scholarly journals Muramyl dipeptide and IL-1 effects on sleep and brain temperature after inhibition of serotonin synthesis

1997 ◽  
Vol 273 (5) ◽  
pp. R1663-R1668 ◽  
Author(s):  
Luca Imeri ◽  
Susanna Bianchi ◽  
Mauro Mancia
Keyword(s):  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Muramyl Dipeptide ◽  
Serotonin Synthesis ◽  
System 2 ◽  
Cortical Temperature ◽  
Second Phases ◽  
Freely Moving

The role of the interactions between serotonin (5-HT) and muramyl dipeptide (MDP) and interleukin-1 (IL-1) in sleep control and thermoregulation was evaluated. To this purpose, MDP and IL-1 were injected intracerebroventricularly at dark onset into freely moving rats pretreated twice intraperitoneally with para-chlorophenylalanine (PCPA) (300 mg/kg), which depletes brain 5-HT and causes insomnia. Fever and slow-wave sleep (SWS) enhancement induced by 150 pmol MDP were completely blocked in PCPA-pretreated rats. Only the first phase of the biphasic increase in SWS induced by 2.5 ng IL-1 was suppressed by PCPA pretreatment, whereas fever remained unaffected. These results suggest that 1) MDP effects on both sleep-wake activity and brain cortical temperature are mediated by the serotonergic system; 2) the mechanisms mediating the first and the second phases of IL-1-induced SWS excess are different: 5-HT could be involved in the first phase, but not in the second one; and 3) the 5-HT system does not appear to be involved in IL-1-induced fever.

Interleukin-1 induces changes in sleep, brain temperature, and serotonergic metabolism

1997 ◽  
Vol 272 (2) ◽  
pp. R601-R606 ◽  
Author(s):  
C. Gemma ◽  
L. Imeri ◽  
M. G. de Simoni ◽  
M. Mancia
Keyword(s):  
Time Course ◽  
Preoptic Area ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Secondary Effect ◽  
Intracerebroventricular Injection ◽  
Early Increase ◽  
Cortical Temperature ◽  
Freely Moving

Simultaneous recordings of sleep-wake activity and of serotonergic metabolism in the medial preoptic area were performed in freely moving rats after the intracerebroventricular injection of interleukin-1 (IL-1) at dark onset. IL-1 (2.5 ng) induced a biphasic increase in slow-wave sleep and an early increase in serotonergic metabolism starting 30 min postinjection. Phasic, state-specific changes (which have been described in spontaneous sleep) were superimposed on this tonic, overall increase in serotonergic metabolism. IL-1 (25 ng) induced an increase in wakefulness and a delayed increase in serotonergic metabolism, which started 120 min postinjection. This suggests that the time course of the serotonergic activation could play a role in mediating IL-1 effects on sleep. Both doses of IL-1 induced a similar and significant increase in brain cortical temperature, suggesting that IL-1 effects on sleep are not a secondary effect of the increase in cortical temperature and that the serotonergic system is not involved in IL-1-induced fever.

905 Role of Cox-2 enzyme in the interleukin-1-induced slow-wave sleep

1997 ◽  
Vol 28 ◽  
pp. S111
Author(s):  
Akira Terao ◽  
Hitoshi Matsumura ◽  
Shinsuke Satoh ◽  
Masayuki Saito ◽  
Osamu Hayaishi
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Interleukin 1 ◽  
Cox 2

An IL-1 receptor and an IL-1 receptor antagonist attenuate muramyl dipeptide- and IL-1-induced sleep and fever

1993 ◽  
Vol 265 (4) ◽  
pp. R907-R913 ◽  
Author(s):  
L. Imeri ◽  
M. R. Opp ◽  
J. M. Krueger
Keyword(s):  
Receptor Antagonist ◽  
Eye Movement ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Dose Range ◽  
Muramyl Dipeptide ◽  
Nrem Sleep ◽  
Type I

It is hypothesized that the somnogenic and pyrogenic effects of muramyl dipeptide (MDP) are mediated via enhanced interleukin-1 (IL-1) production. To test this hypothesis the effects of intracerebroventricular (icv) administration of a recombinant human soluble type I IL-1 receptor (sIL-1r) and of the IL-1 receptor antagonist (IL-1ra) on MDP-induced sleep and fever were evaluated in rabbits. The sIL-1r recognized rabbit IL-1 beta, but it did not affect sleep or brain temperature across the dose range tested (1-50 micrograms) when injected icv into normal rabbits. Pretreatment of rabbits with 50 micrograms sIL-1r or 10 micrograms IL-1ra blocked human recombinant IL-1-enhanced nonrapid eye movement (NREM) sleep and fever. Thus both the sIL-1r and the IL-1ra were effective antagonists of IL-1 actions. When the animals were pretreated with either 50 micrograms sIL-1r or with 10 or 100 micrograms of the IL-1ra, the somnogenic effects of 150 pmol MDP were attenuated. However, the sIL-1r had little effect on MDP-induced febrile responses. These results suggest that the sIL-1r and the IL-1ra can function as antagonists of IL-1 actions in vivo and that MDP-induced sleep and fever are partially mediated by IL-1.

