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Journal articles on the topic 'Peripheral inflammation'

Author: Grafiati

Published: 31 August 2024

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1

De Kock, Marc, Sebastien Loix, and Patricia Lavand'homme. "Ketamine and Peripheral Inflammation." CNS Neuroscience & Therapeutics 19, no. 6 (April 10, 2013): 403–10. http://dx.doi.org/10.1111/cns.12104.

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2

Träger, Ulrike, and Sarah J. Tabrizi. "Peripheral inflammation in neurodegeneration." Journal of Molecular Medicine 91, no. 6 (April 2, 2013): 673–81. http://dx.doi.org/10.1007/s00109-013-1026-0.

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3

Poutler, L. W. "Central inflammation is more important than peripheral inflammation." Respiratory Medicine 91 (November 1997): 9–10. http://dx.doi.org/10.1016/s0954-6111(97)90097-4.

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4

Hamid, Q. A. "Peripheral inflammation is more important than central inflammation." Respiratory Medicine 91 (November 1997): 11–12. http://dx.doi.org/10.1016/s0954-6111(97)90098-6.

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5

Groven, N., E. A. Fors, V. C. Iversen, L. R. White, and S. K. Reitan. "Peripheral inflammation in fibromyalgia syndrome." European Neuropsychopharmacology 27 (October 2017): S634. http://dx.doi.org/10.1016/s0924-977x(17)31194-x.

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6

Lisney, S. J. W. "The development of peripheral inflammation." Pain Forum 4, no. 3 (September 1995): 153–54. http://dx.doi.org/10.1016/s1082-3174(11)80047-4.

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7

Brevetti, Gregorio, Giuseppe Giugliano, Linda Brevetti, and William R. Hiatt. "Inflammation in Peripheral Artery Disease." Circulation 122, no. 18 (November 2, 2010): 1862–75. http://dx.doi.org/10.1161/circulationaha.109.918417.

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8

Signorelli, Salvatore, Elisa Marino, and Salvatore Scuto. "Inflammation and Peripheral Arterial Disease." J 2, no. 2 (April 3, 2019): 142–51. http://dx.doi.org/10.3390/j2020012.

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Peripheral arterial disease (PAD) is an atherosclerotic disease closely associated with high morbidity and mortality in cardiac events. Inflammation is crucial in atherosclerosis both at triggering and in progression. Numerous inflammatory biomarkers (cytokines, matrix metalloproteinases (MMPs), selectin, intracellular adhesion molecule (ICAM), vascular cell adhesion molecule (VCAM) C-reactive protein (CRP), fibrinogen) have been measured in atherosclerotic diseases including PAD. This paper summarizes the data on the inflammatory biomarkers for PAD pathophysiology and highlights the most useful markers in monitoring PAD outcomes.

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9

Callas, Peter, Matthew Allison, Michael Criqui, and Mary Cushman. "Inflammation and peripheral venous disease." Thrombosis and Haemostasis 112, no. 09 (2014): 566–72. http://dx.doi.org/10.1160/th13-10-0860.

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SummaryThe inflammatory response to healing in venous thrombosis might cause vein damage and post-thrombotic syndrome. Inflammation may also be involved in venous insufficiency apart from deep-vein thrombosis. We studied the association of inflammation markers with venous insufficiency in a general population sample. We characterised 2,404 men and women in a general population cohort for peripheral venous disease and its severity using physical exam, symptom assessment, and venous ultrasound. Inflammation markers, C-reactive protein (CRP), fibrinogen, interleukin 1-beta (IL-1-beta), IL-8, IL-10, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, monocyte chemoattractant-1 (MCP-1) and vascular endothelial cell growth factor (VEGF) were compared in 352 case participants with peripheral venous disease and 352 controls with no venous abnormalities frequency matched to cases by age, sex and race. Associations were also evaluated including a subset of 108 cases of severe venous disease, as previously defined. Odds ratios (95% CI), for peripheral venous disease for biomarkers in the top quartile (adjusting for age, race, sex, body mass index and history of venous thrombosis) were 1.8 (1.1–3.0), 1.6 (1.0–2.5) and 1.5 (0.9–2.3) for CRP, fibrinogen and IL-10, respectively. Associations were larger considering cases of severe venous disease, with odds ratios for these three analytes of 2.6 (1.2–5.9), 3.1 (1.3–7.3) and 2.2 (1.1–4.4), and for IL-8: 2.4 (1.1–5.2). There was no association of IL-1-beta, ICAM-1, VCAM-1, E-selectin, MCP-1 or VEGF with overall cases or severe venous disease. In conclusion, a subset of inflammation markers were associated with increased risk of peripheral venous disease, suggesting potential therapeutic targets for treatment.

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Schafer, M., Y. Imai, S. Mousa, I. Antonijevic, G. R. Uhl, and C. Stein. "Peripheral Opioid Analgesia in Inflammation." Anesthesiology 81, SUPPLEMENT (September 1994): A920. http://dx.doi.org/10.1097/00000542-199409001-00919.

