Neuroimmune Interactions (neuroimmune + interaction)

Distribution by Scientific Domains


Selected Abstracts


Differential activation of C1 complement components in rat spinal cord after sciatic nerve injury

JOURNAL OF NEUROCHEMISTRY, Issue 2003
J. Mika
Neuroimmune interactions are discussed to drive neuropathic pain. We used the Bennett model to correlate pain and cellular expression profiles of the complement factors C1q and C1q-associated serine proteases C1r/C1s in lumbar spinal cord. At 2 days C1q mRNA levels increased ipsilateral to the lesion, and peaked at 8 days when allodynia and severe walking problems were present. During regeneration walking problems disappeared together with C1q mRNA levels. C1q biosynthesis was restricted to microglia. Surprisingly, C1s/C1r biosynthesis was not increased after injury suggesting a role for C1q different from classical complement activation. Sustained C1q expression in spinal microglia after lesion in conjunction with pain behavior indicates that microglial C1q may be causally involved in the development and maintenance of neuropathic pain. Acknowledgements:, Supported by BMBF01GG9818, SFB297, DFGWE910/8-3, KBN3P05C00623. [source]


The intestinal barrier and its regulation by neuroimmune factors

NEUROGASTROENTEROLOGY & MOTILITY, Issue 7 2010
. v. Keita
Abstract Background, The ability to control uptake across the mucosa and protect from damage of harmful substances from the lumen is defined as intestinal barrier function. A disturbed barrier dysfunction has been described in many human diseases and animal models, for example, inflammatory bowel disease, irritable bowel syndrome, and intestinal hypersensitivity. In most diseases and models, alterations are seen both of the paracellular pathway, via the tight junctions, and of the transcellular routes, via different types of endocytosis. Recent studies of pathogenic mechanisms have demonstrated the important role of neuroimmune interaction with the epithelial cells in the regulation of barrier function. Neural impulses from extrinsic vagal and/or sympathetic efferent fibers or intrinsic enteric nerves influence mucosal barrier function via direct effects on epithelial cells or via interaction with immune cells. For example, by nerve-mediated activation by corticotropin-releasing hormone or cholinergic pathways, mucosal mast cells release a range of mediators with effects on transcellular, and/or paracellular permeability (for example, tryptase, TNF-,, nerve growth factor, and interleukins). Purpose, In this review, we discuss current physiological and pathophysiological aspects of the intestinal barrier and, in particular, its regulation by neuroimmune factors. [source]


A new paradigm of eosinophil granulocytes: neuroimmune interactions

EXPERIMENTAL DERMATOLOGY, Issue 9 2008
Ulrike Raap
Abstract:, Eosinophil granulocytes have long been regarded as potent effector cells with the potential to release an array of inflammatory mediators involved in cytotoxicity to helminths and tissue destruction in chronic inflammatory diseases such as asthma. However, it has become evident that eosinophils are also involved in regulatory mechanisms modulating local tissue immune responses. Eosinophils take part in remodelling and repair mechanisms and contribute to the localized innate and acquired immune response as well as systemic adaptive immunity. In addition, eosinophils are involved in neuroimmune interactions modulating the functional activity of peripheral nerves. Neuromediators can also modulate the functional activity of eosinophils, revealing bidirectional interactions between the two cell types. Eosinophils are tissue-resident cells and have been found in close vicinity of peripheral nerves. This review describes neuroimmune interactions between eosinophil granulocytes and peripheral nerves and highlights why eosinophils are important in allergic diseases such as asthma. [source]


From Migraine To Chronic Daily Headache: The Biological Basis of Headache Transformation

HEADACHE, Issue 8 2007
Ian D. Meng PhD
Migraine headache carries the potential of transforming into chronic daily headache (CDH) over a period of time. Although several risk factors for migraine progression to CDH have been identified, the biological basis of this transformation is unknown. In this review, the consequences of stressful life events and medication overuse, 2 risk factors associated with the development of CDH, on brain processes involved in headache are examined. The extensive overlap in both neural circuitry and cellular events that occur with stress, medication overuse, and migraine provide insight into potential mechanisms that may lead to CDH. Particular attention is devoted to the effect of stress and medication overuse on peripheral and central neuroimmune interactions that can facilitate pain signaling. These interactions include the degranulation of mast cells in the dura, causing the sensitization of primary afferent neurons, as well as the activation of glial cells in the brain that can lead to central sensitization. It is hypothesized that the biological processes involved in migraine headache are directly impacted by stress, medication overuse, and other risk factors, resulting in a reduced threshold for induction of headache and transformation of episodic migraine to CDH. [source]


Alcohol Consumption Attenuates Febrile Responses to Lipopolysaccharide and Interleukin-1, in Male Rats

ALCOHOLISM, Issue 1 2002
Anna N. Taylor
Background: Chronic and acute alcohol use exert profound modulatory effects on the immune system which manifest as impaired host defense against infections. An important feature of this response is the interaction between the immune and the central nervous systems. This study investigated the effects of 14 days of alcohol exposure on cytokine-mediated neuroimmune interactions that affect the febrile component of the host-defense response. Methods: Adult male rats were fed a liquid diet containing ethanol (EtOH, 5% w/v) for 14 days. Pair-fed and normal chow- and water-fed rats served as controls. Continuous biotelemetric recordings of body temperature and locomotor activity commencing after 14 days of EtOH feeding were used to determine the effects of chronic EtOH on the circadian pattern of temperature and activity, on the febrile response to intraperitoneal (ip) administration of lipopolysaccharide (LPS) and interleukin (IL)-1,, and on fever induced by IL-1, administered intracerebroventricularly. We also examined the effects of EtOH consumption on LPS-induced hypothalamic production of the pyrogenic cytokines IL-1, and tumor necrosis factor-, (TNF,) and on the blood levels of IL-1,, TNF,, IL-6, adrenocorticotropin, and corticosterone at 2, 4, and 6 hr after ip LPS. Results: Fourteen days of EtOH consumption blunted the circadian increases in temperature and activity that normally occur in the dark phase of the light/dark cycle without affecting light-phase temperature or activity. EtOH consumption attenuated fever induced by LPS or IL-1, administered ip during the light phase and significantly reduced hypothalamic production of IL-1,. LPS-induced increases in hypothalamic TNF, and blood cytokines, adrenocorticotropin, and corticosterone were unaffected. Central administration of IL-1, produced a normal febrile response in chronic-EtOH rats. Conclusions: The attenuated LPS- and IL-1,,induced febrile responses in EtOH-consuming rats and the corresponding deficit in hypothalamic production of IL-1, suggest that alcohol may impair IL-1,,mediated neuroimmune communication. [source]