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  • 1
    Online Resource
    Online Resource
    IL-33 Depletion in COVID-19 Lungs
    Elsevier BV ; 2021
    In:  Chest Vol. 160, No. 5 ( 2021-11), p. 1656-1659
    Details
    In: Chest, Elsevier BV, Vol. 160, No. 5 ( 2021-11), p. 1656-1659
    Type of Medium: Online Resource
    ISSN: 0012-3692
    URL: Article
    DOI: 10.1016/j.chest.2021.06.058
    RVK:
    XA 36340
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 2007244-2
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  • 2
    Online Resource
    Online Resource
    Docosahexaenoic acid enhances amphiregulin-mediated bronchial epithelial cell repair processes following organic dust exposure
    American Physiological Society ; 2018
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 314, No. 3 ( 2018-03-01), p. L421-L431
    Details
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 314, No. 3 ( 2018-03-01), p. L421-L431
    Abstract: Injurious dust exposures in the agricultural workplace involve the release of inflammatory mediators and activation of epidermal growth factor receptor (EGFR) in the respiratory epithelium. Amphiregulin (AREG), an EGFR ligand, mediates tissue repair and wound healing in the lung epithelium. Omega-3 fatty acids such as docosahexaenoic acid (DHA) are also known modulators of repair and resolution of inflammatory injury. This study investigated how AREG, DHA, and EGFR modulate lung repair processes following dust-induced injury. Primary human bronchial epithelial (BEC) and BEAS-2B cells were treated with an aqueous extract of swine confinement facility dust (DE) in the presence of DHA and AREG or EGFR inhibitors. Mice were exposed to DE intranasally with or without EGFR inhibition and DHA. Using a decellularized lung scaffolding tissue repair model, BEC recolonization of human lung scaffolds was analyzed in the context of DE, DHA, and AREG treatments. Through these investigations, we identified an important role for AREG in mediating BEC repair processes. DE-induced AREG release from BEC, and DHA treatment following DE exposure, enhanced this release. Both DHA and AREG also enhanced BEC repair capacities and rescued DE-induced recellularization deficits. In vivo, DHA treatment enhanced AREG production following DE exposure, whereas EGFR inhibitor-treated mice exhibited reduced AREG in their lung homogenates. These data indicate a role for AREG in the process of tissue repair after inflammatory lung injury caused by environmental dust exposure and implicate a role for DHA in regulating AREG-mediated repair signaling in BEC.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    URL: Article
    DOI: 10.1152/ajplung.00273.2017
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2018
    detail.hit.zdb_id: 1477300-4
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Malondialdehyde acetaldehyde adduction of surfactant protein D attenuates SARS‐CoV ‐2 spike protein binding and virus neutralization
    Wiley ; 2023
    In:  Alcoholism: Clinical and Experimental Research Vol. 47, No. 1 ( 2023-01), p. 95-103
    Details
    In: Alcoholism: Clinical and Experimental Research, Wiley, Vol. 47, No. 1 ( 2023-01), p. 95-103
    Abstract: Over 43% of the world's population regularly consumes alcohol. Although not commonly known, alcohol can have a significant impact on the respiratory environment. Living in the time of the COVID‐19 pandemic, alcohol misuse can have a particularly deleterious effect on SARS‐CoV‐2‐infected individuals and, in turn, the overall healthcare system. Patients with alcohol use disorders have higher odds of COVID‐19‐associated hospitalization and mortality. Even though the detrimental role of alcohol on COVID‐19 outcomes has been established, the underlying mechanisms are yet to be fully understood. Alcohol misuse has been shown to induce oxidative damage in the lungs through the production of reactive aldehydes such as malondialdehyde and acetaldehyde (MAA). MAA can then form adducts with proteins, altering their structure and function. One such protein is surfactant protein D (SPD), which plays an important role in innate immunity against pathogens. Methods and Results In this study, we examined whether MAA adduction of SPD (SPD‐MAA) attenuates the ability of SPD to bind SARS‐CoV‐2 spike protein, reversing SPD‐mediated virus neutralization. Using ELISA, we show that SPD‐MAA is unable to competitively bind spike protein and prevent ACE2 receptor binding. Similarly, SPD‐MAA fails to inhibit entry of wild‐type SARS‐CoV‐2 virus into Calu‐3 cells, a lung epithelial cell line, as well as ciliated primary human bronchial epithelial cells isolated from healthy individuals. Conclusions Overall, MAA adduction of SPD, a consequence of alcohol overconsumption, represents one mechanism of compromised lung innate defense against SARS‐CoV‐2, highlighting a possible mechanism underlying COVID‐19 severity and related mortality in patients who misuse alcohol.