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11

D'Mello, Charlotte, and Mark G. Swain. "Liver-brain inflammation axis." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 5 (November 2011): G749—G761. http://dx.doi.org/10.1152/ajpgi.00184.2011.

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It is becoming increasingly evident that peripheral organ-centered inflammatory diseases, including chronic inflammatory liver diseases, are associated with changes in central neural transmission that result in alterations in behavior. These behavioral changes include sickness behaviors, such as fatigue, cognitive dysfunction, mood disorders, and sleep disturbances. While such behaviors have a significant impact on quality of life, the changes within the brain and the communication pathways between the liver and the brain that give rise to changes in central neural activity are not fully understood. Traditionally, neural and humoral communication pathways have been described, with the three cytokines TNFα, IL-1β, and IL-6 receiving the most attention in mediating communication between the periphery and the brain, in the setting of peripheral inflammation. However, more recently, we described an immune-mediated communication pathway in experimentally induced liver inflammation whereby, in response to activation of resident immune cells in the brain (i.e., the microglia), peripheral circulating monocytes transmigrate into the brain, leading to development of sickness behaviors. These signaling pathways drive changes in behavior by altering central neurotransmitter systems. Specifically, changes in serotonergic and corticotropin-releasing hormone neurotransmission have been demonstrated and implicated in liver inflammation-associated sickness behaviors. Understanding how the liver communicates with the brain in the setting of chronic inflammatory liver diseases will help delineate novel therapeutic targets that can reduce the burden of symptoms in patients with liver disease.

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12

Krumrych, Wiesław, and Janusz Danek. "Chemiluminescence of Peripheral Blood Neutrophils in Mares with Endometritis." Bulletin of the Veterinary Institute in Pulawy 56, no. 1 (March 1, 2012): 51–56. http://dx.doi.org/10.2478/v10213-012-0010-8.

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Abstract The aim of the study was to evaluate the oxygen metabolism of neutrophils in peripheral blood of mares in relation to intensity of endometrium inflammations. The study involved 36 half-breed mares, aged 4-22 years, showing fertility disturbances. In 26 mares neutrophils were found in uteral smears, which indicated endometritis (15 - moderate inflammation and 11 - severe inflammation). In the rest mares, cytological examination excluded inflammation. Blood samples were evaluated in terms of neutrophils chemiluminescence without stimulation (CL-WS) and with stimulation by opsonised zymosan (CL-OZ). The study demonstrated (only in case of CL-WS) an increase in chemiluminescence of cells in mares with a severe inflammation of the endometrium. The increased chemiluminescence activity was accompanied by a decrease in activation index (OZ/WS) of neutrophils, suggesting some imbalance between production and elimination of reactive oxygen species (ROS). The correlation analysis demonstrated a statistically significant relation between the intensity of the uterus inflammation, which was verified by cytological examination and CL-WS of peripheral blood neutrophils, as well as their activation index. The obtained results suggest that activated neutrophils are an important source of ROS which can play a role in the pathogenesis of endometritis in mares.

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13

Blomqvist, Anders, and David Engblom. "Neural Mechanisms of Inflammation-Induced Fever." Neuroscientist 24, no. 4 (March 20, 2018): 381–99. http://dx.doi.org/10.1177/1073858418760481.

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Fever is a common symptom of infectious and inflammatory disease. It is well-established that prostaglandin E2 is the final mediator of fever, which by binding to its EP3 receptor subtype in the preoptic hypothalamus initiates thermogenesis. Here, we review the different hypotheses on how the presence of peripherally released pyrogenic substances can be signaled to the brain to elicit fever. We conclude that there is unequivocal evidence for a humoral signaling pathway by which proinflammatory cytokines, through their binding to receptors on brain endothelial cells, evoke fever by eliciting prostaglandin E2 synthesis in these cells. The evidence for a role for other signaling routes for fever, such as signaling via circumventricular organs and peripheral nerves, as well as transfer into the brain of peripherally synthesized prostaglandin E2 are yet far from conclusive. We also review the efferent limb of the pyrogenic pathways. We conclude that it is well established that prostaglandin E2 binding in the preoptic hypothalamus produces fever by disinhibition of presympathetic neurons in the brain stem, but there is yet little understanding of the mechanisms by which factors such as nutritional status and ambient temperature shape the response to the peripheral immune challenge.

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14

Ferrari, Carina C., and Rodolfo Tarelli. "Parkinson's Disease and Systemic Inflammation." Parkinson's Disease 2011 (2011): 1–9. http://dx.doi.org/10.4061/2011/436813.

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Peripheral inflammation triggers exacerbation in the central brain's ongoing damage in several neurodegenerative diseases. Systemic inflammatory stimulus induce a general response known as sickness behaviour, indicating that a peripheral stimulus can induce the synthesis of cytokines in the brain. In Parkinson's disease (PD), inflammation was mainly associated with microglia activation that can underlie the neurodegeneration of neurons in thesubstantia nigra(SN). Peripheral inflammation can transform the “primed” microglia into an “active” state, which can trigger stronger responses dealing with neurodegenerative processes. Numerous evidences show that systemic inflammatory processes exacerbate ongoing neurodegeneration in PD patient and animal models. Anti-inflammatory treatment in PD patients exerts a neuroprotective effect. In the present paper, we analyse the effect of peripheral infections in the etiology and progression in PD patients and animal models, suggesting that these peripheral immune challenges can exacerbate the symptoms in the disease.

