Lisa M. Schwiebert

ORCID: 0000-0002-0767-1814
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About
Contact & Profiles
Research Areas
  • Asthma and respiratory diseases
  • Neonatal Respiratory Health Research
  • Exercise and Physiological Responses
  • Cystic Fibrosis Research Advances
  • Immune Response and Inflammation
  • Immune Cell Function and Interaction
  • Pediatric health and respiratory diseases
  • Chemokine receptors and signaling
  • IL-33, ST2, and ILC Pathways
  • COVID-19 and Mental Health
  • Immunotherapy and Immune Responses
  • T-cell and B-cell Immunology
  • Adenosine and Purinergic Signaling
  • Healthcare professionals’ stress and burnout
  • Pharmacological Effects and Assays
  • Inhalation and Respiratory Drug Delivery
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Cytokine Signaling Pathways and Interactions
  • Immune cells in cancer
  • Inflammation biomarkers and pathways
  • Neuroscience of respiration and sleep
  • Antifungal resistance and susceptibility
  • Nitric Oxide and Endothelin Effects
  • Tracheal and airway disorders

University of Alabama at Birmingham
2010-2024

The Graduate Center, CUNY
2023

Pulmonary and Allergy Associates
2014

University of Alabama
1999-2012

Institute of Molecular Biology and Biophysics
1998-2010

Cystic Fibrosis Foundation
1999-2001

Institute of Cell Biology
1999

Johns Hopkins Medicine
1995-1997

New Frontier
1997

Johns Hopkins University
1995-1997

Immune suppression increases the incidence of invasive fungal infections, particularly those caused by opportunistic mold Aspergillus fumigatus. Previous investigations revealed that members TLR family are not absolutely required for host defense against A. fumigatus in nonimmunosuppressed hosts, suggesting other pattern recognition receptors involved. We show this study naive mice (i.e., pharmacologically immunosuppressed) lacking beta-glucan receptor Dectin-1 (Dectin-1(-/-)) more sensitive...

10.4049/jimmunol.0804250 article EN The Journal of Immunology 2009-04-02

These studies provide evidence that cystic fibrosis transmembrane conductance regulator (CFTR) potentiates and accelerates regulatory volume decrease (RVD) following hypotonic challenge by an autocrine mechanism involving ATP release signaling. In wild-type CFTR-expressing cells, CFTR augments constitutive enhances stimulated challenge. itself does not appear to conduct ATP. Instead, is released a separate channel, whose activity potentiated CFTR. Blockade of ion channel blocking drugs,...

10.1074/jbc.m005893200 article EN cc-by Journal of Biological Chemistry 2001-03-01

Sensitization to fungi, such as the mold Aspergillus fumigatus, is increasingly becoming linked with asthma severity. We have previously shown that lung responses generated via β-glucan receptor Dectin-1 are required for defense during acute, invasive A. fumigatus infection. Unexpectedly, in an allergic model of chronic exposure live conidia, recognition led induction multiple proallergic (Muc5ac, Clca3, CCL17, CCL22, and IL-33) proinflammatory (IL-1β CXCL1) mediators compromised function....

10.4049/jimmunol.1201797 article EN The Journal of Immunology 2012-08-30

Monocyte chemotactic protein-4 (MCP-4) is a newly identified C-C chemokine with potent eosinophil chemoattractant properties. We describe studies of its biological activity in vitro to induce chemotaxis peripheral blood eosinophils and histamine release from IL-3-primed basophils. MCP-4 eotaxin caused similar rise intracytoplasmic Ca2+ complete cross-desensitization. also abolished the response MCP-3 partially desensitized macrophage inflammatory protein-1alpha. activated cell migration via...

10.1172/jci119257 article EN Journal of Clinical Investigation 1997-03-01

Abstract Recent reports indicate that aerobic exercise improves the overall physical fitness and health of asthmatic patients. The specific exercise-induced improvements in pathology asthma mechanisms by which these occur, however, are ill-defined; thus, therapeutic potential treatment remains unappreciated. Using an OVA-driven mouse model, we examined role modulating inflammatory responses associated with atopic asthma. Data demonstrate moderate intensity training decreased leukocyte...

