Predictive significance of pro-inflammatory interleukins at newborns with hypoxic-ischemic encephalopathy

Relevance. Hypoxic-ischemic damage to the central nervous system is accompanied by overproduction of pro-inflammatory interleukins in newborns. Perinatal inflammatory responses contribute to unfavorable outcomes. Methods of investigation. The analysis of the cytokine profile in the blood serum was performed in 45 full-term newborns by the method of enzyme-linked immunosorbent assay within 4–96 hours after birth. 32 children had the signs of HIE stage 2, 13 children — HIE stage 3. Unfavorable neurological consequences were formed in 47,4% of children. Research results. Revealed an increase in the levels of IL1β — 17,7 [13,6; 25,4] and IL6 35,2 [24,9; 45,0] in newborns with HIE. A significant increase in pro-inflammatory cytokines was found in patients with unfavorable outcomes compared with favorable ones. When predicting the disabling consequences of DIE, a high predictive value was established for IL1β and IL6. Conclusion. In newborns with hypoxic-ischemic encephalopathy, an increase in serum IL1β and IL6 is observed. It is advisable to use an increase in IL1β >19,4 pg/ml (OR=12,80; 95% CI: 2,90–56,58) and IL6 >40,1 pg/ml (OR=11,33; 95% CI: 2,46–52,15).

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FEATURES KALLIKREIN-KININ SYSTEMS AND DYSFUNCTIONS ENDOTHELIUM AT NEWBORNS WITH HYPOXEMIC DEFEAT OF THE CENTRAL NERVOUS SYSTEM

Bulletin of Siberian Medicine ◽

10.20538/1682-0363-2013-3-106-110 ◽

2013 ◽

Vol 12 (3) ◽

pp. 106-110

Author(s):

V. A. Zhelev ◽

A. S. Pogudina ◽

V. V. Gorev

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Blood Plasma ◽

Inhibitory Activity ◽

Hypoxic Ischemic Encephalopathy ◽

Kinin System ◽

The Central Nervous System ◽

Kallikrein Kinin System ◽

Ischemic Encephalopathy

Proteolytic systems of tissue and blood plasma take part in the processes of adaptation and protection of an organism, as well as in development of pathological reactions. 201 prematurely newborn of various degree gestation with hypoxemic affection of the central nervous system were under observation. We have studied the activity of kallikrein, kallikreinogen in newborns with hypoxic-ischemic encephalopathy. The activity of the kallikrein-kinin system was increased in all the groups against the background of the decreased inhibitory activity of blood plasma of different intensity, which can be used for the prediction of the course of diseases.

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The Role of Mast Cells in Stroke

Cells ◽

10.3390/cells8050437 ◽

2019 ◽

Vol 8 (5) ◽

pp. 437 ◽

Cited By ~ 8

Author(s):

Edoardo Parrella ◽

Vanessa Porrini ◽

Marina Benarese ◽

Marina Pizzi

Keyword(s):

Central Nervous System ◽

Immune Response ◽

Nervous System ◽

Mast Cells ◽

Brain Edema ◽

Hemorrhagic Stroke ◽

Inflammatory Responses ◽

Adult Brain ◽

The Central Nervous System

Mast cells (MCs) are densely granulated perivascular resident cells of hematopoietic origin. Through the release of preformed mediators stored in their granules and newly synthesized molecules, they are able to initiate, modulate, and prolong the immune response upon activation. Their presence in the central nervous system (CNS) has been documented for more than a century. Over the years, MCs have been associated with various neuroinflammatory conditions of CNS, including stroke. They can exacerbate CNS damage in models of ischemic and hemorrhagic stroke by amplifying the inflammatory responses and promoting brain–blood barrier disruption, brain edema, extravasation, and hemorrhage. Here, we review the role of these peculiar cells in the pathophysiology of stroke, in both immature and adult brain. Further, we discuss the role of MCs as potential targets for the treatment of stroke and the compounds potentially active as MCs modulators.