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15

Santo Signorelli, Salvatore, Massimiliano Anzaldi, and Valerio Fiore. "Inflammation in Peripheral Arterial Disease (PAD)." Current Pharmaceutical Design 18, no. 28 (August 8, 2012): 4350–57. http://dx.doi.org/10.2174/138161212802481273.

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16

Djaldetti, Meir. "Piperine – An Immunomodulator and Inflammation Mitigator." Journal of Clinical and Laboratory Research 2, no. 5 (June 3, 2021): 01–04. http://dx.doi.org/10.31579/2768-0487/027.

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Black pepper, one of the most widespread spices, gained the entitlement “King of spices” founded on its peculiar pungent test and therapeutic properties, both owed to its active alkaloid - piperine. Mounting evidence indicates that piperine possesses immunomodulatory and therapeutic activities. The aim of this mini review was to summarize the role of piperine in abolishing inflammation, its part in the immune activity of peripheral blood mononuclear- and a number of other cells, its capacity to elicit production of inflammatory cytokines and its function as a synergist endorsing the beneficial therapeutic effect of conventional anti-inflammatory drugs.

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17

Machado, A., A. J. Herrera, J. L. Venero, M. Santiago, R. M. De Pablos, R. F. Villarán, A. M. Espinosa-Oliva, et al. "Peripheral Inflammation Increases the Damage in Animal Models of Nigrostriatal Dopaminergic Neurodegeneration: Possible Implication in Parkinson's Disease Incidence." Parkinson's Disease 2011 (2011): 1–10. http://dx.doi.org/10.4061/2011/393769.

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Inflammatory processes described in Parkinson’s disease (PD) and its animal models appear to be important in the progression of the pathogenesis, or even a triggering factor. Here we review that peripheral inflammation enhances the degeneration of the nigrostriatal dopaminergic system induced by different insults; different peripheral inflammations have been used, such as IL-1β and the ulcerative colitis model, as well as insults to the dopaminergic system such as 6-hydroxydopamine or lipopolysaccharide. In all cases, an increased loss of dopaminergic neurons was described; inflammation in the substantia nigra increased, displaying a great activation of microglia along with an increase in the production of cytokines such as IL-1β and TNF-α. Increased permeability or disruption of the BBB, with overexpression of the ICAM-1 adhesion molecule and infiltration of circulating monocytes into the substantia nigra, is also involved, since the depletion of circulating monocytes prevents the effects of peripheral inflammation. Data are reviewed in relation to epidemiological studies of PD.

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18

Denes, A., P. Thornton, N. J. Rothwell, and S. M. Allan. "Inflammation and brain injury: Acute cerebral ischaemia, peripheral and central inflammation." Brain, Behavior, and Immunity 24, no. 5 (July 2010): 708–23. http://dx.doi.org/10.1016/j.bbi.2009.09.010.

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19

Mietto, Bruno Siqueira, Klauss Mostacada, and Ana Maria Blanco Martinez. "Neurotrauma and Inflammation: CNS and PNS Responses." Mediators of Inflammation 2015 (2015): 1–14. http://dx.doi.org/10.1155/2015/251204.

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Traumatic injury to the central nervous system (CNS) or the peripheral nervous system (PNS) triggers a cascade of events which culminate in a robust inflammatory reaction. The role played by inflammation in the course of degeneration and regeneration is not completely elucidated. While, in peripheral nerves, the inflammatory response is assumed to be essential for normal progression of Wallerian degeneration and regeneration, CNS trauma inflammation is often associated with poor recovery. In this review, we discuss key mechanisms that trigger the inflammatory reaction after nervous system trauma, emphasizing how inflammations in both CNS and PNS differ from each other, in terms of magnitude, cell types involved, and effector molecules. Knowledge of the precise mechanisms that elicit and maintain inflammation after CNS and PNS tissue trauma and their effect on axon degeneration and regeneration is crucial for the identification of possible pharmacological drugs that can positively affect the tissue regenerative capacity.

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20

Pol, Olga, and Margarita M. Puig. "Expression of Opioid Receptors During Peripheral Inflammation." Current Topics in Medicinal Chemistry 4, no. 1 (January 1, 2004): 51–61. http://dx.doi.org/10.2174/1568026043451519.

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21

Stein, C., A. Herz, and K. Peter. "PERIPHERAL OPIOID RECEPTORS MEDIATING ANALGESIA IN INFLAMMATION." Anesthesiology 71, Supplement (September 1989): A762. http://dx.doi.org/10.1097/00000542-198909001-00762.