10.4049/jimmunol.172.7.4520 article EN The Journal of Immunology 2004-04-01

ATP and its metabolites regulate vascular tone; however, the sources of released in beds are ill defined. As such, we tested hypothesis that all limbs an extracellular purinergic signaling system present endothelial cells: release, receptors, receptor-triggered signal transduction. Primary cultures human cells derived from multiple blood vessels were grown as monolayers studied using a bioluminescence detection assay for into medium. is constitutively exclusively across apical membrane under...

10.1152/ajpcell.01387.2000 article EN AJP Cell Physiology 2002-02-01

Airway epithelium may actively participate in inflammatory responses, such as occur asthma. The presence and regulation of surface molecules on the airway epithelium, however, is incompletely understood. We have determined phenotype human bronchial epithelial cell line BEAS-2B by flow cytometry. confirmed previous observations that cells constitutively express CD29, CD44, CD49a, CD49b, CD49c, CD49d, CD49e, CD49f, CD51, CD54 (ICAM-1), CD61, HLA class 1. were also found to CD9, CD13, CD15,...

10.1165/ajrcmb.17.5.2685 article EN American Journal of Respiratory Cell and Molecular Biology 1997-11-01

The cystic fibrosis transmembrane conductance regulator (CFTR) functions as a low-conductance, cAMP-regulated chloride (Cl-) channel in variety of cell types, such exocrine epithelial cells. Our results demonstrate that human primary endothelial cells isolated from umbilical vein (HUVEC) and lung microvasculature (HLMVEC) also express CFTR determined via RT-PCR immunohistochemical immunoprecipitation analyses. Moreover, Cl- efflux whole patch-clamp analyses reveal HUVEC (n = 6 samples, P <...

10.1152/ajpcell.1998.275.6.c1555 article EN AJP Cell Physiology 1998-12-01

P2X purinergic receptor (P2XR) channels bind ATP and mediate Ca2+ influx — 2 signals that stimulate secretory Cl– transport across epithelia. We tested the hypotheses P2XR are expressed by epithelia P2XRs transduce extracellular into stimulation of Electrophysiological data mRNA analysis human mouse pulmonary other epithelial cells indicate multiple broadly in these tissues they active on both apical basolateral surfaces. Because P2X-selective agonists subtypes, because nasal mucosa cystic...

10.1172/jci7270 article EN Journal of Clinical Investigation 1999-10-01

Aerobic exercise appears to have clinical benefits for many asthmatics, yet a complete understanding of the mechanisms underlying these has not been elucidated at this time.The objective study was determine feasibility larger, future that will define effect aerobic on cellular, molecular, and functional measures in adults with mild-moderate asthma.Recruited subjects were randomized into usual care (sedentary) or moderate intensity treatment groups.Nineteen asthma but without recent history...

10.1186/1710-1492-8-13 article EN cc-by Allergy Asthma and Clinical Immunology 2012-08-03

To delineate the mechanisms that facilitate leukocyte migration into cystic fibrosis (CF) lung, expression of chemokines, including interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), and RANTES, was compared between CF non-CF airway epithelia. The findings presented herein demonstrate that, under either basal conditions or tumor necrosis factor-α (TNF-α)- and/or interferon-γ (IFN-γ)-stimulated conditions, a consistent pattern differences in secretion IL-8 MCP-1 epithelial...

10.1152/ajpcell.1999.276.3.c700 article EN AJP Cell Physiology 1999-03-01

Extracellular nucleotides regulate NaCl transport in some epithelia. However, the effects of nucleotide agonists on renal inner medullary collecting duct (IMCD) are not known. The objective this study was to determine whether ATP and related across mouse IMCD cell line (mIMCD-K2) epithelial monolayers and, if so, via what purinergic receptor subtypes. UTP inhibited Na(+) absorption [measured short-circuit current (I(Na)(sc))] stimulated Cl(-) secretion (I(Cl)(sc))]. Using selective P2...

