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Alcohol consumption leads to an exaggerated inflammatory response after burn injury. Elevated levels of interleukin-6 (IL-6) in patients are associated with increased morbidity and mortality after injury, and high systemic and pulmonary levels of IL-6 have been observed after the combined insult of ethanol exposure and burn injury. To further investigate the role of IL-6 in the pulmonary inflammatory response, we examined leukocyte infiltration and cytokine and chemokine production in the lungs of wild-type and IL-6 knockout mice given vehicle or ethanol (1.11 g/kg) and subjected to a sham or 15% total body surface area burn injury. Levels of neutrophil infiltration and neutrophil chemoattractants were increased to a similar extent in wild-type and IL-6 knockout mice 24 h after burn injury. When ethanol exposure preceded the burn injury, however, a further increase of these inflammatory markers was seen only in the wild-type mice. Additionally, signal transducer and activator of transcription-3 (STAT3) phosphorylation did not increase in response to ethanol exposure in the IL-6 knockout mice, in contrast to their wild-type counterparts. Visual and imaging analysis of alveolar wall thickness supported these findings and similar results were obtained by blocking IL-6 with antibody. Taken together, our data suggest a causal relationship between IL-6 and the excessive pulmonary inflammation observed after the combined insult of ethanol and burn injury. [ABSTRACT FROM AUTHOR]

Laboratory evidence suggests that intestinal permeability is elevated following either binge ethanol exposure or burn injury alone, and this barrier dysfunction is further perturbed when these insults are combined. We and others have previously reported a rise in both systemic and local proinflammatory cytokine production in mice after the combined insult. Knowing that long myosin light-chain kinase (MLCK) is important for epithelial barrier maintenance and can be activated by proinflammatory cytokines, we examined whether inhibition of MLCK alleviated detrimental intestinal responses seen after ethanol exposure and burn injury. To accomplish this, mice were given vehicle or a single binge ethanol exposure followed by a sham or dorsal scald burn injury. Following injury, one group of mice received membrane permeant inhibitor of MLCK (PIK). At 6 and 24 h postinjury, bacterial translocation and intestinal levels of proinflammatory cytokines were measured, and changes in tight junction protein localization and total intestinal morphology were analyzed. Elevated morphological damage, ileal IL-1β and IL-6 levels, and bacterial translocation were seen in mice exposed to ethanol and burn injury relative to either insult alone. This increase was not seen in mice receiving PIK after injury. Ethanol-exposed and burn-injured mice had reduced zonula occludens protein-1 and occludin localization to the tight junction relative to sham-injured mice. However, the observed changes in junctional complexes were not seen in our PIK-treated mice following the combined insult. These data suggest that MLCK activity may promote morphological and inflammatory responses in the ileum following ethanol exposure and burn injury. [ABSTRACT FROM AUTHOR]

Abstract: CD8+ T cells are important for resolution of HSV-2 lesions from the female genital epithelium. It is uncertain whether optimal clearance of viruses such as HSV-2 that cause a limited, non-systemic infection solely requires expression of effector functions by infiltrating CD8+ T lymphocytes, or if the clearance rate is reflective of the expression level of critical effector functions. To address this, CD8+ T cells from normal OT-I mice or OT-I mice deficient in IFNγ (IFNγ−/−) or the IFNγ receptor (IFNγR−/−) were activated in vitro in the presence of IFNγ or IL-4 to generate a series of effector populations (Tc1 and Tc2-like respectively) that secreted different levels of IFNγ and expressed different levels of HSV-specific cytolytic function. Compared with Tc1 cells, Tc2-like cells produced the type 2 cytokines IL-4 and IL-5, exhibited decreased IFNγ secretion, diminished proliferation in vitro, and decreased antigen-specific cytolysis in vivo. Clearance of an ovalbumin-expressing HSV-2 strain (HSV-2 tk− OVA) by adoptively transferred Tc2-like cells was delayed relative to Tc1 cell recipients. Because donor Tc2-like cells proliferated in vivo and infiltrated the infected genital epithelium similar to Tc1 cells, the diminished virus clearance by Tc2-like effector cells correlated with reduced expression of critical effector functions. Together, these results suggest that high level expression of protective T cell functions by effector T cells is necessary for optimal clearance of HSV-2 from the genital epithelium. These results have important implications for vaccines designed to elicit CD8+ T cells against viruses such as HSV-2 that infect the genital tract. [Copyright &y& Elsevier]