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22

Rees, Huw, Kathleen A. Sluka, Karin N. Westlund, and William D. Willis. "Do dorsal root reflexes augment peripheral inflammation?" NeuroReport 5, no. 7 (March 1994): 821–24. http://dx.doi.org/10.1097/00001756-199403000-00021.

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23

Stettner, Mark, Sandra Labus, Jan-philipp Weinberger, Thomas Dehmel, Angelika Derksen, Anne K. Mausberg, and Bernd C. Kieseier. "Schwann cell locomotion during peripheral nerve inflammation." Journal of Neuroimmunology 275, no. 1-2 (October 2014): 72. http://dx.doi.org/10.1016/j.jneuroim.2014.08.189.

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24

Omote, Keiichi, Koji Hazama, Tomoyuki Kawamata, Mikito Kawamata, Yoshito Nakayaka, Masaki Toriyabe, and Akiyoshi Namiki. "Peripheral nitric oxide in carrageenan-induced inflammation." Brain Research 912, no. 2 (September 2001): 171–75. http://dx.doi.org/10.1016/s0006-8993(01)02733-0.

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25

Chesnokova, Vera, Robert N. Pechnick, and Kolja Wawrowsky. "Chronic peripheral inflammation, hippocampal neurogenesis, and behavior." Brain, Behavior, and Immunity 58 (November 2016): 1–8. http://dx.doi.org/10.1016/j.bbi.2016.01.017.

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26

Azhari, Hassan, and Mark G. Swain. "Role of Peripheral Inflammation in Hepatic Encephalopathy." Journal of Clinical and Experimental Hepatology 8, no. 3 (September 2018): 281–85. http://dx.doi.org/10.1016/j.jceh.2018.06.008.

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27

Gray, Marcus, and Gerald Holtmann. "Gut Inflammation: More Than a Peripheral Annoyance." Digestive Diseases and Sciences 62, no. 9 (May 2, 2017): 2205–7. http://dx.doi.org/10.1007/s10620-017-4587-x.

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28

Rittner, Heike L., Christian Lux, Dominika Labuz, Shaaban A. Mousa, Michael Schäfer, Christoph Stein, and Alexander Brack. "Neurokinin-1 Receptor Antagonists Inhibit the Recruitment of Opioid-containing Leukocytes and Impair Peripheral Antinociception." Anesthesiology 107, no. 6 (December 1, 2007): 1009–17. http://dx.doi.org/10.1097/01.anes.0000291454.90754.de.

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Background Neurokinins (e.g., substance P) contribute to pain transmission in the central nervous system, peripheral neurogenic inflammation, and leukocyte recruitment in inflammation. Leukocyte recruitment involves (1) up-regulation of adhesion molecule expression through neurokinin-1 (NK1) receptors on endothelial cells, (2) augmented chemokine production, or (3) chemotaxis through NK1 receptors on leukocytes. In inflammation, leukocytes can trigger endogenous antinociception through release of opioid peptides and activation of opioid receptors on peripheral sensory neurons. The authors hypothesized that NK1 receptor antagonists impair recruitment of opioid-containing leukocytes and stress-induced antinociception. Methods Rats were treated intraperitoneally and intrathecally with peripherally restricted (SR140333) or blood-brain barrier-penetrating (L-733,060) NK1 receptor antagonists and were evaluated for paw pressure thresholds, numbers of infiltrating opioid-containing leukocytes and leukocyte subpopulations, expression of adhesion molecules, NK1 receptors, and chemokines 24-48 h after complete Freund adjuvant-induced hind paw inflammation. Results Systemic and peripherally selective, but not intrathecal, NK1 receptor blockade reduced stress-induced antinociception (control: 177 +/- 9 g, L-733,060: 117 +/- 8 g, and control: 166 +/- 30 g, SR140333: 89 +/- 3 g; both P < 0.05, t test) without affecting baseline hyperalgesia. In parallel, local recruitment of opioid-containing leukocytes was decreased (L-733,060 and SR140333: 56.0 +/- 4.3 and 59.1 +/- 7.9% of control; both P < 0.05, t test). NK1 receptors were expressed on peripheral neurons, infiltrating leukocytes and endothelial cells. Peripheral NK1 receptor blockade did not alter endothelial expression of intercellular adhesion molecule-1 or local chemokine and cytokine production, but decreased polymorphonuclear cell and macrophage recruitment. Conclusions Endogenous inhibition of inflammatory pain is dependent on NK1 receptor-mediated recruitment of opioid-containing leukocytes.

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29

Su, Xiaomin, and Howard J. Federoff. "Immune Responses in Parkinson’s Disease: Interplay between Central and Peripheral Immune Systems." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/275178.

