Tobacco exposure inhibits SPLUNC1-dependent antimicrobial activity

Background: Tobacco smoke exposure impairs the lung´s innate immune response, leading to an increased risk of chronic infections. SPLUNC1 is a secreted, multifunctional innate defense protein that has antimicrobial activity against Gram negative organisms. We hypothesize that tobacco smoke-induced SPLUNC1 dysfunction contributes to the observed defect in innate immunity in tobacco smokers and that this dysfunction can be used as a potential biomarker of harm. Methods: We collected sputum from never-smokers and otherwise healthy smokers. We performed Western blotting to determine SPLUNC1 levels and determined antimicrobial activity against nontypeable Haemophilus influenzae. An in vitro exposure model was utilized to measure the effect of tobacco exposure on human bronchial epithelial culture (HBEC) antimicrobial activity against H. influenzae. The direct effects of cigarette and little cigar smoke exposure on SPLUNC1 function was determined using 24 h growth measurements and LPS binding assays. Results: H. influenzae growth in cigarette smoker´s sputum was significantly greater compared to never-smokers sputum over 24 h. HBEC supernatants and lysates contained significantly higher numbers of H. influenzae following chronic cigarette and little cigar smoke exposure compared to air-exposed controls. Furthermore, SPLUNC1´s antimicrobial activity and LPS-binding capability against both H. influenzae and P. aeruginosa was attenuated following cigarette and little cigar exposure. Conclusions: These data suggest that cigarette and little cigar exposure impairs SPLUNC1´s antimicrobial ability and that this inhibition may serve as a novel biomarker of harm that can be used to assess the toxicity of commercial tobacco products.Fil: Moore, Patrick J.. University of North Carolina; Estados UnidosFil: Sesma, Juliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas; ArgentinaFil: Alexis, Neil E.. University of North Carolina; Estados UnidosFil: Tarran, Robert. University of North Carolina; Estados Unido

Quantification of storm-induced bathymetric change in a back-barrier estuary

© The Author(s), 2016. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Estuaries and Coasts 40 (2017): 22-36, doi:10.1007/s12237-016-0138-5.Geomorphology is a fundamental control on ecological and economic function of estuaries. However, relative to open coasts, there has been little quantification of storm-induced bathymetric change in back-barrier estuaries. Vessel-based and airborne bathymetric mapping can cover large areas quickly, but change detection is difficult because measurement errors can be larger than the actual changes over the storm timescale. We quantified storm-induced bathymetric changes at several locations in Chincoteague Bay, Maryland/Virginia, over the August 2014 to July 2015 period using fixed, downward-looking altimeters and numerical modeling. At sand-dominated shoal sites, measurements showed storm-induced changes on the order of 5 cm, with variability related to stress magnitude and wind direction. Numerical modeling indicates that the predominantly northeasterly wind direction in the fall and winter promotes southwest-directed sediment transport, causing erosion of the northern face of sandy shoals; southwesterly winds in the spring and summer lead to the opposite trend. Our results suggest that storm-induced estuarine bathymetric change magnitudes are often smaller than those detectable with methods such as LiDAR. More precise fixed-sensor methods have the ability to elucidate the geomorphic processes responsible for modulating estuarine bathymetry on the event and seasonal timescale, but are limited spatially. Numerical modeling enables interpretation of broad-scale geomorphic processes and can be used to infer the long-term trajectory of estuarine bathymetric change due to episodic events, when informed by fixed-sensor methods

Flow cytometry of sputum: assessing inflammation and immune response elements in the bronchial airways

The evaluation of sputum leukocytes by flow cytometry is an opportunity to assess characteristics of cells residing in the central airways, yet it is hampered by certain inherent properties of sputum including mucus and large amounts of contaminating cells and debris

Relationship between abuse and neglect in childhood and diabetes in adulthood: Differential effects by sex, national longitudinal study of adolescent health

INTRODUCTION: Few studies have investigated links between child abuse and neglect and diabetes mellitus in nationally representative samples, and none have explored the role of obesity in the relationship. We sought to determine whether child abuse and neglect were associated with diabetes and if so, whether obesity mediated this relationship in a population-representative sample of young adults. METHODS: We used data from 14,493 participants aged 24 to 34 years from Wave IV of the National Longitudinal Study of Adolescent Health to study associations between self-reported child abuse (sexual, physical, or emotional abuse) and neglect as children and diabetes or prediabetes in young adulthood. We conducted sex-stratified logistic regression analyses to evaluate associations in models before and after the addition of body mass index (BMI) as a covariate. RESULTS: Although the prevalence of diabetes was similar for men and women (7.0% vs 6.7%), men were more likely than women to have prediabetes (36.3% vs 24.6%; omnibus P < .001). Among men, recurrent sexual abuse (≥3 lifetime incidents) was significantly associated with diabetes (OR, 3.66; 95% CI, 1.31–10.24), but not with prediabetes. There was no evidence of mediation by BMI. No forms of child abuse or neglect were associated with diabetes or prediabetes among women. CONCLUSIONS: Recurrent sexual abuse is robustly associated with diabetes in young adult men, independently of other forms of child abuse or neglect and BMI. Future research should explore other potential mechanisms for this association to identify avenues for prevention of diabetes among men who have experienced sexual abuse

