Circulating Lymphocyte Subsets Induce Secondary Infection in Acute Pancreatitis

Ding, Lili; Yang, Yimin; Wang, Haijiao; Gao, Pujun

doi:10.3389/fcimb.2020.00128

Cited by 23 publications

(18 citation statements)

References 93 publications

(124 reference statements)

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“…By staining with the anti-CD3 or anti-CD20 antibody, T- and B-lymphocytes were detected more in the interstitium than in the acini of patients with AP [ 26 ]. By contrast, as immune mediators, certain subtypes of lymphocytes could have a detrimental effect on secondary infection in AP [ 27 ]. Similarly, M1 and M2 macrophages have distinct properties in disease progression.…”

Section: Discussionmentioning

confidence: 99%

Diabetic Bone Marrow Cell Injection Accelerated Acute Pancreatitis Progression

Luo

Yan

Zhang

et al. 2021

Journal of Immunology Research

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Acute pancreatitis (AP) is one of the leading causes of hospital admission, 20% of which could progress to the severe type with extensive acinar cell necrosis. Clinical studies have reported that diabetes is an independent risk factor of the incidence of AP and is associated with higher severity than nondiabetic subjects. However, how diabetes participates in AP progression is not well defined. To investigate this question, wild-type (wt) and diabetic db/db mice at the age of 16 weeks were used in the study. AP was induced in wt recipients by 10 injections of 50 μg/kg caerulein with a 1 h interval. One hour after the last caerulein injection, bone marrow cells (BMC) isolated from wt and db/db mice were injected intraperitoneally into the recipients ( 1 × 10 7 cells/recipient). The recipients with no BMC injection served as controls. Thirteen hours after BMC injection, serum lipase activity was 1.8- and 1.3-folds higher in mice that received db/db BMC, compared with those with no injection and wt BMC injection, respectively ( p ≤ 0.02 for both). By H&E staining, the overall severity score was 14.7 for no cell injection and 16.6 for wt BMC injection and increased to 22.6 for db/db BMC injection ( p ≤ 0.002 for both). In particular, mice with db/db BMC injection developed more acinar cell necrosis and vacuolization than the other groups ( p ≤ 0.03 for both). When sections were stained with an antibody against myeloperoxidase (MPO), the density of MPO+ cells in pancreatitis was 1.9- and 1.6-folds higher than wt BMC and no BMC injection groups, separately ( p ≤ 0.02 for both). Quantified by ELISA, db/db BMC produced more IL-6, GM-CSF, and IL-10 compared with wt BMC ( p ≤ 0.04 for all). In conclusion, BMC of db/db mice produced more inflammatory cytokines. In response to acinar cell injury, diabetic BMC aggravated the inflammation cascade and acinar cell injury, leading to the progression of acute pancreatitis.

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Section: Discussionmentioning

confidence: 99%

Diabetic Bone Marrow Cell Injection Accelerated Acute Pancreatitis Progression

Luo

Yan

Zhang

et al. 2021

Journal of Immunology Research

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“…Our assumption concerning the nosocomial origin of COVID-19 was based on the course of the inflammatory component of AP. It is well documented that SIRS lasts about 14 days in patients with AP, gradually leading to compensatory systemic anti-inflammatory syndrome (CARS) with compromising immune system patrolling function and increased risk of infection [6]. Nevertheless, the presence of COVID-19 cannot be excluded on admission, since according to Galanopoulos et al, 2020, patients, presenting exclusively with GI symptoms, have delayed diagnosis of COVID-19 and in their case the first respiratory symptoms appear later [9].…”

Section: Discussionmentioning

confidence: 99%

A case report of severe acute pancreatitis with infected necrosis and concomitant Coronavirus Disease‑19 (COVID‑19): a nosocomial infection or delayed respiratory manifestation of viral disease?