Background: Clinical and laboratory evidence suggests that alcohol consumption prior to burn injury leads to dysregulated immune function and subsequent higher rates of morbidity and mortality. Our laboratory previously observed higher levels of pro-inflammatory cytokines and leukocyte infiltration in the lungs of mice following ethanol and burn injury. To understand the mechanism of the increased inflammatory response, we looked at different signaling initiators of inflammation including toll-like receptors 2 and 4 (TLR2 and 4) pathways. Methods: Wild-type, TLR2, and TLR4 knockout mice were treated with vehicle or a single binge dose of ethanol (1.11 g/kg) and subsequently given a sham or burn injury. Twenty-four hours postinjury, systemic and pulmonary levels of pro-inflammatory cytokines were quantified, and differences in neutrophil infiltration were determined by histological examination. Results: Higher numbers of neutrophils were observed in the lungs of wild-type mice following the combined insult of ethanol and burn injury relative to either injury alone. This increase in leukocyte accumulation was absent in the TLR4 knockout mice. Circulating levels of IL-6 and tumor necrosis factor-α were also elevated in wild-type mice but not in TLR4 knockout mice. Consistent with these findings, pulmonary levels of KC and IL-6 were increased in wild-type mice following burn and ethanol compared to burn injury alone as well as to their TLR4 knockout counterparts. In contrast, TLR2 knockout mice displayed similar levels, to wild-type mice, of neutrophil infiltration as well as IL-6 and KC in the lung. Conclusions: These data suggest that TLR4 signaling is a crucial contributory component in the exuberant inflammation after ethanol and burn injury. However, TLR2 does not appear to play a vital role in the aberrant pulmonary inflammation. [ABSTRACT FROM AUTHOR]

Abstract: This article highlights the research presented at the Alcohol and Trauma Satellite Symposium at the 30th Annual Meeting of the Shock Society. The satellite meeting was held on June 8 and 9 in Baltimore, MD. Its purpose was to discuss recent findings in the areas of alcohol and injury, including the effect of alcohol use on patients in the trauma unit of hospitals. The meeting consisted of three sessions, with plenary talks by invited speakers, short talks from selected abstracts, and a poster session. Participants presented data on the effects of alcohol on organ function, healing, and immune processes after a variety of injuries including burn, hemorrhagic shock, sepsis, and ischemia reperfusion. [Copyright &y& Elsevier]

Abstract: Cell-mediated immunity is extremely important for resolution of infection and for proper healing from injury. However, the cellular immune response is dysregulated following injuries such as burn and hemorrhage. Sex hormones are known to regulate immunity, and a well-documented dichotomy exists in the immune response to injury between the sexes. This disparity is caused by differences in immune cell activation, infiltration, and cytokine production during and after injury. Estrogen and testosterone can positively or negatively regulate the cellular immune response either by aiding in resolution or by compounding the morbidity and mortality. It is apparent that the hormonal dysregulation is dependent not only on the type of injury sustained but also the amount of circulating hormones. Therefore, it may be possible to design sex-specific therapies to improve immunological function and patient outcome. [Copyright &y& Elsevier]

In this study, our goal was to adapt the moss layer transfer technique (MLTT), first developed to restore degraded Sphagnum‐dominated peatland explicitly with a bryophyte layer, to a former in‐situ oil sands well‐pad constructed with nearby mineral fill in northwestern Alberta, Canada. Mineral fill was either completely removed or partially removed with residual fill buried under excavated and decompacted peat, followed by the transfer of donor moss collected from nearby linear features with different plant communities in peatlands. Three years after MLTT, peatland vegetation covers 63% of the site. Carex spp. dominate with 36% coverage, followed by mosses at 12%, including 3% Sphagnum spp. and 8% fen mosses, and shrubs at 8%. Different substrate adjustment treatments and types of donor moss had negligible impact on vegetation development although areas without MLTT remained devoid of mosses and had the lowest peatland species cover. Instead, surface elevation, moisture conditions, and substrate chemistry played important roles in shaping the vegetation communities. The prompt introduction and establishment of peatland donor species through MLTT was crucial to the overall re‐establishment of peatland vegetation. This is the first full pad scale study to prove that a flat, moist peat surface created by the removal and/or burial of mineral fill can support peatland vegetation development, particularly ground layer bryophytes. Overall, the reclaimed well‐pad appears to be on trajectory toward becoming a functional peatland and our approaches should be considered and tested in future well‐pad reclamation trials. [ABSTRACT FROM AUTHOR]