    Type of Medium: Online Resource
    ISSN: 0145-6008 , 1530-0277
    URL: Issue
    URL: Article
    DOI: 10.1111/acer.v47.1
    DOI: 10.1111/acer.14974
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2046886-6
    detail.hit.zdb_id: 3167872-5
    SSG: 15,3
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  • 4
    Online Resource
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    Synergistic Detrimental Effects of Cigarette Smoke, Alcohol, and SARS-CoV-2 in COPD Bronchial Epithelial Cells
    MDPI AG ; 2023
    In:  Pathogens Vol. 12, No. 3 ( 2023-03-22), p. 498-
    Details
    In: Pathogens, MDPI AG, Vol. 12, No. 3 ( 2023-03-22), p. 498-
    Abstract: Lung conditions such as COPD, as well as risk factors such as alcohol misuse and cigarette smoking, can exacerbate COVID-19 disease severity. Synergistically, these risk factors can have a significant impact on immunity against pathogens. Here, we studied the effect of a short exposure to alcohol and/or cigarette smoke extract (CSE) in vitro on acute SARS-CoV-2 infection of ciliated human bronchial epithelial cells (HBECs) collected from healthy and COPD donors. We observed an increase in viral titer in CSE- or alcohol-treated COPD HBECs compared to untreated COPD HBECs. Furthermore, we treated healthy HBECs accompanied by enhanced lactate dehydrogenase activity, indicating exacerbated injury. Finally, IL-8 secretion was elevated due to the synergistic damage mediated by alcohol, CSE, and SARS-CoV-2 in COPD HBECs. Together, our data suggest that, with pre-existing COPD, short exposure to alcohol or CSE is sufficient to exacerbate SARS-CoV-2 infection and associated injury, impairing lung defences.
    Type of Medium: Online Resource
    ISSN: 2076-0817
    URL: Article
    DOI: 10.3390/pathogens12030498
    Language: English
    Publisher: MDPI AG
    Publication Date: 2023
    detail.hit.zdb_id: 2695572-6
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  • 5
    Online Resource
    Online Resource
    Aging leads to dysfunctional innate immune responses to TLR2 and TLR4 agonists
    Springer Science and Business Media LLC ; 2019
    In:  Aging Clinical and Experimental Research Vol. 31, No. 9 ( 2019-9), p. 1185-1193
    Details
    In: Aging Clinical and Experimental Research, Springer Science and Business Media LLC, Vol. 31, No. 9 ( 2019-9), p. 1185-1193
    Type of Medium: Online Resource
    ISSN: 1720-8319
    URL: Article
    DOI: 10.1007/s40520-018-1064-0
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
    detail.hit.zdb_id: 2119282-0
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  • 6
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    Novel role of zinc homeostasis in IL-23 regulation and host defense following bacterial infection
    The American Association of Immunologists ; 2019
    In:  The Journal of Immunology Vol. 202, No. 1_Supplement ( 2019-05-01), p. 62.6-62.6
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 202, No. 1_Supplement ( 2019-05-01), p. 62.6-62.6
    Abstract: Zinc homeostasis is crucial for immune cell activation and intracellular zinc is tightly regulated by zinc transporters. Zinc deficiency is associated with increased prevalence of respiratory bacterial infections. Although the association between zinc and immunity is well established, the mechanisms by which zinc protects against bacteria remain to be elucidated. In human monocytes the zinc transporter Zip8 regulates inflammation in a zinc-dependent manner after LPS exposure. Given the critical role of APCs (macrophages and dendritic cells) in guiding the immune response against bacteria, we sought to determine the role of Zip8 in coordinating the immune response after bacterial exposure. In a