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The etiology of Parkinson’s disease (PD) is complex and most likely involves numerous environmental and heritable risk factors. Recent studies establish that central and peripheral inflammation occurs in the prodromal stage of the disease and sustains disease progression. Aging, heritable risk factors, or environmental exposures may contribute to the initiation of central or peripheral inflammation. One emerging hypothesis is that inflammation plays a critical role in PD neuropathology. Increasing evidence suggest that activation of the peripheral immune system exacerbates the discordant central inflammatory response and synergistically drives neurodegeneration. We provide an overview of current knowledge on the temporal profile of central and peripheral immune responses in PD and discuss the potential synergistic effects of the central and peripheral inflammation in disease development. The understanding of the nature of the chronic inflammation in disease progression and the possible risk factors that contribute to altered central and peripheral immune responses will offer mechanistic insights into PD etiology and pathology and benefit the development of effective tailored therapeutics for human PD.

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30

Marottoli, Felecia M., Yuriko Katsumata, Kevin P. Koster, Riya Thomas, David W. Fardo, and Leon M. Tai. "Peripheral Inflammation, Apolipoprotein E4, and Amyloid-β Interact to Induce Cognitive and Cerebrovascular Dysfunction." ASN Neuro 9, no. 4 (July 14, 2017): 175909141771920. http://dx.doi.org/10.1177/1759091417719201.

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Cerebrovascular dysfunction is rapidly reemerging as a major process of Alzheimer’s disease (AD). It is, therefore, crucial to delineate the roles of AD risk factors in cerebrovascular dysfunction. While apolipoprotein E4 ( APOE4), Amyloid-β (Aβ), and peripheral inflammation independently induce cerebrovascular damage, their collective effects remain to be elucidated. The goal of this study was to determine the interactive effect of APOE4, Aβ, and chronic repeated peripheral inflammation on cerebrovascular and cognitive dysfunction in vivo. EFAD mice are a well-characterized mouse model that express human APOE3 (E3FAD) or APOE4 (E4FAD) and overproduce human Aβ42 via expression of 5 Familial Alzheimer’s disease (5xFAD) mutations. Here, we utilized EFAD carriers [5xFAD+/−/ APOE+/+ (EFAD+)] and noncarriers [5xFAD−/−/ APOE+/+ (EFAD−)] to compare the effects of peripheral inflammation in the presence or absence of human Aβ overproduction. Low-level, chronic repeated peripheral inflammation was induced in EFAD mice via systemic administration of lipopolysaccharide (LPS; 0.5 mg/kg/wk i.p.) from 4 to 6 months of age. In E4FAD+ mice, peripheral inflammation caused cognitive deficits and lowered post-synaptic protein levels. Importantly, cerebrovascular deficits were observed in LPS-challenged E4FAD+ mice, including cerebrovascular leakiness, lower vessel coverage, and cerebral amyloid angiopathy-like Aβ deposition. Thus, APOE4, Aβ, and peripheral inflammation interact to induce cerebrovascular damage and cognitive deficits.

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31

Sehgal, Nalini. "Peripherally Acting Opioids and Clinical Implications for Pain Control." Pain Physician 3;14, no. 3;5 (May 14, 2011): 249–58. http://dx.doi.org/10.36076/ppj.2011/14/249.

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Opioid receptors are widely expressed in the central and peripheral nervous system and in the non-neuronal tissues. Data from animal and human clinical studies support the involvement of peripheral opioid receptors in analgesia, especially in the presence of inflammation. Inflammation has been shown to increase the synthesis of opioid receptors in the dorsal root ganglion neurons and enhance transport and accumulation of opioid receptors in the peripheral terminals of sensory neurons. Under the influence of chemokines and adhesion molecules, opioid peptide-containing immune cells extravasate and accumulate in the injured tissues. Stress, chemokines, cytokines, and other releasing factors in inflamed tissues stimulate these granulocytes to release opioid peptides. Once secreted, opioid peptides bind to and activate peripheral opioid receptors on sensory nerve fibers and produce analgesia by decreasing the excitability of sensory nerves and/or inhibiting release of pro-inflammatory neuropeptides. Research has revealed that local application of exogenous opioid agonists produces a potent analgesic effect by activating peripheral opioid receptors in inflamed tissues. The analgesic activity occurs without activation of opioid receptors in the central nervous system (CNS), and therefore centrally mediated side effects, such as respiratory depression, mental clouding, altered consciousness, or addiction, are not associated with peripheral opioid activity. This discovery has stimulated research on developing peripherally restricted opioid agonists that lack CNS effects. In addition, it has been recognized that opioid receptors modulate inflammation, and that opioids have antiinflammatory effects. The anti-inflammatory actions of opioids are not well known or understood. Conflicting reports on mu-opioids suggest both anti-inflammatory and pro-inflammatory effects. This article will present the basis for peripheral opioid analgesia and describe current research directed at developing novel treatments for pain with improved side effect profiles. Key words: Opioids, opioid receptors, opioid agonists, peripheral nervous system, peripheral opioid receptors

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32

Aries, Michelle, Makayla Cook, and Tiffany Hensley-McBain. "A Pilot Study to Investigate Peripheral Low-Level Chronic LPS Injection as a Model of Neutrophil Activation in the Periphery and Brain in Mice." International Journal of Molecular Sciences 25, no. 10 (May 14, 2024): 5357. http://dx.doi.org/10.3390/ijms25105357.

