Growth Factors and Cytokines in Acute Lung Injury

Deng, Jane C.; Standiford, Theodore J.

doi:10.1002/cphy.c090011

Cited by 20 publications

(24 citation statements)

References 291 publications

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“…Production of pro-inflammatory factors in the lung is considered indicative of the severity of lung injury [21]. To evaluate the production of pro-inflammatory factors following OALT, TNF-α and IL-1β levels were examined by ELISA.…”

Section: Resultsmentioning

confidence: 99%

Dexmedetomidine ameliorates acute lung injury following orthotopic autologous liver transplantation in rats probably by inhibiting Toll-like receptor 4–nuclear factor kappa B signaling

Chi¹,

Wei²,

Gao³

et al. 2015

J Transl Med

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BackgroundTo investigate whether pretreatment with dexmedetomidine (Dex) has a protective effect against acute lung injury (ALI) in an orthotopic autologous liver transplantation (OALT) rat model and to explore the mechanisms responsible for the protective effect of Dex against lung injury.MethodsForty-eight rats underwent OALT and were randomly divided into six groups (n = 8 in each group) that received 10 µg/kg Dex, 50 µg/kg Dex, 50 µg/kg Dex + nonspecific α2-adrenergic receptor (AR) antagonist atipamezole, 50 µg/kg Dex + specific α2B/C-AR antagonist ARC-239, 50 µg/kg Dex + specific α2A-AR antagonist BRL-44408, or the same amount of normal saline. The sham rats (n = 8) underwent anesthesia induction, laparotomy, and separation of the portal vein without liver ischemia and reperfusion. Lung tissue sections were stained with hematoxylin and eosin (HE) to visualize the damage. The expression of Toll-like receptor 4 (TLR4) and the phospho-nuclear factor (NF)-κB p65 subunit as well as inflammatory cytokines was measured.ResultsRats exhibited increased histological lung injury scores and pulmonary edema following OALT. Pretreatment with 50 μg/kg Dex attenuated OALT-induced lung injury in rats, probably by inhibiting the activation of the TLR4–NF-κB signaling pathway. The protective effect of Dex could be blocked by atipamezole or BRL-44408, but not by ARC-239, suggesting these effects of Dex were mediated, at least in part, by the α2A-AR.ConclusionsDex exerts protective effects against ALI following OALT, and this protection is associated with the suppression of TLR4–NF-κB signaling. Thus, pretreatment with Dex may be a useful method for reducing lung damage caused by liver transplantation.

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Section: Resultsmentioning

confidence: 99%

Dexmedetomidine ameliorates acute lung injury following orthotopic autologous liver transplantation in rats probably by inhibiting Toll-like receptor 4–nuclear factor kappa B signaling

Chi¹,

Wei²,

Gao³

et al. 2015

J Transl Med

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“…IL-1β is mainly produced by activated macrophages as a pro-peptide and is cleaved by caspase-1 within the inflammasome into an active enzyme [24]. IL-1β can upregulate cell-surface expression of leukocyte and vascular adhesion molecules and stimulate the production of chemokines required for leukocyte recruitment and activation [25]. Increased levels of IL-1β in ARDS patients correlate with development of pulmonary fibrosis [17,26].…”

Section: Discussionmentioning

confidence: 99%

Insult-dependent effect of bone marrow cell therapy on inflammatory response in a murine model of extrapulmonary acute respiratory distress syndrome

et al. 2013

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IntroductionAdministration of bone marrow-derived cells produces beneficial effects in experimental extrapulmonary acute respiratory distress syndrome (ARDS). However, there are controversies regarding the effects of timing of cell administration and initial insult severity on inflammatory response. We evaluated the effects of bone marrow-derived mononuclear cells (BMDMC) in two models of extrapulmonary ARDS once lung morphofunctional changes had already been installed.MethodsBALB/c mice received lipopolysaccharide (LPS) intraperitoneally (5 mg/kg in 0.5 ml saline) or underwent cecal ligation and puncture (CLP). Control mice received saline intraperitoneally (0.5 ml) or underwent sham surgery. At 24 hours, groups were further randomized to receive saline or BMDMC (2 × 106) intravenously. Lung mechanics, histology, and humoral and cellular parameters of lung inflammation and remodeling were analyzed 1, 3 and 7 days after ARDS induction.ResultsBMDMC therapy led to improved survival in the CLP group, reduced lung elastance, alveolar collapse, tissue and bronchoalveolar lavage fluid cellularity, collagen fiber content, and interleukin-1β and increased chemokine (keratinocyte-derived chemokine and monocyte chemotactic protein-1) expression in lung tissue regardless of the experimental ARDS model. Intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression in lung tissue increased after cell therapy depending on the insult (LPS or CLP).ConclusionsBMDMC therapy at day 1 successfully reduced lung inflammation and remodeling, thus contributing to improvement of lung mechanics in both extrapulmonary ARDS models. Nevertheless, the different inflammatory responses induced by LPS and CLP resulted in distinct effects of BMDMC therapy. These data may be useful in the clinical setting, as they suggest that the type of initial insult plays a key role in the outcome of treatment.

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“…In some patients the edema and ALI will continue to resolve without fibrosis, however others will experience ongoing fibrosis with increased collagen and ECM deposition. An extended fibrotic response is associated with prolonged mechanical ventilation and increased mortality [1,3,5]. …”

Section: Pathogenesis Of Ali/ardsmentioning

confidence: 99%

Acute Lung Injury Regulation by Hyaluronan

Singleton

Lennon

2012

J Aller Ther

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Summary Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS), have high mortality rates with few treatment options. An important regulatory factor in the pathology observed in ALI/ARDS is a disruption of the pulmonary endothelial barrier which, in combination with epithelial barrier disruption, causes leakage of fluid, protein and cells into lung airspaces. Degradation of the glycosaminoglycan, hyaluronan (HA), is involved in reduction of the endothelial glycocalyx, disruption of endothelial cell-cell contacts and activation of HA binding proteins upregulated in ALI/ARDS which promote a loss of pulmonary vascular integrity. In contrast, exogenous administration of high molecular weight HA has been shown to be protective in several models of ALI. This review focuses on the dichotomous role of HA to both promote and inhibit ALI based on its size and the HA binding proteins present. Further, potential therapeutic applications of high molecular weight HA in treating ALI/ARDS are discussed.

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Growth Factors and Cytokines in Acute Lung Injury

Cited by 20 publications

References 291 publications

Dexmedetomidine ameliorates acute lung injury following orthotopic autologous liver transplantation in rats probably by inhibiting Toll-like receptor 4–nuclear factor kappa B signaling

Dexmedetomidine ameliorates acute lung injury following orthotopic autologous liver transplantation in rats probably by inhibiting Toll-like receptor 4–nuclear factor kappa B signaling

Insult-dependent effect of bone marrow cell therapy on inflammatory response in a murine model of extrapulmonary acute respiratory distress syndrome

Acute Lung Injury Regulation by Hyaluronan

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