Destructive Pulmonary Effects of Smoke Inhalation and Simultaneous Alterations in Circulating IL-6, TNF-α, and IFN-γ Levels at Different Burn Depths

Abali, Ayse Ebru; Karakayalı, H.; Özdemir, Binnaz Handan; Bayraktar, Nilüfer; Abbas, Ozan Luay; Haberal, Mehmet

doi:10.1097/bcr.0b013e3182644e9b

Cited by 15 publications

(5 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…If the body's inflammatory response is moderate, the changes in the TNF-α level will be limited, which is conducive to protecting the body and alleviating the body damage and infection. On the contrary, secondary damage may be caused to the tissue, promoting the development of disease (19–21). In this study, with the prolongation of time after burn in rats, TNF-α and Bax expression levels were also increased continuously, while the Bcl-2 expression level was decreased continuously, and the degree of apoptosis became increasingly higher, indicating that the inflammatory response in rats continued to be enhanced and the secondary damage of burn wound was deepened.…”

Section: Discussionmentioning

confidence: 99%

Correlation of the expression of inflammatory factors with expression of apoptosis-related genes Bax and Bcl-2, in burned rats

2018

View full text Add to dashboard Cite

Correlation of the expression of inflammatory factors with expression of apoptosis-related genes, B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X protein (Bax), in burned rats was investigated. Forty healthy Sprague-Dawley rats were selected and randomly divided into SHAM group (n=10), I° burn group (n=10), II° burn group (n=10) and III° burn group (n=10). Changes in tumor necrosis factor-α (TNF-α), Bax messenger ribonucleic acid (mRNA), Bcl-2 mRNA, Bax protein and Bcl-2 protein expression levels were detected. The correlation of TNF-α, Bax and Bcl-2 with the degree of burn in rats was observed, and the correlation of TNF-α with Bax and Bcl-2 was also analyzed. Moreover, Bax mRNA and Bcl-2 mRNA were detected via reverse transcription-quantitative polymerase chain reaction, and TNF-α, Bax protein and Bcl-2 protein were detected via enzyme-linked immunosorbent assay. In burn groups, TNF-α, Bax mRNA and Bax protein levels were significantly increased at each time point compared with those at the previous time point (P<0.05), but Bcl-2 mRNA and protein levels were significantly decreased compared with those at the previous time point (P<0.05). At the same time point, TNF-α, Bax mRNA, Bcl-2 mRNA, Bax protein and Bcl-2 protein expression levels had statistically significant differences between any given two groups (P<0.05). The TNF-α expression level was positively correlated with Bax expression levels and negatively correlated with Bcl-2 expression levels. Additionally, TNF-α, Bax mRNA and Bax protein had positive correlations with the degree of burn and time after burn, while Bcl-2 mRNA and Bcl-2 protein had negative correlations with the degree of burn and time after burn. Continuous monitoring of changes in the TNF-α level can be used as a means to evaluate the degree of burn and apoptosis, and to prevent the deepening of burn wounds, thus facilitating the early clinical evaluation of prognosis.

show abstract

Section: Discussionmentioning

confidence: 99%

Correlation of the expression of inflammatory factors with expression of apoptosis-related genes Bax and Bcl-2, in burned rats

2018

View full text Add to dashboard Cite

show abstract

“…These proinflammatory cytokines induce fever and the production of acute‐phase reactants that contribute to T‐cell activation . A recent in vivo study revealed that pulmonary damage and the systemic inflammatory response might be evaluated by blood levels of IL‐6, tumor necrosis factor alpha, and interferon‐ γ in concomitant smoke inhalation and skin burns . The anti‐inflammatory response following burn injury is characterized by the production of IL‐4 and IL‐10 .…”

Section: Introductionmentioning

confidence: 99%

A time course study about gene expression of post‐thermal injury with DNA microarray

Liu

Tan

et al. 2014

Int J Dermatology

View full text Add to dashboard Cite

show abstract

“…smoke, tissue damage) through pattern recognition receptors expressed on their surface and modulated by Toll like receptor 4 (TLR4). [28,29]…”

Section: Discussionmentioning

confidence: 99%

The effect of smoking status on burn inhalation injury mortality

Knowlin

Stanford

Cairns

et al. 2017

Burns

View full text Add to dashboard Cite

Introduction Three factors that effect burn injury mortality are age, total body surface of burn (TBSA), and inhalation injury. Of the three, inhalation injury is the strongest predictor of mortality thus its inclusion in the revised Baux score (Age + TBSA +17* (Inhalation Injury, 1 = yes, 0 = no)). However, the weighted contribution of specific comorbidities such as smoker status on mortality has traditionally not been accounted for nor studied in this subset of burn patients. We therefore sought to examine the impact of current tobacco and/or marijuana smoking in patients with inhalation injury. Methods A retrospective analysis of patients admitted to a regional burn center from 2002-2012. Independent variables analyzed included basic demographics, burn mechanism, presence of inhalation injury, TBSA, pre-existing comorbidities, and smoker status. Bivariate analysis was performed and logistic regression modeling using significant variables was utilized to estimate odds of mortality. Results There were a total of 7640 patients over the study period. 7% (n=580) of the burn cohort with inhalation injury were included in this study. In-hospital burn mortality for inhalation injury patients was 23%. Current smokers (20%) included cigarette smokers and marijuana users, 19% and 3%, respectively. Preexisting respiratory disease (17%) was present in 36% of smokers compared to 13% of non-smokers (p <0.001). Smokers had significantly lower mortality rate (9%) compared to non-smokers (26%, p <0.01). The logistic regression model for mortality outcomes identified statistically four significant variables: age, TBSA, race, and smoker status (OR = 0.41, 95% CI = 0.18-0.93). Presence of comorbidities, including preexisting respiratory disease, wasn't significant. Conclusion In the sub group of burn patients with inhalation injury, the odds of mortality significantly decreased in pre-existing smokers after adjusting for significant covariates. We postulate that an immune tolerance mechanism that modulates and diminishes the pro-inflammatory response confers a survival advantage in smokers after exposure to acute smoke inhalation injury. Future prospective studies in human and/or animal models are needed to confirm these findings.

show abstract

Destructive Pulmonary Effects of Smoke Inhalation and Simultaneous Alterations in Circulating IL-6, TNF-α, and IFN-γ Levels at Different Burn Depths

Cited by 15 publications

References 26 publications

Correlation of the expression of inflammatory factors with expression of apoptosis-related genes Bax and Bcl-2, in burned rats

Correlation of the expression of inflammatory factors with expression of apoptosis-related genes Bax and Bcl-2, in burned rats

A time course study about gene expression of post‐thermal injury with DNA microarray

The effect of smoking status on burn inhalation injury mortality

Contact Info

Product

Resources

About