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Chinese Journal of Critical Care Medicine(Electronic Edition) ›› 2023, Vol. 16 ›› Issue (06): 475-480. doi: 10.3877/cma.j.issn.1674-6880.2023.06.006

• Original Article • Previous Articles    

Mechanism of regulatory T cells/T helper cell 17 imbalance in patients with pancreatic infection secondary to severe acute pancreatitis

Yahui Sun(), Tiantian Li   

  1. Department of Critical Care, Jinan Laiwu People's Hospital, Jinan 271100, China
    Department of Critical Care Medicine, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan 250021, China
  • Received:2023-05-09 Online:2023-12-31 Published:2024-02-05
  • Contact: Yahui Sun

Abstract:

Objective

To investigate the mechanism of regulatory T cells/T helper cell 17 (Treg/Th17) imbalance in patients with pancreatic infection secondary to severe acute pancreatitis (SAP).

Methods

Sixty SAP patients in Jinan Laiwu People's Hospital from March 2019 to March 2021 were collected, who were divided into a infected group (30 cases) and a uninfected group (30 cases). In addition, 50 healthy persons taking physical examination without symptoms of febrile infection were selected as the control group. The distribution of pathogenic bacteria in the infected patients was detected, the severity of the disease was assessed, and the serum amylase, blood calcium, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), C-reactive protein (CRP) and T cell subgroup levels were measured. Then the mechanism of Treg/Th17 imbalance in patients with pancreatic infection secondary to SAP was analyzed.

Results

Among the pathogens in the infected group, gram-positive bacteria were 56.7% (38/67), and gram-negative bacteria were 43.3% (29/67). The acute physiology and chronic health evaluation (APACHE) II score [(20 ± 4) vs. (14 ± 5), t = 4.814, P < 0.001] and Ranson score [(6.1 ± 2.0) vs. (4.0 ± 1.9), t = 4.116, P < 0.001] in the infected group were higher than those in the uninfected group. There were significant differences in the levels of serum amylase, blood calcium, TNF-α, IL-6 and CRP in the infected, uninfected and control groups, as well as the levels of CD3+, CD4+, CD8+ and CD4+/CD8+ T cell subgroups (F = 1 042.671, 4.018, 6.871, 10 542.863, 306.755, 69.062, 36.185, 37.974, 5.221; all P < 0.05). Further pairwise comparisons found that the serum amylase, TNF-α, IL-6, CRP and CD4+/CD8+ levels of the uninfected and infected groups were significantly higher compared with the control group, which were highest in the infected group (all P < 0.05). The CD3+, CD4+ and CD8+ levels of the uninfected and infected groups were significantly lower compared with the control group, and the CD3+ level was lowest in the infected group (all P < 0.05). The blood calcium level in the infected group was significantly lower compared with the control and uninfected groups (both P < 0.05).

Conclusion

In patients with pancreatic infection caused by pathogenic bacteria, the levels of CD3+, CD4+ and CD8+ decrease, and the CD4+/CD8+ level increases, which promotes the high expression of TNF-α, IL-6 and CRP, and increases the levels of pro-inflammatory factors, causing serious pathological damage.

Key words: Severe acute pancreatitis, Pancreatic infection, Regulatory T cells/T helper cell 17 imbalance, Mechanism study

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