Across Canada's boreal forest, linear disturbances, including cutlines such as seismic lines and roads, crisscross the landscape to facilitate resource exploration and extraction; many of these linear disturbances cross peatland ecosystems. Changes in tree canopy cover and the compression of the peat by heavy equipment alter local thermal, hydrological, and ecological conditions, likely changing carbon exchange on the disturbance, and possibly in the adjacent peatland. We measured bulk density, water table, soil temperature, plant cover, and CO2 and CH4 flux along triplicate transects crossing a winter road through a wooded fen near Peace River, Alberta, Canada. Sample plots were located 1, 5, and 10 m from the road on both sides with an additional three plots on the road. Productivity of the overstory trees, when present, was also determined. The winter road had higher bulk density, shallower water table, higher graminoid cover, and thawed earlier than the adjacent peatland. Tree productivity and CO2 flux varied between the plots, and there was no clear pattern in relation to distance from the road. The plots on the winter road acted as a greater CO2 sink and greater CH4 source compared to the adjacent peatland with plots on the winter road emitting on average (standard error) 479 (138) compared to 41 (10) mg CH4 m−2 day−1 in the adjacent peatland. Considering both gases, global warming potential increased from 70 to 250 g CO2e m−2 year−1 in the undisturbed area to 2100 g CO2e m−2 year−1 on the winter road. Although carbon fluxes on any given cutline through peatland will vary depending on level of compaction, line width and vegetation community shifts, the large number of linear disturbances in Canada's boreal forest and slow recovery on peatland ecosites suggest they could represent an important anthropogenic greenhouse gas source. [ABSTRACT FROM AUTHOR]

Early clearance of a thymidine kinase-deficient strain of herpes simplex virus type 2 from the female genital tract required T-cell-produced gamma interferon (IFN-γ). Transfer of activated CD8+ T cells to irradiated C57BL/6 mice resulted in rapid virus clearance, but clearance was greatly delayed in recipients deficient in the IFN-γ receptor (IFN-γ R). Early virus clearance was demonstrated in radiation chimeras in which IFN-γ R expression was limited to parenchymal cells, but resolution was significantly delayed in chimeras deficient in IFN-γ R expression and chimeras expressing IFN-γ R only on hematopoietic cells. Together, these results suggest that early IFN-γ-mediated protection was manifested mainly by stimulation of genital parenchymal cells. [ABSTRACT FROM AUTHOR]

Across Canada's boreal forest, disturbances from in situ oil sands mining, including well‐pads, significantly impact vast areas of the landscape. The creation of well‐pads requires removal of vegetation and placement of mineral fill, which essentially stops any carbon (C) sequestration on the once peatland ecosystem. It is important that, once no longer in use, these well‐pads are restored as long‐term C (peat) accumulation is what defines peatland ecosystem. However, little is known about the recovery of greenhouse gas exchange post‐restoration of these features. We studied a decommissioned well‐pad located in a treed poor fen that was restored using three soil adjustment treatments (SATs): (1) complete mineral fill removal (Peat‐Dec); (2) partial pad removal and burial under peat layer (BUPL); and (3) mixing mineral and peat by inversion (Mixed‐P‐M). The recreated peat surface was revegetated with donor peatland species using the moss layer transfer technique (MLTT). The objectives of this paper were to (1) quantify plot‐scale seasonal carbon dioxide (CO2) and methane (CH4) exchange of the SATs, 2–4 years post‐restoration compared to reference sites and (2) determine the influence of several environmental variables on CO2 and CH4 exchange. All SATs proved effective in recreating a soil surface needed to support peatland vegetation as shown by similar rates of net ecosystem exchange (NEE). Equally, both types of vegetation reintroduced led this site on a trajectory toward functioning as a net C sink. [ABSTRACT FROM AUTHOR]

