Effect of interleukin-10 (IL-10) on experimental LPS-induced acute lung injury

Inoue, Gen

doi:10.1007/s101560050050

Cited by 57 publications

(45 citation statements)

References 26 publications

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“…Earlier reports have identified increased IL-10 levels following injury of rat sciatic nerve, and a beneficial role of IL-10 has been implicated in tissues such as cardiac muscle, carotid endothelia, and lung epithelia (20)(21)(22). We found that epithelial IL-10Rα mediates the IL-10-driven increase in wound healing.…”

Section: Discussionsupporting

confidence: 57%

Macrophage-derived IL-10 mediates mucosal repair by epithelial WISP-1 signaling

Quirós¹,

Nishio²,

Neumann³

et al. 2017

Journal of Clinical Investigation

158

132

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Section: Discussionsupporting

confidence: 57%

Macrophage-derived IL-10 mediates mucosal repair by epithelial WISP-1 signaling

Quirós¹,

Nishio²,

Neumann³

et al. 2017

Journal of Clinical Investigation

158

132

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“…During the inflammatory stress produced by LPS, a number of proinflammatory cytokines are released into the blood stream to activate the innate immune response that is the first line of defense against the invading microorganisms [1][2][3][4][5]. On the other hand, a second array of anti-inflammatory factors such as the ·-melanocyte-stimulating hormone (·-MSH) [2,6] and the cytokine IL-10 [7,8] are also increased by LPS to diminish the action of an otherwise exacerbated immune response that might induce tissue injury and septic shock [2,3,6,[8][9][10][11][12]. Furthermore, ·-MSH not only blocks the release of a variety of proinflammatory cytokines such as IL-1 [2,3,12,13], IL-2 [13], IL-6 [2,3], IFN-Á [13] and TNF-· [2,3,12,13] but also inhibits their biological effects since it was previously shown that ·-MSH inhibited the stimulatory action of IL-1, IL-2 and IL-6 on corticotropin-releasing hormone release from incubated hypothalami [10,11].…”

Section: Introductionmentioning

confidence: 99%

“…It was shown that ·-MSH inhibits the transcription factor NF-ÎB [14] that stimulates the synthesis of a variety of proinflammatory cytokines such as IL-1, IL-6 and TNF-· [15]. Moreover, ·-MSH increases IL-10 release [16] that also decreases TNF-· synthesis and release [8].…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide-Induced Leptin Synthesis and Release Are Differentially Controlled by Alpha-Melanocyte-Stimulating Hormone

Mastronardi

Srivastava²,

Yu³

et al. 2005

Neuroimmunomodulation

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Objective: Since α-melanocyte-stimulating hormone (α-MSH) inhibits the synthesis and release of proinflammatory cytokines and stimulates the synthesis and release of anti-inflammatory cytokines, and leptin is a cytokine that has anti-inflammatory actions in the presence of lipopolysaccharide (LPS), we hypothesized that α-MSH increases leptin synthesis and release. Methods: α-MSH or 0.9% NaCl (saline) were injected intraperitoneally 15 min prior to intravenous injection of 0.5 ml of saline or LPS (0.15 mg/kg). Thereafter, repeated blood samples were withdrawn over a period of 6 h and plasma leptin concentrations determined. The rats were sacrificed at 6 h and leptin mRNA was measured in epididymal fat pads. Results: Plasma leptin concentrations of the saline-injected control group were unaltered during the 6 h, whereas in the LPS group, leptin was unaltered between 0 and 30 min and thereafter progressively increased between 30 and 360 min by 2.5-fold. α-MSH slightly increased plasma leptin concentrations by 15 min and then increased them further by 120 min, after which they declined towards baseline. The pattern of plasma leptin concentrations in the α-MSH + LPS group was similar to that of the LPS group, except that higher concentrations were observed at 120 min in the rats injected with α-MSH + LPS. LPS increased leptin mRNA by 3-fold at 6 h, whereas it was unaffected in the MSH-treated animals. On the contrary, α-MSH completely blocked the LPS-induced leptin mRNA. Conclusions: Our results suggest that α-MSH increased leptin release without altering its synthesis, but when LPS increased release and synthesis of leptin, α-MSH, although further increasing release, blocked the enhanced synthesis of leptin elicited by LPS.

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“…28 Administration of IL-10 has shown protective effects in LPS-induced lung injury. 29 Interestingly, inhaled IL-10 attenuates biotrauma and mortality in a ventilator-induced lung injury model in rats. 30 We did not observe an attenuation of proinflammatory cytokine levels, pulmonary ICAM-1 levels, or pulmonary neutrophil influx.…”

Section: Discussionmentioning

confidence: 99%

Lidocaine increases the anti‐inflammatory cytokine IL‐10 following mechanical ventilation in healthy mice

Wal

Vaneker

Steegers

et al. 2014

Acta Anaesthesiol Scand

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Background: Mechanical ventilation (MV) induces an inflammatory response that may result in (acute) lung injury. Lidocaine, an amide local anesthetic, has anti-inflammatory properties in vitro and in vivo, possibly due to an attenuation of pro-inflammatory cytokines, intracellular adhesion molecule-1 (ICAM-1), and reduction of neutrophils influx. We hypothesized an attenuation of MV-induced inflammatory response with intravenously administered lidocaine. Methods: Lidocaine (Lido) (2, 4, and 8 mg/kg/h) was intravenously administered during 4 h of MV with a tidal volume of 8 ml/ kg, positive end expiratory pressure 1,5 cmH2O and FiO2 0.4. We used one ventilated control (CON) group receiving vehicle. After MV, mice were euthanized, and lungs and blood were immediately harvested, and cytokine levels and ICAM-1 levels were measured in plasma and lung homogenates. Pulmonary neutrophils influx was determined in LEDER-stained slices of lungs. Anesthetic need was determined by painful hind paw stimulation. Results: Lidocaine-treated animals (Lido 2, 4 and 8 mg/kg/h) showed higher interleukin (IL)-10 plasma levels compared to control animals. Lidocaine treatment with 8 mg/kg/h (Lido 8) resulted in higher IL-10 in lung homogenates. No differences were observed in pro-inflammatory cytokines, ICAM-1, and pulmonary influx between the different ventilated groups. Conclusions: Intravenously administered lidocaine increases levels of plasma IL-10 with infusion from 2, 4, and 8 mg/kg/h and pulmonary levels of IL-10 with 8 mg/kg/h in a murine mechanical ventilation model. Intravenously administered lidocaine appears to reduce anesthetic need in mice.

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Effect of interleukin-10 (IL-10) on experimental LPS-induced acute lung injury

Cited by 57 publications

References 26 publications

Macrophage-derived IL-10 mediates mucosal repair by epithelial WISP-1 signaling

Macrophage-derived IL-10 mediates mucosal repair by epithelial WISP-1 signaling

Lipopolysaccharide-Induced Leptin Synthesis and Release Are Differentially Controlled by Alpha-Melanocyte-Stimulating Hormone

Lidocaine increases the anti‐inflammatory cytokine IL‐10 following mechanical ventilation in healthy mice

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