Interleukin-1-induced lung neutrophil accumulation and oxygen metabolite-mediated lung leak in rats

Leff, Jonathan A.; Baer, Jeanne W.; Bodman, M. E.; Kirkman, J. M.; Shanley, Paul F.; Patton, Lavonne M.; Beehler, Connie J.; McCord, Joe M.; Repine, John E.

doi:10.1152/ajplung.1994.266.1.l2

Cited by 49 publications

(18 citation statements)

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“…PQ-induced ROS can activate intracellular transcription factors such as NF-κB [13], thereby enhancing IL-1β expression. IL-1β can upregulate the expression of endothelial intercellular adhesion molecules essential for the recruit of inflammatory cells to an area of inflammation [18]. In an in vivo experiment, we found that the production of IL-1β and IL-18 in the PQpoisoning group of rats, BALF increased obviously in a time-dependent manner compared with the control.…”

Section: Discussionmentioning

confidence: 73%

NLRP3 Inflammasome Activation Is Essential for Paraquat-Induced Acute Lung Injury

et al. 2014

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The innate immune response is important in paraquat-induced acute lung injury, but the exact pathways involved are not elucidated. The objectives of this study were to determine the specific role of the NLRP3 inflammasome in the process. Acute lung injury was induced by administering paraquat (PQ) intraperitoneally. NLRP3 inflammasome including NLRP3, ASC, and caspase-1 mRNA and protein expression in lung tissue and IL-1β and IL-18 levels in BALF were detected at 4, 8, 24, and 72 h after PQ administration in rats. Moreover, rats were pretreated with 10, 30, and 50 mg/kg NLRP3 inflammasome blocker glybenclamide, respectively, 1 h before PQ exposure. At 72 h after PQ administration, lung histopathology changes, NLRP3, ASC, and caspase-1 protein expression, as well as secretion of cytokines including IL-1β and IL-18 in BALF were investigated. The NLRP3 inflammasome including NLRP3, ASC, caspase-1 expression, and cytokines IL-1β and IL-18 levels in PQ poisoning rats were significantly higher than that in the control group. NLRP3 inflammasome blocker glybenclamide pretreatment attenuated lung edema, inhibited the NLRP3, ASC, and caspase-1 activation, and reduced IL-1β and IL-18 levels in BALF. In the in vitro experiments, IL-1β and IL-18 secreted from RAW264.7 mouse macrophages treated with paraquat were attenuated by glybenclamide. In conclusion, paraquat can induce IL-1β/IL-18 secretion via NLRP3-ASC-caspase-1 pathway, and the NLRP3 inflammasome is essential for paraquat-induced acute lung injury.

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Section: Discussionmentioning

confidence: 73%

NLRP3 Inflammasome Activation Is Essential for Paraquat-Induced Acute Lung Injury

et al. 2014

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“…Discussion IL-Ia has been shown to increase neutrophil adhesion to endothelium (37,38) and lung neutrophil accumulation (39), to induce its own gene expression in endothelial cells (40), to stimulate the production of lipid mediators (13,17,19,20,41) and the synthesis of collagen by fibroblasts (42), and to induce basic fibroblast growth factor production by vascular smooth muscle cells (43). This information, in the aggregate, provides a powerful rationale for the postulate that some of the activities of IL-I may playa role in the development of chronic inflammatory pulmonary hypertension.…”

Section: Lung Histologymentioning

confidence: 97%

Interleukin-1 receptor antagonist treatment reduces pulmonary hypertension generated in rats by monocrotaline.

Voelkel

Tuder²,

Bridges³

et al. 1994

Am J Respir Cell Mol Biol

197

146

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Chronic pulmonary hypertension is associated with significant vascular remodeling. We demonstrated recently in the monocrotaline (MCT) and chronic hypoxia rat models of pulmonary hypertension that treatment with platelet-activating factor (PAF) antagonists inhibited the development of chronic pulmonary hypertension. PAF and other lipid mediators interact with interleukin-1. We postulated that chronic treatment with a recombinant human interleukin-1 receptor antagonist (IL-1ra) would inhibit development of chronic pulmonary hypertension in animal models. Rats were either injected with (60 mg/kg) MCT or exposed to a stimulated high altitude of 16,000 feet; half of the animals were treated with twice-daily injections (2 mg/kg) of IL-1ra. At 3 wk after MCT injection or 3 wk of hypoxic exposure, pulmonary artery pressure and right heart ventricle weight/(left ventricle and septum weight), RV/(LV + S), were measured. IL-1ra treatment reduced pulmonary hypertension and right heart hypertrophy in the MCT model, but not in the chronic hypoxia model. Measurement of lung homogenate IL-1 alpha by radioimmunoassay showed elevated levels in the MCT-treated rats throughout the 3-wk observation period. IL-1ra treatment reduced the levels of IL-1 alpha in lung tissue in most of the MCT-treated rats. MCT treatment was also associated with an increase in lung mRNA for IL-1 alpha, IL-1 beta, and IL-1ra. Immunohistology, using an antibody against rat IL-1 alpha, revealed staining of alveolar structures and of vascular and bronchial smooth muscle. In situ hybridization using a human IL-1 alpha cDNA probe demonstrated increased expression of the IL-1 alpha gene in the lung cells after endotoxin or MCT treatment. Northern blot analysis demonstrated low-level expression of IL-1 alpha mRNA in extracts of normal rat lung and increased expression after endotoxin or MCT treatment. We conclude that chronic treatment with human IL-1ra inhibited the development of pulmonary hypertension in the inflammatory (MCT) model, but not in the chronically hypoxic rats. This result indicates that IL-1 participates in the pathogenesis of some forms of pulmonary hypertension.

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“…Additionally, glibenclamide's inhibitory effect on neutrophil migration is somewhat indirectly mediated by its inhibition of NLRP3 inflammasome assembly. NLRP3 inflammasome is the key for IL-1 β maturation, and IL-1 β upregulates the expression of endothelial intercellular adhesion molecules essential for the recruitment of neutrophils to the area of inflammation [94–96]. …”

Section: Mechanisms Of Glibenclamide Underlying Its Anti-inflammatmentioning

confidence: 99%

A Protective Role of Glibenclamide in Inflammation-Associated Injury

Zhang

Lin

Zhang

et al. 2017

Mediators of Inflammation

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Glibenclamide is the most widely used sulfonylurea drug for the treatment of type 2 diabetes mellitus (DM). Recent studies have suggested that glibenclamide reduced adverse neuroinflammation and improved behavioral outcomes following central nervous system (CNS) injury. We reviewed glibenclamide's anti-inflammatory effects: abundant evidences have shown that glibenclamide exerted an anti-inflammatory effect in respiratory, digestive, urological, cardiological, and CNS diseases, as well as in ischemia-reperfusion injury. Glibenclamide might block KATP channel, Sur1-Trpm4 channel, and NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome activation, decrease the production of proinflammatory mediators (TNF-α, IL-1β, and reactive oxygen species), and suppress the accumulation of inflammatory cells. Glibenclamide's anti-inflammation warrants further investigation.

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Interleukin-1-induced lung neutrophil accumulation and oxygen metabolite-mediated lung leak in rats

Cited by 49 publications

References 0 publications

NLRP3 Inflammasome Activation Is Essential for Paraquat-Induced Acute Lung Injury

NLRP3 Inflammasome Activation Is Essential for Paraquat-Induced Acute Lung Injury

Interleukin-1 receptor antagonist treatment reduces pulmonary hypertension generated in rats by monocrotaline.

A Protective Role of Glibenclamide in Inflammation-Associated Injury

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