Background Ethanol ( Et OH) exposure prior to traumatic injury, such as a burn, elevates systemic and local inflammatory responses and increases morbidity and mortality. Adipose is a large tissue mass that is often inflamed during obesity or other stresses, which disturbs metabolic homeostasis. To date, there has been little investigation into the inflammatory response of adipose tissue after combined Et OH exposure and burn injury. Methods Two Et OH exposure regimens were utilized to examine the role of inflammation in adipose tissue after Et OH and burn injury. Mice were either given a single or episodic binge exposure to Et OH or saline followed by scald (burn) or sham injury 30 minutes later. Twenty-four hours post injury, serum and adipose tissue were collected for assessment of inflammatory mediators. Results Single binge Et OH alone induced no inflammation in adipose when compared with sham vehicle-treated mice. However, single binge Et OH followed by burn injury induced significant elevations in m RNA and protein concentrations of pro-inflammatory mediators interleukin-6 ( IL-6), KC, and monocyte chemoattractant protein 1 compared with either insult alone or sham vehicle group. Additionally, Et OH exposure and burn injury significantly blunted inducible nitric oxide synthase (i NOS), indicating a complex inflammatory response. Episodic binge Et OH exposure followed by burn injury exacerbated the postburn adipose inflammatory response. The magnitude of the episodic binge-induced inflammatory parameters postburn were 2- to 5-fold greater than the response detected after a single exposure of Et OH, indicating Et OH-induced potentiation of burn-induced inflammatory response. Finally, inflammatory loci and crown-like structures in adipose were significantly increased by episodic binge Et OH and burn injury. Conclusions This is the first report of binge and burn-induced crown-like structure formation. Evidence presented herein suggests an important role for alcohol and burn as an additional mediator of adipose inflammation in postburn injury, a common complication in burn patients. [ABSTRACT FROM AUTHOR]

The article discusses a study which analyzed if the graded severity of smoke inhalation is depicted in acute pulmonary inflammatory response to injury. Study authors obtained bronchoalveolar lavage fluid from 60 patients within 14 hour after burn injury, who underwent bronchoscopy for suspected smoke inhalation. They concluded that the degree of inhalation injury influences burn patient morbidity and results to changes in multiple alveolar inflammatory proteins.

Abstract: Interferon gamma (IFNγ) is important for immune resistance to herpes simplex virus (HSV) infection. To examine the influence of IFNγ on the development of HSV-specific immune responses and test for IFNγ-independent adaptive immune mechanisms of protection, IFNγ-deficient mice (IFNγ−/−) were immunized with thymidine kinase-deficient HSV-2 (HSV-2 333tk−). HSV-specific cellular and humoral responses were elicited in immunized IFNγ−/− mice resulting in increased resistance relative to non-immune C57BL/6J (B6) mice following challenge with fully virulent HSV-2. CD8+ T cells from IFNγ−/− mice displayed cytotoxic activity and secreted TNFα. HSV-specific CD4+ T cells from immunized IFNγ−/− mice secreted IL-4, TNFα, and IL-17, but unlike T cells from HSV-immune B6 mice, could not clear virus from genital tissue following adoptive transfer. HSV-immune IFNγ−/− mice produced predominantly IgG1 HSV-specific antibodies while immune B6 mice produced predominantly IgG2c antibodies. Transfer of equivalent amounts of HSV-specific antibodies from either strain to naïve mice imparted equivalent early resistance against infection of the genital epithelia. However, protection against neurological symptoms mediated by immune B6 antibodies was superior late in infection. Taken together, these results demonstrate that the limited resistance of HSV-immune IFNγ−/− mice to HSV-2 infection resulted from the action of HSV-specific Ab rather than IFNγ-independent effector functions of T cells. Further, protection against neurological manifestations of HSV-2 infection was superior in mice receiving Ab from immune B6 mice suggesting that Ab-mediated protective mechanisms involving IFNγ-induced IgG subclasses were more effective once virus had spread to neural tissues. [Copyright &y& Elsevier]

