Splenic Atrophy in Experimental Severe Acute Pancreatitis

Yasuda, Takeo; Takeyama, Yoshifumi; Ueda, Takashi; Takase, Kozo; Nishikawa, Junsuke; Kuroda, Yoshikazu

doi:10.1097/00006676-200205000-00007

Cited by 25 publications

(20 citation statements)

References 16 publications

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“…We have successfully reproduced this animal model in previous studies [18] . Researchers have used this model to evaluate immunoinflammatory response related to severe acute pancreatitis [6,16,21] . In the present study, the IL-2, IL-10, and IFN-␥ productivity was measured in ConA-stimulated splenocytes.…”

Section: Discussionmentioning

confidence: 99%

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Protective Effects of Ulinastatin on Proliferation and Cytokine Release of Splenocytes from Rats with Severe Acute Pancreatitis

Kang

Shao

et al. 2006

Eur Surg Res

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Aim: To clarify the contributions of ulinastatin to cellular immune responses in vivo, we examined the functional alterations of splenocytes and quantitatively evaluated the effects of ulinastatin on the splenocyte function during experimental severe acute pancreatitis. Methods: Severe acute pancreatitis was induced in rats by retrograde injection of 3% sodium deoxycholate. Thirty minutes after induction of pancreatitis, the rats were randomly assigned to four groups, receiving either saline or 50,000 U/kg of ulinastatin, respectively. Splenocytes were obtained aseptically and stimulated with concanavalin A for 24 h. Then the proliferative activity of cultured splenocytes was measured by using an MTT cellular proliferation assay, and the cytokine concentrations in the culture supernatants were measured by enzyme-linked immunosorbent assays. Results: Upon stimulation, the release of interleukin-2, interleukin-10, and interferon-γ was significantly decreased in the splenocytes from rats with pancreatitis as compared with those from sham operation and control groups. The splenocyte proliferation was also significantly suppressed in this group. In contrast, the proliferative as well as the cytokine-releasing capacities of the splenocytes from rats treated with ulinastatin were significantly increased as compared with those from rats with pancreatitis. Conclusions: The deficiencies in proliferation and cytokine release in response to antigen stimulation demonstrated an anergic state of splenocytes during severe acute pancreatitis. Treatment with ulinastatin contributed to the recovery of the immune function by improving proliferative responses and cytokine release of splenocytes. These data suggest that a protease-modulating therapy may be an effective strategy for the treatment of immunosuppression induced by severe acute pancreatitis.

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Section: Discussionmentioning

confidence: 99%

“…Yasuda et al [16] reported that, in severe acute pancreatitis, splenic atrophy occurred as a result of reduction in splenocytes which indicated an impairment of the cellular immunity. Moreover, Curley et al [17] demonstrated a diminished production of interleukin (IL)-2 by splenocytes isolated from mice with severe acute pancrea titis.…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Ulinastatin on Proliferation and Cytokine Release of Splenocytes from Rats with Severe Acute Pancreatitis

Kang

Shao

et al. 2006

Eur Surg Res

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“…Differently from the thymus, however, no apoptosis was detected in the splenocytes from the rats with pancreatitis. 46 Peripheral lymphocytes in the rats with pancreatitis were significantly decreased due to apoptosis compared with those in sham-operated rats. With antecedent splenectomy, peripheral lymphocyte counts were significantly lower than those in rats without splenectomy.…”

Section: Apoptosis Of Lymphocytes and Lymphatic Tissuesmentioning

confidence: 92%

“…46 In splenocytes harvested 24 h after the induction of pancreatitis, proliferative activity was lowered, and IL-2 secretion in response to concanavalin A was also depressed. The results obtained suggested that the Th1/Th2 balance tended toward Th1 suppression as a whole in severe pancreatitis.…”

Section: Apoptosis Of Lymphocytes and Lymphatic Tissuesmentioning

confidence: 98%

Significance of apoptotic cell death in systemic complications with severe acute pancreatitis

Takeyama

2005

J Gastroenterol

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In severe acute pancreatitis, multiple organ failure in the early stage after onset, and sepsis in the late stage, due to infection of pancreatic or peripancreatic devitalized tissue, contribute to its high mortality. In analogy with sepsis, evidence has accumulated of the significance of apoptotic cell death in the systemic manifestations associated with acute pancreatitis. Since we identified apoptosis-inducing activity in pancreatitis-associated ascitic fluid in 1995, a number of investigators, including our group, have reported, through animal experiments, that apoptosis occurred in the parenchymal cells constituting organs, such as alveolar epithelial cells in the lung, renal tubular cells in the kidney, and hepatocytes in the liver, and this apoptosis was involved in organ dysfunction with severe acute pancreatitis. Moreover, through clinical and experimental investigations, apoptosis has been revealed to be involved in the mechanism of infectious complications in acute pancreatitis. Namely, apoptosis in lymphatic tissues and peripherally circulating lymphocytes is involved in the impairment of cellular immunity, and apoptosis in gut epithelial cells is implicated in bacterial translocation. These results suggest that apoptotic cell death may play a considerable role in affecting mortality and morbidity in severe acute pancreatitis. Control of apoptosis could be a potent strategy for improvement of the clinical outcome in severe acute pancreatitis.

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“…Particularly, Curley et al reported a significant decrease in the proportion of helper T cells in severe acute pancreatitis. 5 Moreover, we have reported that thymic atrophy and splenic atrophy occur in rat experimental severe acute pancreatitis 7,8 and that peripheral lymphocyte reduction due to apoptosis is linked to the development of subsequent infectious complications in patients with severe acute pancreatitis. 9,10 Recently, the concept of "Th1 (helper T cell type 1)/ Th2 (helper T cell type 2) balance" has been introduced for understanding the pathophysiological response during many diseases.…”

Section: Introductionmentioning

confidence: 99%

Significant elevation of serum interleukin-18 levels in patients with acute pancreatitis

et al. 2006

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Splenic Atrophy in Experimental Severe Acute Pancreatitis

Abstract: These results indicate that splenic atrophy resulting from splenocyte reduction occurs in rat experimental severe acute pancreatitis. It is suggested that splenocytes are recruited into systemic circulation in response to peripheral lymphocyte reduction as a result of apoptosis.

Cited by 25 publications

References 16 publications

Protective Effects of Ulinastatin on Proliferation and Cytokine Release of Splenocytes from Rats with Severe Acute Pancreatitis

Protective Effects of Ulinastatin on Proliferation and Cytokine Release of Splenocytes from Rats with Severe Acute Pancreatitis

Significance of apoptotic cell death in systemic complications with severe acute pancreatitis

Significant elevation of serum interleukin-18 levels in patients with acute pancreatitis

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