et al. 2021

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The association between COVID‑19 and acute pancreatitis (AP) has been extensively analyzed in recent research and review papers worldwide. It should be noted that most studies have focused on AP as a COVID‑19 complication and/or an extra‑pulmonary manifestation of the disease, although the investigation reports on the cases of prior pancreatitis and subsequent COVID‑19 infection are limited. The aim of this case report is to describe the treatment protocol and clinical outcome of a patient with acute necrotizing pancreatitis who developed nosocomial COVID‑19.. Case presentation. The data were collected from patient S., a 42‑year‑old male admitted with AP to the intensive care unit of Kyiv City Clinical Emergency Hospital, in October 2020. This study was reviewed and approved by the local Ethics Committee (Protocol No 25‑15‑60). The patient signed written informed consent to participate in the study, after having been informed of all relevant aspects that could influence his decision. The patient, primarily diagnosed with AP, was admitted to the hospital without a PCR test for detecting SARS‑CoV‑2. 21 days after his admission to the hospital, the patient developed COVID‑19. AP progression to severe AP with infected necrosis, the development of systemic inflammatory response syndrome and multiple organ failure necessitated operative pancreatic debridement, which was postponed due to severe acute respiratory failure. Operative pancreatic debridement was performed on the 45th day of hospital stay after the resolution of COVID‑19‑associated pneumonia. The postoperative period was typical for the disease severity and the extent of the surgery, and was complicated by external pancreatic and colonic fistulas. The length of hospital stay for this patient was 115 days which included 20 days of treatment and monitoring in the intensive care unit due to pneumonia. He was discharged after clinical symptom improvement. Conclusions. It is imperative to screen patients presenting with AP for SARS‑CoV‑2 in order to avoid misdiagnosis and inappropriate treatment strategy. Further detailed investigation of mechanisms of pancreatic injury in patients with SARS‑CoV‑2 is necessary.

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“…SAP is defined with local or remote organ dysfunction (2), accounting for the majority of the death rate. Damaged pancreatic acinar cells induce a systemic inflammatory response syndrome (SIRS) by releasing cytokines, chemokines, and immune cells, such as such as IL-1b, IL-6, Th1, and Th17 (3)(4)(5). Compensatory antiinflammatory syndrome (CARS) is a regulatory procedure limiting the excessive inflammatory response, involving regulatory immune cells, such as regulatory T cells (Tregs) and type 2 macrophages (M2) (6,7).…”

Section: Introductionmentioning

confidence: 99%

Myeloid-Derived Suppressor Cells in Patients With Acute Pancreatitis With Increased Inhibitory Function

et al. 2022

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Acute pancreatitis (AP) is pancreatic or systemic inflammation without or with motion organ dysfunction. Severe acute pancreatitis (SAP) is the main cause of death for patients with AP. A pro-/anti-inflammatory imbalance is considered the key regulation of disease severity. However, the real mechanism of SAP remains unclear. This study aimed to identify the frequency and specific roll of myeloid-derived suppressor cell (MDSC) in AP. We evaluated MDSC frequency and disease severity by analyzing MDSCs in the peripheral blood of healthy controls (HCs) and patients with mild acute pancreatitis (MAP) and SAP by flow cytometry. We also compared the frequency and inhibitory ability of MDSCs from HCs and SAP, and finally detected the reason for the difference in inhibitory ability. AP was marked by expansion of MDSCs as well as its subsets, granulocytic MDSCs (G-MDSCs) and monocytic MDSCs (M-MDSCs). The proportion of MDSC in the peripheral blood mononuclear cells of patients with AP was increased and positively correlated with AP severity. The frequency of MDSC was decreased after treatment compared with pre-treatment. CD3+ T cells were remarkably inhibited by MDSC derived from the patients with SAP. In the expression of arginase-1 (Arg-1) and reactive oxygen species (ROS), the MDSCs from patients with SAP increased. These findings demonstrated that MDSCs expanded in the peripheral blood in patients with AP, especially in those with SAP. Moreover, the inhibitory ability of MDSCs was increased in the patients with SAP compared with that in the HCs. The enhanced suppressive function was possibly caused by an overexpression of Arg-1 and ROS.

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Circulating Lymphocyte Subsets Induce Secondary Infection in Acute Pancreatitis

Cited by 23 publications

References 93 publications

Diabetic Bone Marrow Cell Injection Accelerated Acute Pancreatitis Progression

Diabetic Bone Marrow Cell Injection Accelerated Acute Pancreatitis Progression

A case report of severe acute pancreatitis with infected necrosis and concomitant Coronavirus Disease‑19 (COVID‑19): a nosocomial infection or delayed respiratory manifestation of viral disease?

Myeloid-Derived Suppressor Cells in Patients With Acute Pancreatitis With Increased Inhibitory Function

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