis

Michalski¹,

Selvaggi²,

Bartel³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Although it is recognized that neurogenic influences contribute to progression of chronic inflammatory diseases, the molecular basis of neuroimmune interactions in the pathogenesis of chronic pancreatitis (CP) is not well defined. Here we report that responsiveness of peripheral blood mononuclear cells (PBMC) to the neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) is altered in CP. Expression of PACAP and its receptors in human CP was analyzed with quantitative RT-PCR, laser-capture microdissection, and immunohistochemistry. Regulation of PACAP expression was studied in coculture systems using macrophages and acinar cells. Responsiveness of donor and CP PBMC to PACAP was determined based on cytokine profiles and NF-kappaB activation of LPS- or LPS+PACAP-exposed cells. Although donor and CP PBMC responded equally to LPS, PACAP-mediated counteraction of LPS-induced cytokine response was switched from inhibiting TNF-alpha to decreasing IL-1beta and increasing IL-10 secretion. The change of PACAP-mediated anti-inflammatory pattern was associated with altered activation of NF-kappaB: compared with LPS alone, a combination of LPS and PACAP had no effect on NF-kappaB p65 nuclear translocation in CP PBMC, whereas NF-kappaB was significantly decreased in donor PBMC. According to laser-capture microdissection and coculture experiments, PBMC also contributed to generation of a PACAP-rich intrapancreatic environment by upregulating PACAP expression in macrophages encountering apoptotic pancreatic acini. The nociceptive status of CP patients correlated with pancreatic PACAP levels and with IL-10 bias of PACAP-exposed CP PBMC. Thus the ability of PBMC to produce and to respond to PACAP might influence neuroimmune interactions that regulate pain and inflammation in CP.

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“…The pancreas is infi ltrated by lymphocytes in chronic pancreatitis [3][4][5][6] and this appears to at least partially be mediated by upregulation of chemokines in the infl amed gland [7] . In the peripheral blood of chronic pancreatitis patients, several studies have shown a dysregulated distribution of lymphocytes that in some cases is reversed after pancreatic resection [8][9][10][11] . T lymphocytes appear to play a key role in the infl ammatory process in chronic pancreatitis and constitute a large part of both the cell population infi ltrating the pancreas and the dysregulated cell population in peripheral blood.…”

Section: Introductionmentioning

confidence: 99%