Lipopolysaccharide induces substance P in sympathetic ganglia via ganglionic interleukin-1 production

Shadiack, Annette M.; Carlson, Christopher; Ding, Minzhen; Hart, Ronald P.; Jonakait, G. Miller

doi:10.1016/0165-5728(94)90180-5

Cited by 30 publications

(17 citation statements)

References 25 publications

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“…Efferent actions of sensory nerve fibers are achieved by bioactive substances (mainly sensory neuropeptides), which are released from sensory nerve fibers to interact with their receptors on the cells of the surrounding tissues [10][11][12][13]. LPS [14][15][16] and cytokines [12,15,17] can induce the release of sensory neuropeptides, presumably via stimulation of unmyelinated sensory neurons. Neonatal capsaicin treatment results in a significant degeneration of thin sensory neurons and marked depletion of the sensory neuropeptides [11].…”

Section: Discussionmentioning

confidence: 99%

“…The involvement of the afferent function in the development of fever is well documented [4][5][6][7]9]. In addition, several lines of evidence suggest that the efferent action of sensory nerves could play an important role in fever: (i) lipopolysaccharide (LPS), either directly or indirectly [14][15][16], cytokines [12,15,17] and other inflammatory mediators can induce the release of sensory neuropeptides, presumably via stimulation of unmyelinated sensory neurons; (ii) sensory neuropeptides, in turn, can modulate the activity of cells involved in the inflammatory response and affect the production of pyrogenic cytokines by peripheral cells [18][19][20][21] and brain [18,20,22,23] immunocompetent cells. We hypothesized that alterations in cytokine production, induced by sensory neuropeptides, can significantly affect the development of fever.…”

Section: Introductionmentioning

confidence: 99%

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Role of Capsaicin-Sensitive Afferents in Fever and Cytokine Responses during Systemic and Local Inflammation in Rats

Gourine

Rudolph

Korsak

et al. 2001

Neuroimmunomodulation

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Objective: Peripheral afferents play an important role in fever. In the present study, we investigated the role of capsaicin-sensitive afferents in fever and cytokine responses during systemic (induced by intraperitoneal lipopolysaccharide, LPS) and local (induced by injection of Freund’s incomplete adjuvant, FIA, into the paw) inflammation. Methods: Fevers in rats (8–10 weeks of age) whose capsaicin-sensitive afferents were depleted by neonatal capsaicin (50 mg/kg) treatment were compared to those of rats treated as neonates with vehicle. To investigate a possible involvement of cytokines, plasma levels of interleukin-6 (IL-6) and tumor necrosis factor (TNF) were measured during LPS- and FIA-induced fever in rats after capsaicin-induced desensitization. Body temperature was measured by biotelemetry. IL-6 and TNF bioactivities in plasma were determined using bioassays. Results: The initial but not the late phase of LPS (50 µg/kg)-induced fever was markedly higher (∼1.0°C) in rats whose capsaicin-sensitive neurons were destroyed by neonatal capsaicin treatment. Capsaicin-induced desensitization also resulted in significantly higher plasma levels of IL-6 and TNF 1 but not 4 h after LPS challenge. In contrast, the day after injection with FIA (0.1 ml), rats treated with capsaicin had significantly lower body temperatures compared with vehicle-treated animals. No differences were found in plasma levels of IL-6 and TNF between capsaicin- and vehicle-treated animals in response to FIA. Conclusions: These data indicate that the role of capsaicin-sensitive afferents in fever depends on the type of inflammatory response. During systemic inflammation, capsaicin-sensitive afferents may be involved in modulating fever by regulating the levels of pyrogenic cytokines. During local inflammation, the late phase of fever is partially mediated via capsaicin-sensitive afferents.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Role of Capsaicin-Sensitive Afferents in Fever and Cytokine Responses during Systemic and Local Inflammation in Rats