Brain temperature changes coupled to sleep states persist during interleukin 1-enhanced sleep

1986 ◽  
Vol 250 (1) ◽  
pp. R96-R103 ◽  
Author(s):  
J. Walter ◽  
D. Davenne ◽  
S. Shoham ◽  
C. A. Dinarello ◽  
J. M. Krueger
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Temperature Changes ◽  
Arousal State ◽  
Intraventricular Infusion ◽  
Sleep Cycles

The effects of human interleukin 1 (IL 1) on the architecture of rabbit sleep-wake cycles and brain temperature (Tbr) changes coupled to states of vigilance were examined. Cerebral intraventricular infusion of IL 1 induced increased slow-wave sleep (SWS), increased electroencephalographic slow-wave (0.5-4 Hz) amplitudes, and fever. Heat-inactivated IL 1 failed to elicit these responses. IL 1 also significantly inhibited rapid-eye-movement (REM) sleep; however, inactivated IL 1 also reduced REM sleep; thus some of the IL 1-induced REM reduction may be related to the infusion process. The duration and number of sleep cycles (REM-to-REM interval) were unaffected by IL 1. Similarly, Tbr changes that normally occur during the transition from one arousal state to another remained unchanged after IL 1 infusion, even though rabbits were simultaneously febrile. We conclude that IL 1 selectively enhances SWS while leaving sleep cycles and Tbr changes coupled to states of vigilance undisturbed.

Recombinant tumor necrosis factor and interleukin 1 enhance slow-wave sleep

1987 ◽  
Vol 253 (1) ◽  
pp. R142-R149 ◽  
Author(s):  
S. Shoham ◽  
D. Davenne ◽  
A. B. Cady ◽  
C. A. Dinarello ◽  
J. M. Krueger
Keyword(s):  
Immune Response ◽  
Tumor Necrosis Factor ◽  
Slow Wave ◽  
Tumor Necrosis ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Temperature Changes ◽  
Recombinant Tumor Necrosis Factor ◽  
Necrosis Factor

The cytokines interleukin 1 (IL 1) and interferon (IFN) are immune response modifiers that are also pyrogenic and somnogenic. Tumor necrosis factor (TNF) (cachectin) is another pyrogenic monocyte product whose production can be elicited by somnogenic agents such as endotoxin. Human recombinant TNF (rTNF), therefore, was assayed for somnogenic activity. Intravenous (iv) or intracerebroventricular (ICV) injections of rTNF enhanced slow-wave sleep (SWS) and electroencephalographic slow-wave (0.5-4.0 Hz) activity. Recombinant TNF also suppressed rapid-eye-movement sleep (REM) and induced biphasic fevers whether given by intravenous or ICV injection. Responses to rTNF were compared with those elicited by human recombinant beta-IL 1 (rIL 1). Sleep responses elicited by rIL 1 were similar to those previously reported for native IL 1 and to those elicited by rTNF. However, unlike rTNF, rIL 1 induced monophasic fevers. Animal behavior and brain temperature changes that occur during the transition from one arousal state to another remained undisturbed after either rTNF or rIL 1 treatment. The fact that TNF and IL 1 as well as other immunoactive substances, e.g., IFN, muramyl peptides, and endotoxin, enhance SWS suggests that SWS is linked to the immune response. We conclude that TNF, in addition to IL 1 and IFN, is an endogenous somnogen.

Role of inflammation in the development of colorectal cancer

2020 ◽  
Vol 20 ◽  
Author(s):  
Sridhar Muthusami ◽  
R. Ileng Kumaran ◽  
Kokelavani Nampalli Babu ◽  
Sneha Krishnamoorthy ◽  
Akash Guruswamy ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Chronic Inflammation ◽  
Interleukin 1 ◽  
Cell Types ◽  
Model Systems ◽  
Cytokine Gene Expression ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Proinflammatory Molecules

: Chronic inflammation can lead to the development of many diseases including cancer. Inflammatory bowel disease (IBD) that includes both ulcerative colitis (UC) and Crohn's disease (CD) are risk factors for the development of colorectal cancer (CRC). Many cytokines produced primarily by the gut immune cells either during or in response to localized inflammation in the colon and rectum are known to stimulate the complex interactions between the different cell types in the gut environment resulting in acute inflammation. Subsequently, chronic inflammation together with genetic and epigenetic changes has been shown to lead to the development and progression of CRC. Various cell types present in the colon such as enterocytes, Paneth cells, goblet cells and macrophages express receptors for inflammatory cytokines and respond to tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6 and other cytokines. Among the several cytokines produced, TNF-α and IL-1β are the key proinflammatory molecules that play critical roles in the development of CRC. The current review is intended to consolidate the published findings to focus on the role of proinflammatory cytokines, namely TNF-α and IL-1β, on inflammation (and the altered immune response) in the gut, to better understand the development of CRC in IBD, using various experimental model systems, preclinical and clinical studies. Moreover, this review also highlights the current therapeutic strategies available (monotherapy and combination therapy), to alleviate the symptoms or treat inflammationassociated CRC by using monoclonal antibodies or aptamers to block proinflammatory molecules, inhibitors of tyrosine kinases in inflammatory signaling cascade, competitive inhibitors of proinflammatory molecules, and the nucleic acid drugs like small activating RNAs (saRNAs) or microRNA (miRNA) mimics to activate tumor suppressor or repress oncogene/proinflammatory cytokine gene expression.

