Clinical observation of immunity in patients with secondary infection from severe acute pancreatitis

Shen, Yinfeng; Cui, Naiqiang

doi:10.1007/s00011-012-0467-1

Cited by 24 publications

(17 citation statements)

References 32 publications

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“…The shift in microbial community structure was reported to induce the expression of TNFα and IL-6 expression in intestine [8] and then exaggerated the intestinal barrier injury in IBD. Acute pancreatitis is characterized by excessive release of inflammatory cytokines in both system and intestine [9]. …”

Section: Introductionmentioning

confidence: 99%

Dysbiosis of intestinal microbiota and decrease in paneth cell antimicrobial peptide level during acute necrotizing pancreatitis in rats

et al. 2017

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ObjectivesIntestinal barrier dysfunction plays an important role in acute necrotizing pancreatitis (ANP) and intestinal microbiota dysbiosis was involved in intestinal barrier failure. Paneth cells protect intestinal barrier and are associated with intestinal microbiota. Here, we investigated changes in intestinal microbiota and antimicrobial peptides of Paneth cells in ileum during ANP.MethodsRats with ANP were established by retrograde injection of 3.5% sodium taurocholate into biliopancreatic duct and sacrificed at 24h and 48h, respectively. Injuries of pancreas and distal ileum were evaluated by histopathological score. Intestinal barrier function was assessed by plasma diamine oxidase activity (DAO) and D-lactate. Systemic and intestinal inflammation was evaluated by TNFα, IL-1β and IL-17A concentration by ELISA, respectively. 16S rRNA high throughput sequencing on fecal samples was used to investigate the changes in intestinal microbiota in the ANP group at 48h. Lysozyme and α-defensin5 were measured by real-time PCR, western blot and immunofluoresence.ResultsANP rats had more severe histopathological injuries in pancreas and distal ileum, injured intestinal barrier and increased expression of TNFα, IL-1β and IL-17A in plasma and distal ileum compared with those of the sham-operated (SO) group. Principal component analysis (PCA) showed structural segregation between the SO and ANP groups. Operational taxonomic unit (OTU) number and ACE index revealed decreased microbiota diversity in the ANP group. Taxonomic analysis showed dysbiosis of intestinal microbiota structure. At phyla level, Saccharibacteria and Tenericutes decreased significantly. At genus level, Escherichia-Shigella and Phascolarctobacterium increased significantly, while Candidatus_Saccharimonas, Prevotellaceae_UCG-001, Lachnospiraceae_UCG-001, Ruminiclostridium_5 and Ruminococcaceae_UCG-008 decreased significantly. Lysozyme and α-defensin5 mRNA expression levels decreased significantly in ANP group at 48h. Protein expression of lysozyme decreased in ANP groups at 24h and 48h. Meanwhile, the relative abundance of Escherichia-Shigella correlated inversely with the decrease in lysozyme.ConclusionThe disorder in intestinal microbiota and decreases of Paneth cell antimicrobial peptides might participate in the pathogenesis of intestinal barrier dysfunction during ANP.

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Section: Introductionmentioning

confidence: 99%

Dysbiosis of intestinal microbiota and decrease in paneth cell antimicrobial peptide level during acute necrotizing pancreatitis in rats

et al. 2017

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“…Despite persistent efforts and rapid advances in early anti-inflammatory and organ-supportive treatment measures, the mortality rate remains high, and infectious complications are the dominant cause of late mortality [3,4]. Early immune dysfunction followed by immunosuppression is associated with infectious complications [5]. Immunosuppression occurs in the early phase of AP, leading to susceptibility of the host to infectious complications and then to systemic sepsis in the late stage [6,7].…”

Section: Introductionmentioning

confidence: 99%

sPD‐L1 Expression is Associated with Immunosuppression and Infectious Complications in Patients with Acute Pancreatitis

Chen

Liu

et al. 2017

Scand J Immunol

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Acute pancreatitis (AP) with infectious complications has high mortality because of early-stage immunosuppression. The programmed cell death-1 (PD-1)/programmed cell death ligand 1 (PD-L1) pathway is an important host immunosuppression mechanism. Soluble PD-L1 (sPD-L1) expression regulates co-inhibitory signals in malignancies or autoimmune disorders; however, its effects in AP are unknown. Here, we evaluated whether serum sPD-L1 is involved in immune dysfunction and assessed its relationship with infectious complications in early AP. Blood samples were obtained from 56 patients with acute pancreatitis and 21 healthy individuals in this prospective study. Serum sPD-L1 levels within 48 h after AP onset were tested by enzyme-linked immunosorbent assays. Relevant immune parameters (human leucocyte antigen-DR, lymphocyte count) and inflammatory markers (C-reactive protein, white blood cell count) were analysed. sPD-L1 was significantly upregulated in patients with early AP, especially those with infectious complications, compared to healthy controls. Significant negative correlations were observed among monocyte HLA-DR expression, lymphocyte count and sPD-L1 levels in AP. Multivariate regression indicated that sPD-L1 was an independent risk factor for infectious complications in AP. The findings suggest that increased sPD-L1 expression appears to be involved in the development of immunosuppression in the early stage of AP and that sPD-L1 might be an early parameter for prediction of infectious complications in patients with AP.

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“…Shen et al [8] reported that the levels of TNF-α and IL-6 in a MODS group of SAP patients differed from those of a non-MODS group, with higher levels on days 3 and 7, and lower levels on day 14 in the early stage. Shen and Cui [9] reported that the cytokine levels in an infected group differed from those in a noninfected group, with a rise in TNF-α and IL-6 through the first 2 weeks, but dropping at 1 month. Moreover, IL-10 and IL-4 increased initially, but then dropped over the next 3 weeks in the late stage.…”

Section: Discussionmentioning

confidence: 97%

“…Some researchers suggest that the excessive inflammatory immune response to SAP mediates pathological damage and that immune dysregulation plays an important role in infection and organ dysfunction [8,9]. However, few studies have investigated the relationship between the severity of the event and immune dysregulation in the course of SAP.…”

Section: Introductionmentioning

confidence: 97%

Relationship between the degree of severe acute pancreatitis and patient immunity

Shen

Deng

et al. 2014

Surg Today

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Clinical observation of immunity in patients with secondary infection from severe acute pancreatitis

Abstract: An early excessive immune response followed by a subsequent immune deficiency is closely related to secondary SAP infection.

Cited by 24 publications

References 32 publications

Dysbiosis of intestinal microbiota and decrease in paneth cell antimicrobial peptide level during acute necrotizing pancreatitis in rats

Dysbiosis of intestinal microbiota and decrease in paneth cell antimicrobial peptide level during acute necrotizing pancreatitis in rats

sPD‐L1 Expression is Associated with Immunosuppression and Infectious Complications in Patients with Acute Pancreatitis

Relationship between the degree of severe acute pancreatitis and patient immunity

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