The Tachykinin Neuroimmune Connection in Inflammatory Pain

Weihe, Eberhard; Nöhr, Donatus; Müller, Sabine; Büchler, Markus W.; Friess, Helmut; Zentel, H.J.

doi:10.1111/j.1749-6632.1991.tb33116.x

Cited by 48 publications

(19 citation statements)

References 23 publications

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“…Martinez et al [23] also demonstrated that antigenic stimulation and inflammation induce the secretion and release of VIP from the lymphoid cells. SP is one of the primary mediators of neurogenic inflammations [24]. It has been implicated in regulation of nociception, vasoactivity and modulating of the immune function as neurotransmitter.…”

Section: Discussionmentioning

confidence: 99%

Neuroimmune Interactions in Experimental Colitis

Fehér¹,

Altdorfer²,

Bagaméri³

et al. 2001

Neuroimmunomodulation

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With its abundance of neurons and immunocytes, the gut is a potentially important site for the study of the interaction between the nervous and immune systems. In this electron microscopic study we have investigated the distribution of substance P (SP)- and vasoactive intestinal polypeptide (VIP)-immunoreactive (IR) nerve terminals and the immunocytes during experimental colitis in the rat. A mild colitis was induced by a luminal enema containing trinitrobenzene sulfonic acid. The most severe inflammation was detected after 2 days and the density and the distribution of the SP- and VIP-IR nerve terminals as well as the immunocompetent cells were studied at that time. Many SP- and VIP-IR nerve terminals were observed in a very close situation to the inflammatory cells. The number of VIP-IR nerve terminals slightly increased in the inflamed area. The gap between the axolemma of the nerve terminals and immunocytes was 20–200 nm. Some lymphocytes and plasma cells were also IR for SP in the inflamed area, whereas no IR immunocytes were observed in the control and in noninflamed area from the same animal. The very close apposition of the SP- and VIP-IR nerve terminals to the inflammatory cells as well as the presence of SP-IR immunocytes in inflamed area support the suggestion that bidirectional neuroimmunomodulation exists in the colon.

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Section: Discussionmentioning

confidence: 99%

Neuroimmune Interactions in Experimental Colitis

Fehér¹,

Altdorfer²,

Bagaméri³

et al. 2001

Neuroimmunomodulation

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“…SP acting on endothelial NK1 receptors plays an important role in peripheral inflammatory reactions and diseases by enhancing venular permeability and leukocyte diapedesis via interactions with proinflammatory cytokines and endothelial cell adhesion molecules (Weihe et al, 1991;Shepheard et al, 1993;Bowden et al, 1994;Nakagawa et al, 1995;Maggi, 1997;Saban et al, 1997;Quinlan et al, 1999a,b). Cerebrovenular endothelial cells have been suggested to bind SP after interleukin-1 administration in vitro (Cioni et al, 1998).…”

Section: Evidence Of a Role Of Endothelial Nk1 Receptors In The Neuromentioning

confidence: 99%

Adaptive Plasticity in Tachykinin and Tachykinin Receptor Expression after Focal Cerebral Ischemia Is Differentially Linked to GABAergic and Glutamatergic Cerebrocortical Circuits and Cerebrovenular Endothelium

et al. 2001

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To test the hypothesis of an involvement of tachykinins in destabilization and hyperexcitation of neuronal circuits, gliosis, and neuroinflammation during cerebral ischemia, we investigated cell-specific expressional changes of the genes encoding substance P (SP), neurokinin B (NKB), and the tachykinin/ neurokinin receptors (NK1, NK2, and NK3) after middle cerebral artery occlusion (MCAO) in the rat. Our analysis by quantitative in situ hybridization, immunohistochemistry, and confocal microscopy was concentrated on cerebrocortical areas that survive primary infarction but undergo secondary damage. Here, SP-encoding preprotachykinin-A and NK1 mRNA levels and SP-like immunoreactivity were transiently increased in GABAergic interneurons at 2 d after MCAO. Coincidently, MCAO caused a marked expression of SP and NK1 in a subpopulation of glutamatergic pyramidal cells, and in some neurons SP and NK1 mRNAs were coinduced. Elevated levels of the NKBencoding preprotachykinin-B mRNA and of NKB-like immunoreactivity at 2 and 7 d after MCAO were confined to GABAergic interneurons. In parallel, the expression of NK3 was markedly downregulated in pyramidal neurons. MCAO caused transient NK1 expression in activated cerebrovenular endothelium within and adjacent to the infarct. NK1 expression was absent from activated astroglia or microglia. The differential ischemia-induced plasticity of the tachykinin system in distinct inhibitory and excitatory cerebrocortical circuits suggests that it may be involved in the balance of endogenous neuroprotection and neurotoxicity by enhancing GABAergic inhibitory circuits or by facilitating glutamate-mediated hyperexcitability. The transient induction of NK1 in cerebrovenular endothelium may contribute to ischemiainduced edema and leukocyte diapedesis. Brain tachykinin receptors are proposed as potential drug targets in stroke.

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“…However, none of these concepts can explain the pain syndrome in these patients conclusively. Recent studies using modern molecular biology techniques have led to the postulation that direct alterations of nerves and changes in neurotransmitters might cause pain in patients with CP [9][10][11].…”

Section: Growth Factors In Chronic Pancreatitismentioning

confidence: 99%