Nasal PMN response to repeated challenge with endotoxin in healthy volunteers

We have employed nasal challenge with lipopolysaccharide (LPS) followed by nasal lavage (NL) to experimentally induce and examine upper airway inflammation in human volunteers. It is unclear however whether adaptation within individuals occurs following repeated nasal challenge. This was a pilot study to determine if repeated nasal LPS challenge yields attenuation of markers of inflammation (primarily neutrophil response) in the NL fluid of healthy humans

Vaping-Induced Proteolysis Causes Airway Surface Dehydration

Proteases such as neutrophil elastase cleave and activate the epithelial sodium channel (ENaC), causing airway dehydration. Our current study explores the impact of increased protease levels in vapers’ airways on ENaC activity and airway dehydration. Human bronchial epithelial cultures (HBECs) were exposed to bronchoalveolar lavage fluid (BALF) from non-smokers, smokers and vapers. Airway surface liquid (ASL) height was measured by confocal microscopy as a marker of hydration. ENaC cleavage was measured by Western blotting. Human peripheral blood neutrophils were treated with a menthol-flavored e-liquid (Juul), and the resulting secretions were added to HBECs. BALF from smokers and vapers significantly and equally increased ENaC activity and decreased ASL height. The ASL height decrease was attenuated by protease inhibitors. Non-smokers’ BALF had no effect on ENaC or ASL height. BALF from smokers and vapers, but not non-smokers, induced ENaC cleavage. E-liquid-treated neutrophil secretions cleaved ENaC and decreased ASL height. Our study demonstrated that elevated protease levels in vapers’ airways have functional significance since they can activate ENaC, resulting in airway dehydration. Lung dehydration contributes to diseases like cystic fibrosis (CF), chronic obstructive pulmonary disease (COPD) and asthma. Thus, our data predict that vaping, like smoking, will cause airway surface dehydration that likely leads to lung disease

When worlds collide: Invader-driven benthic habitat complexity alters predatory impacts of invasive and native predatory fishes

Interactions between multiple invasive alien species (IAS) might increase their ecological impacts, yet relatively few studies have attempted to quantify the effects of facilitative interactions on the success and impact of aquatic IAS. Further, the effect of abiotic factors, such as habitat structure, have lacked consideration in ecological impact prediction for many high-profile IAS, with most data acquired through simplified assessments that do not account for real environmental complexities. In the present study, we assessed a potential facilitative interaction between a predatory invasive fish, the Ponto-Caspian round goby (Neogobius melanostomus), and an invasive bivalve, the Asian clam (Corbicula fluminea). We compared N. melanostomus functional responses (feeding-rates under different prey densities) to a co-occurring endangered European native analogue fish, the bullhead (Cottus gobio), in the presence of increased levels of habitat complexity driven by the accumulation of dead C. fluminea biomass that persists within the environment (i.e. 0, 10, 20 empty bivalve shells). Habitat complexity significantly influenced predation, with consumption in the absence of shells being greater than where 10 or 20 shells were present. However, at the highest shell density, invasive N. melanostomus maximum feeding-rates and functional response ratios were substantially higher than those of native C. gobio. Further, the Relative Impact Potential metric, by combining per capita effects and population abundances, indicated that higher shell densities exacerbate the relative impact of the invader. It therefore appears that N. melanostomus can better tolerate higher IAS shell abundances when foraging at high prey densities, suggesting the occurrence of an important facilitative interaction. Our data are thus fully congruent with field data that link establishment success of N. melanostomus with the presence of C. fluminea. Overall, we show that invader-driven benthic habitat complexity can alter the feeding-rates and thus impacts of predatory fishes, and highlight the importance of inclusion of abiotic factors in impact prediction assessments for IAS

Effect of Obesity on Acute Ozone-Induced Changes in Airway Function, Reactivity, and Inflammation in Adult Females

We previously observed greater ozone-induced lung function decrements in obese than non-obese women. Animal models suggest that obesity enhances ozone-induced airway reactivity and inflammation. In a controlled exposure study, we compared the acute effect of randomized 0.4ppm ozone and air exposures (2 h with intermittent light exercise) in obese (N = 20) (30<BMI<40Kg/m2) vs. non-obese (N = 20) (BMI<25Kg/m2) non-smoking 18–35 year old women. We measured spirometry and bronchial reactivity to inhaled methacholine (3h post-exposure). Inflammation and obesity markers were assessed in the blood (pre, 4h post, and 20h post exposures) and induced-sputum (4h post-exposures and on 24h pre-exposure training day, no exercise): measures of C reactive protein (CRP) (blood only), leptin (blood only), adiponectin, interleukins IL-6, IL-1b, and IL-8, and tumor necrosis factor alpha, and sputum cell differential cell counts. The pre- to post-exposure decrease in forced vital capacity after ozone (adjusted for the change after air exposure) was significantly greater in the obese group (12.5+/-7.5 vs. 8.0+/-5.8%, p<0.05). Post ozone exposure, 6 obese and 6 non-obese subjects responded to methacholine at ≤ 10mg/ml (the maximum dose); the degree of hyperresponsiveness was similar for the two groups. Both BMI groups showed similar and significant ozone-induced increases in sputum neutrophils. Plasma IL-6 was increased by exercise (4 hr post air exposure vs. pre) only in the obese but returned to pre-air exposure levels at 20hr post-exposure. Plasma IL-6 was significantly increased at 4hr post ozone exposure in both groups and returned to pre-exposure levels by 20h post-exposure. These results confirm our previous findings of greater post-ozone spirometric decrements in obese young women. However, acute ozone-induced airway reactivity to methacholine and airway inflammation did not differ by obesity at the exposure and exercise levels used