Changes in Adaptive and Innate Immunity in Patients with Acute Pancreatitis and Systemic Inflammatory Response Syndrome

Mylona, Vassiliki; Koussoulas, Vassilios; Tzivras, Dimitrios; Makrygiannis, Elias; Georgopoulou, Panagiota; Koratzanis, George; Giamarellos‐Bourboulis, Evangelos J.; Tzivras, Michalis

doi:10.1159/000329460

Cited by 26 publications

(12 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The presented findings indicate that when sepsis develops, NK cells are reprogrammed toward the biosynthesis of IFNγ and of IL‐23. In a recent study of our group, NK cells were isolated early upon presentation of signs of systemic inflammation in a cohort of patients with acute edematous pancreatitis . Stimulation with LPS produced great amounts of TNFα and IL‐6 from NK cells of patients with acute pancreatitis, whatever did not happen with the enrolled population of sepsis patients in the current study.…”

Section: Discussionmentioning

confidence: 75%

The functional role of natural killer cells early in clinical sepsis

Giannikopoulos¹,

Antonopoulou

Kalpakou³

et al. 2012

APMIS

Self Cite

View full text Add to dashboard Cite

Although much information is available for the function of circulating monocytes when signs of sepsis are apparent, little is known for natural killer (NK) cells. NK cells were isolated from 10 healthy controls and from 103 patients with sepsis within the first 24 h from diagnosis. NK cells were stimulated with lipopolysaccharide for cytokine production. Release of tumor necrosis factor-alpha and of interleukin (IL)-6 was below the limit of detection. Release of IL-23 and of interferon-gamma (IFNγ) was significantly greater among patients than among healthy volunteers. Release of IFNγ was pronounced in septic shock. Patients were divided into two subgroups based on the ratio of IFNγ to IL-23 released by the NK cells after stimulation: those with ratio ≤5 and 28-day survival 13.5%, and those with ratio >5 and 28-day survival 29.4% (p: 0.048). It is concluded that early after clinical development of sepsis, NK cells remain active for the production of IFNγ. Their activity is associated with the final outcome.

show abstract

Section: Discussionmentioning

confidence: 75%

The functional role of natural killer cells early in clinical sepsis

Giannikopoulos¹,

Antonopoulou

Kalpakou³

et al. 2012

APMIS

Self Cite

View full text Add to dashboard Cite

show abstract

“…Toxic ingredients released from the damaged structures such as ROS and RNS, products of arachidonic acid metabolism (prostaglandins, leukotrienes, thromboxanes), and other noxious agents work as propagators of sterile inflammation and chemoattractants for inflammatory cells, leading to the increased production of pro-inflammatory cytokines (e.g., TNFα, IL-6, IL-8). This is accompanied by vascular endothelium damage, increased vascular permeability, and processes of intensified coagulation and fibrinolysis [52,53,54,55]. Local pancreatic inflammation could develop into systemic inflammatory response (SIRS), often leading to multiple organ dysfunction (MODS) and septic shock [55,56].…”

Section: Melatonin System and Acute Pancreatitismentioning

confidence: 99%

“…This is accompanied by vascular endothelium damage, increased vascular permeability, and processes of intensified coagulation and fibrinolysis [52,53,54,55]. Local pancreatic inflammation could develop into systemic inflammatory response (SIRS), often leading to multiple organ dysfunction (MODS) and septic shock [55,56]. …”

Section: Melatonin System and Acute Pancreatitismentioning

confidence: 99%

Effects of Melatonin and Its Analogues on Pancreatic Inflammation, Enzyme Secretion, and Tumorigenesis

Jaworek

Leja-Szpak

Nawrot-Porąbka

et al. 2017

IJMS

View full text Add to dashboard Cite

Melatonin is an indoleamine produced from the amino acid l-tryptophan, whereas metabolites of melatonin are known as kynuramines. One of the best-known kynuramines is N1-acetyl-N1-formyl-5-methoxykynuramine (AFMK). Melatonin has attracted scientific attention as a potent antioxidant and protector of tissue against oxidative stress. l-Tryptophan and kynuramines share common beneficial features with melatonin. Melatonin was originally discovered as a pineal product, has been detected in the gastrointestinal tract, and its receptors have been identified in the pancreas. The role of melatonin in the pancreatic gland is not explained, however several arguments support the opinion that melatonin is probably implicated in the physiology and pathophysiology of the pancreas. (1) Melatonin stimulates pancreatic enzyme secretion through the activation of entero-pancreatic reflex and cholecystokinin (CCK) release. l-Tryptophan and AFMK are less effective than melatonin in the stimulation of pancreatic exocrine function; (2) Melatonin is a successful pancreatic protector, which prevents the pancreas from developing of acute pancreatitis and reduces pancreatic damage. This effect is related to its direct and indirect antioxidant action, to the strengthening of immune defense, and to the modulation of apoptosis. Like melatonin, its precursor and AFMK are able to mimic its protective effect, and it is commonly accepted that all these substances create an antioxidant cascade to intensify the pancreatic protection and acinar cells viability; (3) In pancreatic cancer cells, melatonin and AFMK activated a signal transduction pathway for apoptosis and stimulated heat shock proteins. The role of melatonin and AFMK in pancreatic tumorigenesis remains to be elucidated.