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Histamine H4 Receptor Optimizes T Regulatory Cell Frequency and Facilitates Anti-Inflammatory Responses within the Central Nervous System

The Journal of Immunology ◽

10.4049/jimmunol.1101498 ◽

2011 ◽

Vol 188 (2) ◽

pp. 541-547 ◽

Cited By ~ 40

Author(s):

Roxana del Rio ◽

Rajkumar Noubade ◽

Naresha Saligrama ◽

Emma H. Wall ◽

Dimitry N. Krementsov ◽

...

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Inflammatory Responses ◽

T Regulatory Cell ◽

Cell Frequency ◽

Histamine H4 Receptor ◽

Regulatory Cell ◽

The Central Nervous System ◽

Anti Inflammatory ◽

H4 Receptor

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Neurological Deficit and Disturbances in Higher Nervous Activity during Modeling of Perinatal Hypoxic-Ischemic Damage to the Central Nervous System in Rat Pups

Bulletin of Experimental Biology and Medicine ◽

10.1023/b:bebm.0000008973.15597.58 ◽

2003 ◽

Vol 136 (3) ◽

pp. 242-245 ◽

Cited By ~ 4

Author(s):

S. V. Lebedev ◽

N. N. Volodin ◽

D. V. Blinov ◽

I. P. Lazarenko ◽

S. O. Rogatkin ◽

...

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Neurological Deficit ◽

Nervous Activity ◽

Ischemic Damage ◽

Rat Pups ◽

Higher Nervous Activity ◽

The Central Nervous System

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Paeoniflorin Attenuates Inflammatory Pain by Inhibiting Microglial Activation and Akt-NF-κB Signaling in the Central Nervous System

Cellular Physiology and Biochemistry ◽

10.1159/000490076 ◽

2018 ◽

Vol 47 (2) ◽

pp. 842-850 ◽

Cited By ~ 14

Author(s):

Bo Hu ◽

Guangtao Xu ◽

Xiaomin Zhang ◽

Long Xu ◽

Hong Zhou ◽

...

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Signaling Pathway ◽

Inflammatory Pain ◽

Microglial Activation ◽

Enzyme Linked Immunosorbent Assay ◽

Pain Model ◽

The Central Nervous System

Background/Aims: Paeoniflorin (PF) is known to have anti-inflammatory and paregoric effects, but the mechanism underlying its analgesic effect remains unclear. The aim of this study was to clarify the effect of PF on Freund’s complete adjuvant (CFA)-induced inflammatory pain and explore the underlying molecular mechanism. Methods: An inflammatory pain model was established by intraplantar injection of CFA in C57BL/6J mice. After intrathecal injection of PF daily for 8 consecutive days, thermal and mechanical withdrawal thresholds, the levels of inflammatory factors TNF-α, IL-1β and IL-6, microglial activity, and the expression of Akt-NF-κB signaling pathway in the spinal cord tissue were detected by animal ethological test, cell culture, enzyme-linked immunosorbent assay, immunofluorescence histochemistry, and western blot. Results: PF inhibited the spinal microglial activation in the CFA-induced pain model. The production of proinflammatory cytokines was decreased in the central nervous system after PF treatment both in vivo and in vitro. PF further displayed a remarkable effect on inhibiting the activation of Akt-NF-κB signaling pathway in vivo and in vitro. Conclusion: These results suggest that PF is a potential therapeutic agent for inflammatory pain and merits further investigation.

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Several forms of callitachykinins are distributed in the central nervous system and intestine of the blowfly Calliphora vomitoria.

Journal of Experimental Biology ◽

10.1242/jeb.198.12.2527 ◽

1995 ◽

Vol 198 (12) ◽

pp. 2527-2536

Author(s):

D R Nässel ◽

M Y Kim ◽

C T Lundquist

Keyword(s):