Background and Aims: Peatland methane (CH) fluxes may vary between plant types; however, in mixed communities, the specific role of each species is difficult to distinguish. The goal of this study was to determine the individual and interacting effect of moss, graminoid and shrub plant functional types on CH dynamics of experimentally planted plots in a rewetted minerotrophic peatland. Methods: We measured CH flux, pore water CH concentration and CH production and oxidation potential in pure stands of reintroduced Tomenthypnum nitens (Hedw.) Loeske, Carex aquatilis Wahlenb, or Myrica gale L., as well as mixtures of T. nitens + C. aquatilis and T. nitens + M. gale. Methane flux was also measured on bare peat plots. Results: The presence of both the graminoid C. aquatilis and the shrub M. gale resulted in the highest CH production potential in near surface peat (10 cm). The presence of moss ( T. nitens) and C. aquatilis significantly increased CH oxidation potential. Water table position was a significant control on CH flux, but the presence of C. aquatilis maintained higher flux even at dry plots. Plots including C. aquatilis had significantly lower pore water CH concentration at 30 cm depth, likely reflecting CH oxidation and transport. Conclusions: Management of restored sites aiming to reduce CH flux should focus on hydrology, i.e. water table position. The presence of graminoids enhances CH flux, while moss presence may result in lower CH emission. [ABSTRACT FROM AUTHOR]

Abstract: On November 18, 2011, the 16th annual Alcohol and Immunology Research Interest Group (AIRIG) meeting was held at Loyola University Medical Center in Maywood, Illinois. The focus of this year''s meeting was alcohol''s effect on epigenetic changes and possible outcomes induced by these changes. Two sessions, which consisted of talks from invited speakers as well as presentations of selected abstracts, were held in addition to a poster session. Participants presented information on alcohol-induced alterations in histone modifications and gene expression along with immunologic responses to alcohol. Speakers shared new research specifically on histone deacetylase enzyme expression and modifications due to alcohol and the downstream effect of these modifications may have on gene expression and tissue damage. Additional studies suggested that alcohol exacerbates inflammation when combined with other insults such as infection, trauma, inhalation injury, and disease. [Copyright &y& Elsevier]

The 15th annual meeting of the Alcohol and Immunology Research Interest Group was held on November 19, 2010, at Loyola University Medical Center in Maywood, IL. This year, the focus of the meeting was on alcohol's effect on the immune system in both clinical and experimental systems. The event consisted of three sessions, which featured plenary talks from invited speakers along with oral presentations from selected abstracts, in addition to a poster session. Participants presented a variety of information on ethanol-induced effects on infection susceptibility and resolution, oxidative stress, and organ inflammation. Specifically, speakers presented new insights on the mechanism of alcohol-mediated deleterious effects in the lung, liver, skin, and neuroendocrine system, as well as on immune cells in both in vivo and in vitro systems. Additional oral presentations suggested possible mechanisms of how alcohol-induced reactive oxygen species promote immune dysregulation both locally and systemically. [ABSTRACT FROM AUTHOR]

Abstract: The 15th annual meeting of the Alcohol and Immunology Research Interest Group was held on November 19, 2010, at Loyola University Medical Center in Maywood, IL. This year, the focus of the meeting was on alcohol’s effect on the immune system in both clinical and experimental systems. The event consisted of three sessions, which featured plenary talks from invited speakers along with oral presentations from selected abstracts, in addition to a poster session. Participants presented a variety of information on ethanol-induced effects on infection susceptibility and resolution, oxidative stress, and organ inflammation. Specifically, speakers presented new insights on the mechanism of alcohol-mediated deleterious effects in the lung, liver, skin, and neuroendocrine system, as well as on immune cells in both in vivo and in vitro systems. Additional oral presentations suggested possible mechanisms of how alcohol-induced reactive oxygen species promote immune dysregulation both locally and systemically. [Copyright &y& Elsevier]

The article discusses the clinical practice guidelines issued by the American Academy of Family Physicians (AAFP) on atrial fibrillation (AF) diagnosis and management. Topics explored include the presentation of AF symptoms such as irregular heart rate and extreme fatigue, the need for primary care physicians to educate AF patients about medication cost and possible side effects of anticoagulants, and the use of lenient rate control instead of strict rate control in patients with AF.