show abstract

“…The first group consisted of patients with infectious diseases in whom plasma was obtained ≤24 hours after presentation: viral lower respiratory tract infections (LRTI) (n = 25; Table 3), measles [15] (n = 43), infectious mononucleosis caused by either Epstein-Barr virus (EBV) [16] or cytomegalovirus (CMV) infection (n = 16), bacterial and viral respiratory co-infections (n = 20; Table 3), bacterial sepsis [17], stratified into sepsis, severe sepsis and septic shock [18] (n = 156), and candidemia [19] (n = 26). The second group comprised of patients with non-infectious inflammation: Crohn's disease (n = 15), gout (n = 36), autoinflammatory syndromes (n = 15), rheumatoid arthritis (n = 20), and pancreatitis [20] (n = 22). Patients with autoinflammatory syndromes consisted mainly of patients with well-known, genetically confirmed autoinflammatory diseases, like hyperimmunoglobulin-D syndrome, familial Mediterranean fever, Muckle-Wells syndrome and tumor necrosis factor receptor-1 associated syndrome (TRAPS).…”

Section: Biomarker Studymentioning

confidence: 99%

The discriminative capacity of soluble Toll-like receptor (sTLR)2 and sTLR4 in inflammatory diseases

et al. 2014

View full text Add to dashboard Cite

BackgroundThe extracellular domains of cytokine receptors are released during inflammation, but little is known about the shedding of Toll-like receptors (TLR) and whether they can be used as diagnostic biomarkers.MethodsThe release of sTLR2 and sTLR4 was studied in in-vitro stimulations, as well as in-vivo during experimental human endotoxemia (n = 11, 2 ng/kg LPS), and in plasma of 394 patients with infections (infectious mononucleosis, measles, respiratory tract infections, bacterial sepsis and candidemia) or non-infectious inflammation (Crohn’s disease, gout, rheumatoid arthritis, autoinflammatory syndromes and pancreatitis). Using C-statistics, the value of sTLR2 and sTLR4 levels for discrimination between infections and non-infectious inflammatory diseases, as well as between viral and bacterial infections was analyzed.ResultsIn-vitro, peripheral blood mononuclear cells released sTLR2 and sTLR4 by exposure to microbial ligands. During experimental human endotoxemia, plasma concentrations peaked after 2 hours (sTLR4) and 4 hours (sTLR2). sTLR4 did not correlate with cytokines, but sTLR2 correlated positively with TNFα (rs = 0.80, P < 0.05), IL-6 (rs = 0.65, P < 0.05), and IL-1Ra (rs = 0.57, P = 0.06), and negatively with IL-10 (rs = -0.58, P = 0.06), respectively. sTLR4 had a similar area under the ROC curve [AUC] for differentiating infectious and non-infectious inflammation compared to CRP: 0.72 (95% CI 0.66-0.79) versus 0.74 (95% CI 0.69-0.80) [P = 0.80], while sTLR2 had a lower AUC: 0.60 (95% CI 0.54-0.66) [P = 0.0004]. CRP differentiated bacterial infections better from viral infections than sTLR2 and sTLR4: AUC 0.94 (95% CI 0.90-0.96) versus 0.58 (95% CI 0.51-0.64) and 0.75 (95% CI 0.70-0.80), respectively [P < 0.0001 for both].ConclusionssTLRs are released into the circulation, and suggest the possibility to use sTLRs as diagnostic tool in inflammatory conditions.

show abstract

Changes in Adaptive and Innate Immunity in Patients with Acute Pancreatitis and Systemic Inflammatory Response Syndrome

Cited by 26 publications

References 19 publications

The functional role of natural killer cells early in clinical sepsis

The functional role of natural killer cells early in clinical sepsis

Effects of Melatonin and Its Analogues on Pancreatic Inflammation, Enzyme Secretion, and Tumorigenesis

The discriminative capacity of soluble Toll-like receptor (sTLR)2 and sTLR4 in inflammatory diseases

Contact Info

Product

Resources

About