Central Nervous System ◽

Nervous System ◽

High Performance ◽

The Body ◽

Enzyme Linked Immunosorbent Assay ◽

Additional Material ◽

Immunoreactive Material ◽

The Central Nervous System ◽

Entire Central Nervous System ◽

The Brain

We have examined the distribution of two tachykinin-related neuropeptides, callitachykinin I and II (CavTK-I and CavTK-II), isolated from whole-animal extracts of the blowfly Calliphora vomitoria. Extracts of dissected brains, thoracic-abdominal ganglia and midguts of adult blowflies and the entire central nervous system of larval flies were analysed by high performance liquid chromatography (HPLC) combined with enzyme-linked immunosorbent assay (ELISA) for the presence of CavTKs. To identify the two neuropeptides by HPLC, we used the retention times of synthetic CavTK-I and II as reference and detection with an antiserum raised to locustatachykinin II (shown here to recognise both CavTK-I and II). The brain contains only two immunoreactive components, and these have exactly the same retention times as CavTK-I and II. The thoracic-abdominal ganglia and midgut contain immunoreactive material eluting like CavTK-I and II as well as additional material eluting later. The larval central nervous system (CNS) contains material eluting like CavTK-I and II as well as a component that elutes earlier. We conclude that CavTK-I and II are present in all assayed tissues and that additional, hitherto uncharacterised, forms of tachykinin-immunoreactive material may be present in the body ganglia and midgut as well as in the larval CNS. An antiserum was raised to CavTK-II for immunocytochemistry. This antiserum, which was found to be specific for CavTK-II in ELISA, labelled all the neurones and midgut endocrine cells previously shown to react with the less selective locustatachykinin antisera. It is not clear, however, whether CavTK-I and II are colocalised in all LomTK-immunoreactive cells since there is no unambiguous probe for CavTK-I.

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Arachidonic Acid Derivatives and Neuroinflammation

CNS & Neurological Disorders - Drug Targets ◽

10.2174/1871527320666210208130412 ◽

2021 ◽

Vol 20 ◽

Author(s):

Era Gorica ◽

Vincenzo Calderone

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Arachidonic Acid ◽

Prostaglandin E2 ◽

Phospholipase A2 ◽

Inflammatory Responses ◽

The Central Nervous System ◽

The Brain ◽

Arachidonic Acid Derivatives

: Neuroinflammation is characterized by dysregulated inflammatory responses localized within the brain and spinal cord. Neuroinflammation plays a pivotal role in the onset of several neurodegenerative disorders and is considered a typical feature of these disorders. Microglia perform primary immune surveillance and macrophage-like activities within the central nervous system. Activated microglia are predominant players in the central nervous system response to damage related to stroke, trauma, and infection. Moreover, microglial activation per se leads to a proinflammatory response and oxidative stress. During the release of cytokines and chemokines, cyclooxygenases and phospholipase A2 are stimulated. Elevated levels of these compounds play a significant role in immune cell recruitment into the brain. Cyclic phospholipase A2 plays a fundamental role in the production of prostaglandins by releasing arachidonic acid. In turn, arachidonic acid is biotransformed through different routes into several mediators that are endowed with pivotal roles in the regulation of inflammatory processes. Some experimental models of neuroinflammation exhibit an increase in cyclic phospholipase A2, leukotrienes, and prostaglandins such as prostaglandin E2, prostaglandin D2, or prostacyclin. However, findings on the role of the prostacyclin receptors have revealed that their signalling suppresses Th2-mediated inflammatory responses. In addition, other in vitro evidence suggests that prostaglandin E2 may inhibit the production of some inflammatory cytokines, attenuating inflammatory events such as mast cell degranulation or inflammatory leukotriene production. Based on these conflicting experimental data, the role of arachidonic acid derivatives in neuroinflammation remains a challenging issue.

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Systemic Catecholaminergic Deficiency in Depressed Patients with and without Coronary Artery Disease

Journal of Clinical Medicine ◽

10.3390/jcm10050986 ◽

2021 ◽

Vol 10 (5) ◽

pp. 986

Author(s):

Uta Hoppmann ◽

Harald Engler ◽

Sabrina Krause ◽

Edit Rottler ◽

Julia Hoech ◽

...