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Lipopolysaccharide-induced (LPS) inflammation is used as model to understand the role of inflammation in brain diseases. However, no studies have assessed the ability of peripheral low-level chronic LPS to induce neutrophil activation in the periphery and brain. Subclinical levels of LPS were injected intraperitoneally into mice to investigate its impacts on neutrophil frequency and activation. Neutrophil activation, as measured by CD11b expression, was higher in LPS-injected mice compared to saline-injected mice after 4 weeks but not 8 weeks of injections. Neutrophil frequency and activation increased in the periphery 4–12 h and 4–8 h after the fourth and final injection, respectively. Increased levels of G-CSF, TNFa, IL-6, and CXCL2 were observed in the plasma along with increased neutrophil elastase, a marker of neutrophil extracellular traps, peaking 4 h following the final injection. Neutrophil activation was increased in the brain of LPS-injected mice when compared to saline-injected mice 4–8 h after the final injection. These results indicate that subclinical levels of peripheral LPS induces neutrophil activation in the periphery and brain. This model of chronic low-level systemic inflammation could be used to understand how neutrophils may act as mediators of the periphery–brain axis of inflammation with age and/or in mouse models of neurodegenerative or neuroinflammatory disease.

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33

Weaver, Lehn K., Niansheng Chu, and Edward M. Behrens. "TLR9-mediated inflammation drives a Ccr2-independent peripheral monocytosis through enhanced extramedullary monocytopoiesis." Proceedings of the National Academy of Sciences 113, no. 39 (September 12, 2016): 10944–49. http://dx.doi.org/10.1073/pnas.1524487113.

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Monocytes are innate immune cells that interact with their environment through the expression of pattern recognition receptors, including Toll-like receptors (TLRs). Both monocytes and TLRs are implicated in driving persistent inflammation in autoimmune diseases. However, cell-intrinsic mechanisms to control inflammation, including TLR tolerance, are thought to limit inflammatory responses in the face of repeated TLR activation, leaving it unclear how chronic TLR-mediated inflammation is maintained in vivo. Herein, we used a well-characterized model of systemic inflammation to determine the mechanisms allowing sustained TLR9 responses to develop in vivo. Monocytes were identified as the main TLR9-responsive cell and accumulated in peripherally inflamed tissues during TLR9-driven inflammation. Intriguingly, canonical mechanisms controlling monocyte production and localization were altered during the systemic inflammatory response, as accumulation of monocytes in the liver and spleen developed in the absence of dramatic increases in bone marrow monocyte progenitors and was independent of chemokine (C-C motif) receptor 2 (Ccr2). Instead, TLR9-driven inflammation induced a Ccr2-independent expansion of functionally enhanced extramedullary myeloid progenitors that correlated with the peripheral accumulation of monocytes in both wild-type and Ccr2−/− mice. Our data implicate inflammation-induced extramedullary monocytopoiesis as a peripheral source of newly produced TLR9 responsive monocytes capable of sustaining chronic TLR9 responses in vivo. These findings help to explain how chronic TLR-mediated inflammation may be perpetuated in autoimmune diseases and increase our understanding of how monocytes are produced and positioned during systemic inflammatory responses.

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34

Mengr, Anna, Veronika Strnadová, Štěpán Strnad, Vladimír Vrkoslav, Helena Pelantová, Marek Kuzma, Thomas Comptdaer, et al. "Feeding High-Fat Diet Accelerates Development of Peripheral and Central Insulin Resistance and Inflammation and Worsens AD-like Pathology in APP/PS1 Mice." Nutrients 15, no. 17 (August 23, 2023): 3690. http://dx.doi.org/10.3390/nu15173690.

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Alzheimer’s disease (AD) is a progressive brain disorder characterized by extracellular amyloid-β (Aβ) plaques, intracellular neurofibrillary tangles formed by hyperphosphorylated Tau protein and neuroinflammation. Previous research has shown that obesity and type 2 diabetes mellitus, underlined by insulin resistance (IR), are risk factors for neurodegenerative disorders. In this study, obesity-induced peripheral and central IR and inflammation were studied in relation to AD-like pathology in the brains and periphery of APP/PS1 mice, a model of Aβ pathology, fed a high-fat diet (HFD). APP/PS1 mice and their wild-type controls fed either a standard diet or HFD were characterized at the ages of 3, 6 and 10 months by metabolic parameters related to obesity via mass spectroscopy, nuclear magnetic resonance, immunoblotting and immunohistochemistry to quantify how obesity affected AD pathology. The HFD induced substantial peripheral IR leading to central IR. APP/PS1-fed HFD mice had more pronounced IR, glucose intolerance and liver steatosis than their WT controls. The HFD worsened Aβ pathology in the hippocampi of APP/PS1 mice and significantly supported both peripheral and central inflammation. This study reveals a deleterious effect of obesity-related mild peripheral inflammation and prediabetes on the development of Aβ and Tau pathology and neuroinflammation in APP/PS1 mice.

