Defining Doctoral-Prepared Health Scientists' Identity.

Teamwork skills across disciplines are increasingly required for delivery of quality health care. To meet this expectation, healthcare professionals, researchers, policymakers, and educators must embrace and employ the tenets associated with teamwork. In addition, health professions faculty are expected to prepare entry-level professionals for interprofessional practice and scholarship.

Understanding Student Preferences in the Selection of a Graduate Allied Health Program: A Conjoint Analysis Study.

Issue: As the healthcare landscape rapidly changes, graduate allied health programs must position themselves to educate the next generation of healthcare professionals in a highly competitive landscape. No studies have directly measured the relative importance of attributes in program selection by prospective healthcare students.

Methods: We surveyed graduate healthcare management program applicants in the 2018 admissions cycle (n=512) to determine which attributes were most important in program choice.

Dendritic cells and alveolar macrophages mediate IL-13-induced airway inflammation and chemokine production.

Background: IL-13 in the airway induces pathologies that are highly characteristic of asthma, including mucus metaplasia, airway hyperreactivity (AHR), and airway inflammation. As such, it is important to identify the IL-13-responding cell types that mediate each of the above pathologies. For example, IL-13's effects on epithelium contribute to mucus metaplasia and AHR.

12/15-lipoxygenase is an interleukin-13 and interferon-γ counterregulated-mediator of allergic airway inflammation.

Interleukin-13 and interferon-γ are important effectors of T-helper cells. Interleukin-13 increases expression of the arachidonic acid-metabolizing enzyme, 15-lipoxygenase-1, in a variety of cell types. 15-lipoxygenase-1 is dramatically elevated in the airways of subjects with asthma.

Expression of IL-4 receptor alpha on smooth muscle cells is not necessary for development of experimental allergic asthma.

Background: Airflow in the lungs of patients with allergic asthma is impaired by excessive mucus production and airway smooth muscle contractions. Elevated levels of the cytokines IL-4 and IL-13 are associated with this pathology. In vitro studies have suggested that IL-4 receptor alpha (IL-4Ralpha) signaling on smooth muscle cells is critical for airway inflammation and airway hyperresponsiveness.

Epithelium, inflammation, and immunity in the upper airways of humans: studies in chronic rhinosinusitis.

The purpose of this review is to discuss recent findings made during studies of the upper airways and sinuses of people with chronic rhinosinusitis (CRS) in the context of the literature. CRS is a chronic inflammatory disorder affecting nearly 30 million Americans and is generally resistant to therapy with antibiotics and glucocorticoids (Meltzer EO and coworkers, J Allergy Clin Immunol 2004;114:155-212). We have formed a collaboration that consists of otolaryngologists, allergists, and basic scientists to address the underlying immunologic and inflammatory processes that are occurring in, and possibly responsible for, this disease.

CD11b+ myeloid cells are the key mediators of Th2 cell homing into the airway in allergic inflammation.

STAT6-mediated chemokine production in the lung is required for Th2 lymphocyte and eosinophil homing into the airways in allergic pulmonary inflammation, and thus is a potential therapeutic target in asthma. However, the critical cellular source of STAT6-mediated chemokine production has not been defined. In this study, we demonstrate that STAT6 in bone marrow-derived myeloid cells was sufficient for the production of CCL17, CCL22, CCL11, and CCL24 and for Th2 lymphocyte and eosinophil recruitment into the allergic airway.

12/15-Lipoxygenase deficiency protects mice from allergic airways inflammation and increases secretory IgA levels.

Background: Induction of 15-lipoxygenase-1 (15-LO-1) has been observed in the airways of subjects with asthma, although its physiologic role in the airways has remained largely undefined.

Objectives: We sought to test the hypothesis that the mouse 15-LO-1 ortholog 12/15-LO contributes to the development of allergic airways inflammation.

Methods: Two models were used to evaluate wild-type and 12/15-LO-deficient mice.

Interleukin-4, interleukin-13, signal transducer and activator of transcription factor 6, and allergic asthma.

Interleukin (IL)-4 and IL-13 share many biological activities. To some extent, this is because they both signal via a shared receptor, IL-4Ralpha. Ligation of IL-4Ralpha results in activation of Signal Transducer and Activator of Transcription factor 6 (STAT6) and Insulin Receptor Substrate (IRS) molecules.

The epithelial anion transporter pendrin is induced by allergy and rhinovirus infection, regulates airway surface liquid, and increases airway reactivity and inflammation in an asthma model.

Asthma exacerbations can be triggered by viral infections or allergens. The Th2 cytokines IL-13 and IL-4 are produced during allergic responses and cause increases in airway epithelial cell mucus and electrolyte and water secretion into the airway surface liquid (ASL). Since ASL dehydration can cause airway inflammation and obstruction, ion transporters could play a role in pathogenesis of asthma exacerbations.

Epithelium: at the interface of innate and adaptive immune responses.

Several diseases of the airways have a strong component of allergic inflammation in their cause, including allergic rhinitis, asthma, polypoid chronic rhinosinusitis, eosinophilic bronchitis, and others. Although the roles played by antigens and pathogens vary, these diseases have in common a pathology that includes marked activation of epithelial cells in the upper airways, the lower airways, or both. Substantial new evidence indicates an important role of epithelial cells as both mediators and regulators of innate immune responses and adaptive immune responses, as well as the transition from innate immunity to adaptive immunity.

IL-4 receptor signaling in Clara cells is required for allergen-induced mucus production.

Excessive mucus production is an important pathological feature of asthma. The Th2 cytokines IL-4 and IL-13 have both been implicated in allergen-induced mucus production, inflammation, and airway hyperreactivity. Both of these cytokines use receptors that contain the IL-4Ralpha subunit, and these receptors are expressed on many cell types in the lung.

Dissecting asthma using focused transgenic modeling and functional genomics.

Background: Asthma functional genomics studies are challenging because it is difficult to relate gene expression changes to specific disease mechanisms or pathophysiologic features. Use of simplified model systems might help to address this problem. One such model is the IL-13/Epi (IL-13-overexpressing transgenic mice with STAT6 expression limited to epithelial cells) focused transgenic mouse, which isolates the effects of a single mediator, IL-13, on a single cell type, the airway epithelial cell.