Keyword(s):

Coronary Artery Disease ◽

Central Nervous System ◽

Nervous System ◽

Coronary Artery ◽

Social Stress ◽

Stress Test ◽

Enzyme Linked Immunosorbent Assay ◽

Inflammation Markers ◽

The Central Nervous System ◽

Artery Disease

Background: Stress and depression are known to contribute to coronary artery disease (CAD) with catecholamines (CA), altering the balance to a pro- and anti-inflammatory stetting and potentially playing a key role in the underlying pathophysiology. This study aimed to elucidate the impact of social stress on the CA system and inflammation markers in patients suffering from CAD and depression. Methods: 93 subjects were exposed to the Trier Social Stress Test (TSST). Based on the results of the depression subscale of the Hospital Anxiety and Depression Scale (HADS, German Version) and the presence/absence of CAD, they were divided into four groups. A total of 21 patients suffered from CAD and depression (+D+CAD), 26 suffered from CAD alone (−D+CAD), and 23 suffered from depression only (+D−CAD); another 23 subjects served as healthy controls (−D−CAD). Subjects were registered at 09:00 AM at the laboratory. A peripheral venous catheter was inserted, and after a 60-min-resting period, the TSST was applied. Prior to and 5, 15, 30, and 60 min after the stress test, plasma epinephrine, norepinephrine, and dopamine concentrations (High Performance Liquid Chromatography (HPLC)) were measured together with the inflammation markers interleukin-6 (IL-6) and monocyte chemotactic protein-1 (MCP-1). High-sensitive C-reactive protein (hs-CRP, Enzyme-linked Immunosorbent Assay (ELISA)) was measured prior to TSST. Results: (+D−CAD) and (+D+CAD) patients showed significantly lower epinephrine and dopamine levels compared to the (−D+CAD) and (−D−CAD) participants at baseline (prior to TSST). Over the whole measurement period after the TSST, no inter-group difference was detected. Partial correlation (controlling for age, gender and Body Mass Index (BMI)) revealed a significant direct relation between MCP-1 and norepinephrine (r = 0.47, p = 0.03) and MCP-1 and epinephrine (r = 0.46, p = 0.04) in patients with −D+CAD at rest. Conclusions: The stress response of the CA system was not affected by depression or CAD, whereas at baseline we detected a depression-related reduction of epinephrine and dopamine release independent of CAD comorbidity. Reduced norepinephrine and dopamine secretion in the central nervous system in depression, known as ‘CA-deficit hypothesis’, are targets of antidepressant drugs. Our results point towards a CA-deficit in the peripheral nervous system in line with CA-deficit of the central nervous system and CA exhaustion in depression. This might explain somatic symptoms such as constipation, stomach pain, diarrhoea, sweating, tremor, and the influence of depression on the outcome of somatic illness such as CAD.

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Can depression be associated with the immune response

10.5327/1516-3180.443 ◽

2021 ◽

Author(s):

Maurício Machado Lenhardt ◽

Dauana Schwartz ◽

Bruna K. de F. Silva

Keyword(s):

Central Nervous System ◽

Immune Response ◽

Nervous System ◽

Depressive Symptoms ◽

Immune System ◽

Literature Review ◽

The Central Nervous System ◽

Biochemical Components ◽

Therapeutic Protocols ◽

Pro Inflammatory Cytokines

Introduction: Depression is a disease of uncertain installation and etiology, the imbalance of neurotransmitters is involved in this process, and stress can be an activator of pro-inflammatory cytokines and trigger depressive symptoms. The organism undergoes modulations due to biochemical changes and these are linked to molecular and biochemical components and by the survival instinct, the human body is stimulated to release substances as a form of protection. The objective of this study is to describe the possible association between a loss of homeostasis of the central nervous system (CNS), changes in the modulation of the immune system, and the development of depressive symptoms. Methods: This is an integrative literature review, available in the virtual health databases: PubMed, MEDLINE, SciELO, and Google Scholar published between the years 2010 to 2020. Results: Studies indicate that cytokines can interfere with the homeostasis of the CNS and that the imbalance of catecholamines and indoleamine is involved in the process of depression. In this sense, studies have focused on neuromodulation by blocking neurotransmitters and neuroreceptors to regulate the immune system. Conclusion: It’s already established that the imbalance in the release and reuptake of neurotransmitters is associated with the onset of the depression, however, current studies show that there may also be an association with the homeostasis of the immune system. Therapeutic protocols aren’t based on the correlation between the immune system and the onset of the disease, so further studies are needed to strengthen this relationship.

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