Gourine

Rudolph

Korsak

et al. 2001

Neuroimmunomodulation

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“…Possible autocrine actions of IL-6 in injured sensory neurons might include changes in the synthesis of peptides, growth-associated molecules, or apoptosis-related molecules. IL-6 from neurons might possibly influence the synthesis of trophic molecules or glial fibrillary acidic protein (Woodham et al, 1989) by satellite glial cells just as IL-1 and TNF-a stimulate the synthesis of NGF and LIF by nonneuronal cells in the CNS and PNS (Lindholm et al, 1987;Yoshida and Gage, 1992;Shadiack et al, 1994). IL-6 synthesized in sensory neurons presumably is transported in both central and peripheral axons and therefore in position to act on Schwann cells in the nerve and astrocytes or neurons in the spinal cord.…”

Section: Rt-pcrmentioning

confidence: 99%

Induction of interleukin-6 in axotomized sensory neurons

et al. 1995

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RNA from rat dorsal root ganglia was analyzed in search of potentially beneficial cytokines that are induced in dorsal root ganglia by nerve injury. By reverse transcription, the PCR, and Southern blotting, interleukin-6 mRNA was detected during development but not in normal adult dorsal root ganglia, reappeared within 1 d of sciatic nerve transection, was maximally increased after 2 and 4 d, and decreased below the threshold of detection within 1 week. By RNase protection assay, interleukin-6 mRNA was consistently present in RNA from dorsal root ganglia removed from rats 4 d following transection but not in control dorsal root ganglia. Interleukin-6 bioactivity was also present in dorsal root ganglia following nerve injury. By in situ hybridization, interleukin-6 mRNA was localized within large and medium- sized axotomized neurons. In summary, some sensory neurons respond to axotomy with a brisk transient increase in synthesis of interleukin-6. Injury to the sciatic nerve also induced mRNAs for interleukin-1 beta and tumor necrosis factor-alpha in dorsal root ganglia. The inductions of interleukin-1 beta and tumor necrosis factor-alpha mRNAs were later and more sustained than that of interleukin-6 mRNA. The cellular sources of these two cytokines have not been defined.

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“…Thus, rat CD4 + T cells pretreated with dexamethasone exhibit increased levels of mRNA for IL-10. 21 Similarly, during experimental endotoxemia or cardiopulmonary bypass, or in multiple sclerosis patients having an acute relapse, the treatment with GCs is associated with an increased plasma IL-10 secretion. 20,22,23 This might have resulted from a direct stimulatory effect of GCs on T cell IL-10 production and/or from the disinhibition of the restraining inputs of IL-12 and IFN-γ on monocyte/lymphocyte IL-10 production.…”

Section: Systemic Effects Of Gcsmentioning

confidence: 99%

Glucocorticoids and the Th1/Th2 Balance

2004

Horm Metab Res

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Evidence accumulated over the last 5-10 years indicates that glucocorticoids (GCs) inhibit the production of interleukin (IL)-12, interferon (IFN)-␥, IFN-␣, and tumor necrosis factor (TNF)-␣ by antigen-presenting cells (APCs) and T helper (Th)1 cells, but upregulate the production of IL-4, IL-10, and IL-13 by Th2 cells. Through this mechanism increased levels of GCs may systemically cause a selective suppression of the Th1-cellular immunity axis, and a shift toward Th2-mediated humoral immunity, rather than generalized immunosuppression. During an immune response and inflammation, the activation of the stress system, and thus increased levels of systemic GCs through induction of a Th2 shift, may actually protect the organism from systemic "overshooting" with Th1/pro-inflammatory cytokines and other products of activated macrophages with tissue-damaging potential. However, conditions associated with significant changes of GCs levels, such as acute or chronic stress or cessation of chronic stress, severe exercise, and pregnancy and postpartum, through modulation of the Th1/Th2 balance may affect the susceptibility to or the course of infections as well as autoimmune and atopic/ allergic diseases.

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Lipopolysaccharide induces substance P in sympathetic ganglia via ganglionic interleukin-1 production

Cited by 30 publications

References 25 publications

Role of Capsaicin-Sensitive Afferents in Fever and Cytokine Responses during Systemic and Local Inflammation in Rats

Role of Capsaicin-Sensitive Afferents in Fever and Cytokine Responses during Systemic and Local Inflammation in Rats

Induction of interleukin-6 in axotomized sensory neurons

Glucocorticoids and the Th1/Th2 Balance

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