novel myeloid-specific Zip8KO mouse model we observed that intranasal instillation of S. pneumoniae resulted in a significant increase of infiltrating neutrophils in the airways of Zip8KO mice when compared to WT counterparts. Analysis of BAL fluid revealed elevated levels of CXCL1 and IL-23 in the Zip8KO mice. To determine whether dendritic cells potentially play a role in the observed response, BMDCs were generated from Zip8KO and WT mice. LPS stimulation produced mature BMDCs with high CD11c and MHC-II expression in both groups. No significant changes were observed in the production of most cytokines examined (TNF-α, CXCL1, IL-6, IL-12), except for IL-23 which was consistently increased in the stimulated Zip8KO cells in comparison to WT control DCs. These results potentially reveal a vital axis that couples zinc homeostasis to IL-23 production in myeloid cells and ultimately host defense against invasive bacterial pathogens. To what extent this alters pathogen clearance and host recovery is the focus of future studies.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.202.Supp.62.6
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2019
    detail.hit.zdb_id: 1475085-5
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  • 7
    Online Resource
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    TLR 2 and TLR 4 Expression and Inflammatory Cytokines are Altered in the Airway Epithelium of Those with Alcohol Use Disorders
    Wiley ; 2015
    In:  Alcoholism: Clinical and Experimental Research Vol. 39, No. 9 ( 2015-09), p. 1691-1697
    Details
    In: Alcoholism: Clinical and Experimental Research, Wiley, Vol. 39, No. 9 ( 2015-09), p. 1691-1697
    Abstract: The lung has a highly regulated system of innate immunity to protect itself from inhaled microbes and toxins. The first line of defense is mucociliary clearance, but if invaders overcome this, inflammatory pathways are activated. Toll‐like receptors ( TLR s) are expressed on the airway epithelium. Their signaling initiates the inflammatory cascade and leads to production of inflammatory cytokines such as interleukin (IL) ‐6 and IL ‐8. We hypothesized that airway epithelial insults, including heavy alcohol intake or smoking, would alter the expression of TLR s on the airway epithelium. Methods Bronchoscopy with bronchoalveolar lavage and brushings of the airway epithelium was performed in otherwise healthy subjects who had normal chest radiographs and spirometry. A history of alcohol use disorders ( AUD s) was ascertained using the Alcohol Use Disorders Identification Test ( AUDIT ), and a history of cigarette smoking was also obtained. Age, gender, and nutritional status in all groups were similar. We used real‐time polymerase chain reaction (PCR) to quantitate TLR1 to 9 and enzyme‐linked immune assay to measure tumor necrosis factor‐ α , IL ‐6, and IL ‐8. Results Airway brushings were obtained from 26 nonsmoking/non‐ AUD subjects, 28 smoking/non‐ AUD subjects, 36 smoking/ AUD subjects, and 17 nonsmoking/ AUD subjects. We found that TLR 2 is up‐regulated in AUD subjects, compared to nonsmoking/non‐ AUD subjects, and correlated with their AUDIT scores. We also measured a decrease in TLR 4 expression in AUD subjects that correlated with AUDIT score. IL ‐6 and IL ‐8 were also increased in bronchial washings from AUD subjects. Conclusions We have previously demonstrated in normal human bronchial epithelial cells that in vitro alcohol exposure up‐regulates TLR 2 through a NO / cGMP / PKG ‐dependent pathway, resulting in up‐regulation of inflammatory cytokine production after Gram‐positive bacterial product stimulation. Our current translational study confirms that TLR 2 is also up‐regulated in humans with AUD s.
