Expression and regulation of interleukin‐10 and interleukin‐10 receptor in rat astroglial and microglial cells

Ledeboer, Annemarie; Brevé, John; Wierinckx, Anne; Jagt, Saskia Van Der; Bristow, Adrian; Leysen, Josée E.; Tilders, F. J. H.; Dam, Anne‐Marie van

doi:10.1046/j.1460-9568.2002.02200.x

Cited by 169 publications

(128 citation statements)

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“…We demonstrate that systemic administration of this agent significantly inhibits N. meningitidis and B. burgdorferi-induced CNS gliosis, demyelination, and associated inflammatory cytokine elevations while attenuating concomitant decreases in IL-10 levels. As such, endogenous SP may augment inflammation within the brain in two ways, first by elevating levels of inflammatory mediators, and second by lowering levels of a cytokine that are thought to contribute to the immunoquiescent environment of the healthy CNS (30,31).…”

Section: Discussionmentioning

confidence: 99%

Neurogenic Exacerbation of Microglial and Astrocyte Responses toNeisseria meningitidisandBorrelia burgdorferi

Chauhan

Sterka

Gray

et al. 2008

The Journal of Immunology

109

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Although glial cells are recognized for their roles in maintaining neuronal function, there is growing appreciation of the ability of resident CNS cells to initiate and/or augment inflammation following trauma or infection. The tachykinin, substance P (SP), is well known to augment inflammatory responses at peripheral sites and its presence throughout the CNS raises the possibility that this neuropeptide might serve a similar function within the brain. In support of this hypothesis, we have recently demonstrated the expression of high affinity receptors for SP (Neurokinin-1 (NK-1) receptors) on microglia and shown that this tachykinin can significantly elevate bacterially induced inflammatory prostanoid production by isolated cultures of these cells. In the present study, we demonstrate that endogenous SP/NK-1R interactions are an essential component in the initiation and/or progression of CNS inflammation in vivo following exposure to two clinically relevant bacterial CNS pathogens, Neisseria meningitidis and Borrelia burgdorferi. We show that in vivo elevations in inflammatory cytokine production and decreases in the production of an immunosuppressive cytokine are markedly attenuated in mice genetically deficient in the expression of the NK-1R or in mice treated with a specific NK-1R antagonist. Furthermore, we have used isolated cultures of microglia and astrocytes to demonstrate that SP can augment inflammatory cytokine production by these resident CNS cell types following exposure to either of these bacterial pathogens. Taken together, these studies indicate a potentially important role for neurogenic exacerbation of resident glial immune responses in CNS inflammatory diseases, such as bacterial meningitis.

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Section: Discussionmentioning

confidence: 99%

Neurogenic Exacerbation of Microglial and Astrocyte Responses toNeisseria meningitidisandBorrelia burgdorferi

Chauhan

Sterka

Gray

et al. 2008

The Journal of Immunology

109

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“…IL-10 knockout mice showed decreased latency to immobility in a forced swim test where administration of IL-10 was able to reverse behavior of helplessness (42). IL-10 receptor 1 is located on rat microglia, and responds to inflammatory stimuli, such as lipopolysaccharide (LPS) injection (43). It inhibits pro-inflammatory cytokine production by glial cells stimulated by LPS in a dose-dependent manner (44).…”

Section: Inflammatory Cytokine Concentration In Depressionmentioning

confidence: 99%

Role of inflammatory cytokines in depression: Focus on interleukin-1β

et al. 2016

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Abstract. According to the World Health Organization, major depression will become the leading cause of disability worldwide by the year 2030. Despite extensive research into the mechanisms underlying this disease, the rate, prevalence and disease burden has been on the rise, particularly in the industrialized world. Epidemiological studies have shown biological and biochemical differences in disease characteristics and treatment responses in different age groups. Notable differences have been observed in the clinical presentation, co-prevalence with other diseases, interaction with the immune system and even in the outcome. Thus, there is an increased interest in characterizing these differences, particularly in terms of contribution of different factors, including age, cytokines and immunotherapy. Research into the possible mechanisms of these interactions may reveal novel opportunities for future pharmacotherapy. The aim of the present review is to document recent literature regarding the impact of inflammatory mechanisms on the pathophysiology of the depressive disorder.

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“…As a result, "4-h-cultured" neutrophils become very responsive to IL-10 in terms of STAT3 tyrosine phosphorylation and suppressor of cytokine signaling (SOCS)-3 protein synthesis, unlike freshly isolated neutrophils. Importantly, modulation of IL-10R1 expression has been reproduced in cell types other than neutrophils [12][13][14][15], indicating that the regulated expression of IL-10R1 represents a general mechanism to control responsiveness to IL-10. In addition, because experimental evidence suggests that new protein synthesis is required for IL-10 to inhibit LPS-induced cytokine production in human neutrophils and monocytes [16,17], our findings might have identified IL-10R1 as at least one of the newly synthesized polypeptide(s) involved.…”

Section: Introductionmentioning

confidence: 99%