10.1152/ajprenal.1999.277.4.f552 article EN AJP Renal Physiology 1999-10-01

Transforming growth factor (TGF)-β mediates hypoxia-induced inhibition of alveolar development in the newborn lung. TGF-β is regulated primarily at level activation latent TGF-β. Fibroblasts expressing Thy-1 (CD90) inhibit activation. We hypothesized that loss due to hypoxia may be a mechanism by which increases and animals deficient will simulate effects on lung development. To determine if occurred during hypoxia, non-transgenic (C57BL/6) wild-type (WT) mice exposed were evaluated for mRNA...

10.1152/ajplung.90603.2008 article EN AJP Lung Cellular and Molecular Physiology 2009-03-07

Section:ChooseTop of pageAbstract <<MATERIALS AND METHODSRESULTSDISCUSSIONReferencesCITING ARTICLES

10.1165/rcmb.2009-0038oc article EN American Journal of Respiratory Cell and Molecular Biology 2009-05-08

Section:ChooseTop of pageAbstract <<MATERIALS AND METHODSRESULTSDISCUSSIONReferencesCITING ARTICLES

10.1165/rcmb.2010-0226oc article EN American Journal of Respiratory Cell and Molecular Biology 2010-09-21

Cytokines produced by activated macrophages and Th2 cells within the lung play a key role in asthma-associated airway inflammation. Additionally, recent studies suggest that molecule CD40 modulates immune responses. Because epithelial can act as effector through expression of inflammatory mediators, epithelium is now considered important generation Therefore, goal present study was to examine effects proinflammatory Th2-derived cytokines on function epithelia. The results show express...

10.4049/jimmunol.165.4.2214 article EN The Journal of Immunology 2000-08-15

Previous studies have suggested that the asthmatic responses of airway inflammation, remodeling, and hyperresponsiveness (AHR) are interrelated; in this study, we used exercise to examine nature interrelationship. Mice were sensitized challenged with ovalbumin (OVA); mice then exercised via running on a motorized treadmill at moderate intensity. Data indicate that, within lungs OVA-treated mice, attenuated production inflammatory mediators, including chemokines KC, RANTES, MCP-1...

10.1165/rcmb.2008-0172oc article EN American Journal of Respiratory Cell and Molecular Biology 2008-07-18

Despite the identification of 1,000 mutations in cystic fibrosis gene product CFTR, there remains discordance between CFTR genotype and lung disease phenotype. The study therefore, has expanded beyond its chloride channel activity into other possible functions, such as role a regulator expression. Findings indicate that plays expression RANTES airway epithelia. is chemokine been implicated regulation mucosal immunity pathogenesis inflammatory diseases. Results demonstrate triggers via...

10.1128/mcb.23.2.594-606.2003 article EN Molecular and Cellular Biology 2003-01-01

The effect of dexamethasone on human MHC class II expression was examined various cell types including lymphocytes, monocytes, and epithelial cells. Dexamethasone decreased the surface HLA-DR -DP, but not HLA-DQ, lymphocytic lines that constitutively express these molecules. In addition, dexamethasome down-regulated mRNA levels HLA-DRA, HLA-DQB, in Jijoye cells, a lymphoblastic line. Similarly, monocytic upon IFN-γ treatment. total, results suggest inhibits both constitutive IFN-γ-inducible...

10.1006/cimm.1995.1181 article EN cc-by-nc-nd Cellular Immunology 1995-10-01

The mechanisms for the development of bronchiectasis and airway hyperreactivity have not been fully elucidated. Although genetic, acquired diseases environmental influences may play a role, it is also possible that motile cilia can influence this disease process. We hypothesized deletion key intraflagellar transport molecule, IFT88, in mature mice causes loss cilia, resulting remodeling. Airway were deleted by knockout remodeling pulmonary function evaluated. In IFT88(-) there was...

10.1152/ajplung.00095.2013 article EN AJP Lung Cellular and Molecular Physiology 2013-11-09
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