    Type of Medium: Online Resource
    ISSN: 0145-6008 , 1530-0277
    URL: Issue
    URL: Article
    DOI: 10.1111/acer.2015.39.issue-9
    DOI: 10.1111/acer.12803
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 2046886-6
    detail.hit.zdb_id: 3167872-5
    SSG: 15,3
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  • 8
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    Online Resource
    Malondialdehyde Acetaldehyde-Adduction Changes Surfactant Protein D Structure and Function
    Frontiers Media SA ; 2022
    In:  Frontiers in Immunology Vol. 13 ( 2022-5-20)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 13 ( 2022-5-20)
    Abstract: Alcohol consumption with concurrent cigarette smoking produces malondialdehyde acetaldehyde (MAA)-adducted lung proteins. Lung surfactant protein D (SPD) supports innate immunity via bacterial aggregation and lysis, as well as by enhancing macrophage-binding and phagocytosis. MAA-adducted SPD (SPD-MAA) has negative effects on lung cilia beating, macrophage function, and epithelial cell injury repair. Because changes in SPD multimer structure are known to impact SPD function, we hypothesized that MAA-adduction changes both SPD structure and function. Purified human SPD and SPD-MAA (1 mg/mL) were resolved by gel filtration using Sephadex G-200 and protein concentration of each fraction determined by Bradford assay. Fractions were immobilized onto nitrocellulose by slot blot and assayed by Western blot using antibodies to SPD and to MAA. Binding of SPD and SPD-MAA was determined fluorometrically using GFP-labeled Streptococcus pneumoniae (GFP-SP). Anti-bacterial aggregation of GFP-SP and macrophage bacterial phagocytosis were assayed by microscopy and permeability determined by bacterial phosphatase release. Viral injury was measured as LDH release in RSV-treated airway epithelial cells. Three sizes of SPD were resolved by gel chromatography as monomeric, trimeric, and multimeric forms. SPD multimer was the most prevalent, while the majority of SPD-MAA eluted as trimer and monomer. SPD dose-dependently bound to GFP-SP, but SPD-MAA binding to bacteria was significantly reduced. SPD enhanced, but MAA adduction of SPD prevented, both aggregation and macrophage phagocytosis of GFP-SP. Likewise, SPD increased bacterial permeability while SPD-MAA did not. In the presence of RSV, BEAS-2B cell viability was enhanced by SPD, but not protected by SPD-MAA. Our results demonstrate that MAA adduction changes the quaternary structure of SPD from multimer to trimer and monomer leading to a decrease in the native anti-microbial function of SPD. These findings suggest one mechanism for increased pneumonia observed in alcohol use disorders.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    DOI: 10.3389/fimmu.2022.866795
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2606827-8
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  • 9
    Online Resource
    Online Resource
    Oxidative stress associated with aging activates protein kinase Cε, leading to cilia slowing
    American Physiological Society ; 2018
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 315, No. 5 ( 2018-11-01), p. L882-L890
    Details
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 315, No. 5 ( 2018-11-01), p. L882-L890
    Abstract: Older people are four times more likely to develop pneumonia than younger people. As we age, many components of pulmonary innate immunity are impaired, including slowing of mucociliary clearance. Ciliary beat frequency (CBF) is a major determinant of mucociliary clearance, and it slows as we age. We hypothesized that CBF is slowed in aging because of increased oxidative stress, which activates PKCε signaling. We pharmacologically inhibited PKCε in ex vivo mouse models of aging. We measured a slowing of CBF with aging that was reversed with inhibition using the novel PKC inhibitor, Ro-31-8220, as well as the PKCε inhibitor, PKCe141. Inhibition of PKCε using siRNA in mouse trachea also returned CBF to normal. In addition, antioxidants decrease PKCε activity and speed cilia. We also aged wild-type and PKCε KO mice and measured CBF. The PKCε KO mice were spared from the CBF slowing of aging. Using human airway epithelial cells from younger and older donors at air-liquid interface (ALI), we inhibited PKCε with siRNA. We measured a slowing of CBF with aging that was reversed with siRNA inhibition of PKCε. In addition, we measured bead clearance speeds in human ALI, which demonstrated a decrease in bead velocity with aging and a return to baseline after inhibition of PKCε. In summary, in human and mouse models, aging is associated with increased oxidant stress, which activates PKCε and slows CBF.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    URL: Article
    DOI: 10.1152/ajplung.00033.2018
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2018
    detail.hit.zdb_id: 1477300-4
    SSG: 12
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  • 10
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    Alcohol and cannabis use alter pulmonary innate immunity
    Elsevier BV ; 2019
    In:  Alcohol Vol. 80 ( 2019-11), p. 131-138
    Details
    In: Alcohol, Elsevier BV, Vol. 80 ( 2019-11), p. 131-138
    Type of Medium: Online Resource
    ISSN: 0741-8329
    URL: Article
    DOI: 10.1016/j.alcohol.2018.11.002
    RVK:
    XA 17485
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
    detail.hit.zdb_id: 1483410-8
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