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35

Brack, Alexander, Dominika Labuz, Anu Schiltz, Heike L. Rittner, Halina Machelska, Michael Schäfer, Regina Reszka, and Christoph Stein. "Tissue Monocytes/Macrophages in Inflammation." Anesthesiology 101, no. 1 (July 1, 2004): 204–11. http://dx.doi.org/10.1097/00000542-200407000-00031.

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Background Opioid-containing leukocytes migrate to peripheral sites of inflammation. On exposure to stress, opioid peptides are released, bind to opioid receptors on peripheral sensory neurons, and induce endogenous antinociception. In later stages of Freund's complete adjuvant-induced local inflammation, monocytes/macrophages are a major opioid-containing leukocyte subpopulation, but these cells also produce proalgesic cytokines. In this study, the role of tissue monocytes/macrophages in hyperalgesia and in peripheral opioid-mediated antinociception was investigated. Methods After intraplantar injection of Freund's adjuvant, leukocyte subpopulations and opioid-containing leukocytes were analyzed by flow cytometry in the inflamed paw in the presence or absence of monocyte/macrophage depletion by intraplantar injection of clodronate-containing liposomes (phosphate-buffered saline and empty liposomes served as controls). Paw volume was measured with a plethysmometer. Hyperalgesia was determined by measuring heat-induced paw withdrawal latency and paw pressure threshold. Paw pressure threshold was also measured after swim stress and injection of fentanyl. Results At 48 and 96 h of inflammation, it was found that (1). monocytes/macrophages were the largest leukocyte subpopulation (> 55% of all leukocytes) and the predominant producers of opioid peptides (71-77% of all opioid-containing leukocytes in the paw), (2). clodronate-containing liposomes depleted monocytes/macrophages by 30-35% (P < 0.05), (3). hyperalgesia was unaltered by liposome injection (P > 0.05), and (4) opioid-containing leukocytes and swim stress but not fentanyl-induced antinociception were significantly decreased by clodronate-containing liposomes (P < 0.05, P > 0.05, all by t test; opioid-containing cells and swim stress-induced increase of paw pressure threshold were reduced by 35-42% and 20%, respectively). Conclusion Partial depletion of tissue monocytes/macrophages impairs peripheral endogenous opioid-mediated antinociception without affecting hyperalgesia.

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Gu, Dandan, Yiming Xia, Zihan Ding, Jiaxi Qian, Xi Gu, Huiyuan Bai, Maorong Jiang, and Dengbing Yao. "Inflammation in the Peripheral Nervous System after Injury." Biomedicines 12, no. 6 (June 5, 2024): 1256. http://dx.doi.org/10.3390/biomedicines12061256.

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Nerve injury is a common condition that occurs as a result of trauma, iatrogenic injury, or long-lasting stimulation. Unlike the central nervous system (CNS), the peripheral nervous system (PNS) has a strong capacity for self-repair and regeneration. Peripheral nerve injury results in the degeneration of distal axons and myelin sheaths. Macrophages and Schwann cells (SCs) can phagocytose damaged cells. Wallerian degeneration (WD) makes the whole axon structure degenerate, creating a favorable regenerative environment for new axons. After nerve injury, macrophages, neutrophils and other cells are mobilized and recruited to the injury site to phagocytose necrotic cells and myelin debris. Pro-inflammatory and anti-inflammatory factors involved in the inflammatory response provide a favorable microenvironment for peripheral nerve regeneration and regulate the effects of inflammation on the body through relevant signaling pathways. Previously, inflammation was thought to be detrimental to the body, but further research has shown that appropriate inflammation promotes nerve regeneration, axon regeneration, and myelin formation. On the contrary, excessive inflammation can cause nerve tissue damage and pathological changes, and even lead to neurological diseases. Therefore, after nerve injury, various cells in the body interact with cytokines and chemokines to promote peripheral nerve repair and regeneration by inhibiting the negative effects of inflammation and harnessing the positive effects of inflammation in specific ways and at specific times. Understanding the interaction between neuroinflammation and nerve regeneration provides several therapeutic ideas to improve the inflammatory microenvironment and promote nerve regeneration.

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Jansen, L.-A. R., L. A. Forster, X. L. Smith, M. Rubaharan, A. Z. Murphy, and D. J. Baro. "Changes in peripheral HCN2 channels during persistent inflammation." Channels 15, no. 1 (January 1, 2021): 165–79. http://dx.doi.org/10.1080/19336950.2020.1870086.

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Mallard, Carina. "Central and peripheral inflammation in developmental brain injury." Reproductive Toxicology 56 (August 2015): 4–5. http://dx.doi.org/10.1016/j.reprotox.2015.07.010.

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Kim, Ryul, Han-Joon Kim, Aryun Kim, Mihee Jang, Ahro Kim, Yoon Kim, Dallah Yoo, Jin Hee Im, Ji-Hyun Choi, and Beomseok Jeon. "Does peripheral inflammation contribute to multiple system atrophy?" Parkinsonism & Related Disorders 64 (July 2019): 340–41. http://dx.doi.org/10.1016/j.parkreldis.2019.03.020.