scholarly journals Hippocampal Interneurons are Required for Trace Eyeblink Conditioning in Mice

2021 ◽  
Author(s):  
Wei-Wei Zhang ◽  
Rong-Rong Li ◽  
Jie Zhang ◽  
Jie Yan ◽  
Qian-Hui Zhang ◽  
...  
Keyword(s):  
Eyeblink Conditioning ◽  
Pyramidal Cells ◽  
Conditioned Eyeblink ◽  
Cellular Mechanisms ◽  
Sustained Activity ◽  
Early Acquisition ◽  
Freely Moving ◽  
Trace Eyeblink Conditioning

AbstractWhile the hippocampus has been implicated in supporting the association among time-separated events, the underlying cellular mechanisms have not been fully clarified. Here, we combined in vivo multi-channel recording and optogenetics to investigate the activity of hippocampal interneurons in freely-moving mice performing a trace eyeblink conditioning (tEBC) task. We found that the hippocampal interneurons exhibited conditioned stimulus (CS)-evoked sustained activity, which predicted the performance of conditioned eyeblink responses (CRs) in the early acquisition of the tEBC. Consistent with this, greater proportions of hippocampal pyramidal cells showed CS-evoked decreased activity in the early acquisition of the tEBC. Moreover, optogenetic suppression of the sustained activity in hippocampal interneurons severely impaired acquisition of the tEBC. In contrast, suppression of the sustained activity of hippocampal interneurons had no effect on the performance of well-learned CRs. Our findings highlight the role of hippocampal interneurons in the tEBC, and point to a potential cellular mechanism subserving associative learning.

scholarly journals The Potential Role of IL1RAP on Tumor Microenvironment-Related Inflammatory Factors in Stomach Adenocarcinoma

2021 ◽  
Vol 20 ◽  
pp. 153303382199528
Author(s):  
Qing Lv ◽  
Qinghua Xia ◽  
Anshu Li ◽  
Zhiyong Wang
Keyword(s):  
Tumor Microenvironment ◽  
Interleukin 1 ◽  
Mrna Level ◽  
Inflammatory Factors ◽  
Stomach Carcinoma ◽  
Downstream Target ◽  
Volume Weight

This study was performed to investigate the role of interleukin-1 receptor accessory protein (IL1RAP) in stomach carcinoma in vitro and in vivo, determine whether IL1RAP knockdown could regulate the development of stomach carcinoma, and elucidate the relationship between IL1RAP knockdown and inflammation by tumor microenvironment-related inflammatory factors in stomach carcinoma. We first used TCGA and GEPIA systems to predict the potential function of IL1RAP. Second, western blot and RT-PCR were used to analyze the expression, or mRNA level, of IL1RAP at different tissue or cell lines. Third, the occurrence and development of stomach carcinoma in vitro and in vivo were observed by using IL1RAP knockdown lentivirus. Finally, the inflammation of stomach carcinoma in vitro and in vivo was observed. Results show that in GEPIA and TCGA systems, IL1RAP expression in STAD tumor tissue was higher than normal, and high expression of IL1RAP in STAD patients had a worse prognostic outcome. Besides, GSEA shown IL1RAP was negative correlation of apopopsis, TLR4 and NF-κB signaling pathway. We also predicted that IL1RAP may related to IL-1 s, IL-33, and IL-36 s in STAD. The IL1RAP expression and mRNA level in tumor, or MGC803, cells were increased. Furthermore, IL1RAP knockdown by lentivirus could inhibit stomach carcinoma development in vitro and in vivo through weakening tumor cell proliferation, migration, invasion, therefore reducing tumor volume, weight, and biomarker levels, and increasing apoptotic level. Finally, we found IL1RAP knockdown could increase inflammation of tumor microenvironment-related inflammatory factors of stomach carcinoma, in vitro and in vivo. Our study demonstrates that IL1RAP is possibly able to regulate inflammation and apoptosis in stomach carcinoma. Furthermore, TLR4, NF-κB, IL-1 s, IL-33, and IL-36 s maybe the downstream target factor of IL1RAP in inflammation. These results may provide a new strategy for stomach carcinoma development by regulating inflammation.

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