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Depino, Amaicha Mara. "Peripheral and central inflammation in autism spectrum disorders." Molecular and Cellular Neuroscience 53 (March 2013): 69–76. http://dx.doi.org/10.1016/j.mcn.2012.10.003.

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41

Gentle, M. J., and V. L. Tilston. "Reduction in Peripheral Inflammation by Changes in Attention." Physiology & Behavior 66, no. 2 (April 1999): 289–92. http://dx.doi.org/10.1016/s0031-9384(98)00297-2.

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42

Willison, Hugh, Guido Stoll, Klaus V. Toyka, Thomas Berger, and Hans-Peter Hartung. "Autoimmunity and inflammation in the peripheral nervous system." Trends in Neurosciences 25, no. 3 (March 2002): 127–29. http://dx.doi.org/10.1016/s0166-2236(00)02120-2.

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Holz, O., R. A. Jörres, and H. Magnussen. "Monitoring central and peripheral airway inflammation in asthma." Respiratory Medicine 94 (September 2000): S7—S12. http://dx.doi.org/10.1016/s0954-6111(00)80134-1.

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HOLZ, O. "Monitoring central and peripheral airway inflammation in asthma." Respiratory Medicine 94 (September 2000): S7—S12. http://dx.doi.org/10.1016/s0954-6111(00)90117-3.

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Carlton, S. M., and R. E. Coggeshall. "Inflammation-induced changes in peripheral glutamate receptor populations." Brain Research 820, no. 1-2 (February 1999): 63–70. http://dx.doi.org/10.1016/s0006-8993(98)01328-6.

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Savarraj, Jude P. J., Kaushik Parsha, Georgene W. Hergenroeder, Liang Zhu, Suhas S. Bajgur, Sungho Ahn, Kiwon Lee, et al. "Systematic model of peripheral inflammation after subarachnoid hemorrhage." Neurology 88, no. 16 (March 17, 2017): 1535–45. http://dx.doi.org/10.1212/wnl.0000000000003842.

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Objective:To investigate inflammatory processes after aneurysmal subarachnoid hemorrhage (aSAH) with network models.Methods:This is a retrospective observational study of serum samples from 45 participants with aSAH analyzed at multiple predetermined time points: <24 hours, 24 to 48 hours, 3 to 5 days, and 6 to 8 days after aSAH. Concentrations of cytokines were measured with a 41-plex human immunoassay kit, and the Pearson correlation coefficients between all possible cytokine pairs were computed. Systematic network models were constructed on the basis of correlations between cytokine pairs for all participants and across injury severity. Trends of individual cytokines and correlations between them were examined simultaneously.Results:Network models revealed that systematic inflammatory activity peaks at 24 to 48 hours after the bleed. Individual cytokine levels changed significantly over time, exhibiting increasing, decreasing, and peaking trends. Platelet-derived growth factor (PDGF)-AA, PDGF-AB/BB, soluble CD40 ligand, and tumor necrosis factor-α (TNF-α) increased over time. Colony-stimulating factor (CSF) 3, interleukin (IL)-13, and FMS-like tyrosine kinase 3 ligand decreased over time. IL-6, IL-5, and IL-15 peaked and decreased. Some cytokines with insignificant trends show high correlations with other cytokines and vice versa. Many correlated cytokine clusters, including a platelet-derived factor cluster and an endothelial growth factor cluster, were observed at all times. Participants with higher clinical severity at admission had elevated levels of several proinflammatory and anti-inflammatory cytokines, including IL-6, CCL2, CCL11, CSF3, IL-8, IL-10, CX3CL1, and TNF-α, compared to those with lower clinical severity.Conclusions:Combining reductionist and systematic techniques may lead to a better understanding of the underlying complexities of the inflammatory reaction after aSAH.

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Antonijevic, I., SA Mousa, M. Schafer, and C. Stein. "Perineurial defect and peripheral opioid analgesia in inflammation." Journal of Neuroscience 15, no. 1 (January 1, 1995): 165–72. http://dx.doi.org/10.1523/jneurosci.15-01-00165.1995.

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Ruda, M. A. "Altered Nociceptive Neuronal Circuits After Neonatal Peripheral Inflammation." Science 289, no. 5479 (July 28, 2000): 628–30. http://dx.doi.org/10.1126/science.289.5479.628.

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Edwards, L. J., B. Sharrack, A. Ismail, H. Tumani, and C. S. Constantinescu. "Central inflammation versus peripheral regulation in multiple sclerosis." Journal of Neurology 258, no. 8 (March 9, 2011): 1518–27. http://dx.doi.org/10.1007/s00415-011-5973-5.

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Park, Hi-Joon, Mi-Sook Hong, Ji Suk Lee, Kang-Hyun Leem, Chang-Ju Kim, Jin-Woo Kim, and Sabina Lim. "Effects ofAralia continentalis on hyperalgesia with peripheral inflammation." Phytotherapy Research 19, no. 6 (2005): 511–13. http://dx.doi.org/10.1002/ptr.1693.

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