The cytokines interleukin-1β and tumor necrosis factor-α stimulate CFTR-mediated fluid secretion by swine airway submucosal glands

Baniak, Nicholas; Luan, Xiaojie; Grunow, Amber; Machen, Terry E.; Ianowski, Juan P.

doi:10.1152/ajplung.00058.2012

Cited by 25 publications

(37 citation statements)

References 38 publications

(51 reference statements)

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“…CFTR is required for normal fluid secretion, which washes mucins and antimicrobial compounds from the submucosal glands into the airway lumen (7)(8)(9)(10)(12)(13)(14)(15). The loss of CFTR-mediated fluid secretion reduces ASL secretion, supporting the hypothesis that CFTR mutations lead to reduced secretion of antimicrobial compounds and mucins into the airway lumen, facilitating chronic infection and inflammation (3,6,35,36).…”

Section: Resultsmentioning

confidence: 83%

“…29), triggering the release of proinflammatory cytokines into the submucosa within several minutes (30). The cytokines diffuse from the surface epithelium to the glands located ∼150 μm away (31,32), stimulating CFTR-dependent ASL secretion (13). Flagellin also will induce mucin expression within 18-24 h and further contribute to bacteria clearance (33,34).…”

Section: Resultsmentioning

confidence: 99%

“…In addition, human CF airways, 1-d-old CF piglets, newborn CFTR −/− ferrets, and CFTR −/− mice fail to respond to stimulatory signals that normally elicit strong ASL secretion (6)(7)(8)(9). Consequently, it has been proposed that abnormal secretion of fluid and mucin in response to bacterial infection may contribute to the pathogenesis of CF lung disease (7)(8)(9)(10)(12)(13)(14)(15); however, the central questions of whether bacteria trigger ASL secretion in the airways, and the role of CFTR in such a process, have not been explored previously, owing to the lack of a suitable experimental technique.…”

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confidence: 99%

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Pseudomonas aeruginosa triggers CFTR-mediated airway surface liquid secretion in swine trachea

Luan

Campanucci

Nair

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Significance Cystic fibrosis (CF) is a genetic disorder caused by mutations in the gene encoding for the anion channel cystic fibrosis transmembrane conductance regulator (CFTR). Several organs are affected in CF, but most of the morbidity and mortality comes from lung disease caused by the failure to clear bacteria. Bacterial clearance depends on a layer of airway surface liquid (ASL) covering the airways, rich in antimicrobial compounds and mucins, that removes bacteria from the airway through mucociliary clearance. This study provides the first demonstration that inhalation of bacteria triggers CFTR-dependent ASL secretion. We suggest that this response to inhaled pathogens is an important but previously unknown part of the innate immune response that would be missing in CF patients, resulting in reduced bacterial killing and facilitating infection.

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Section: Resultsmentioning

confidence: 83%

Section: Resultsmentioning

confidence: 99%

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confidence: 99%

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Pseudomonas aeruginosa triggers CFTR-mediated airway surface liquid secretion in swine trachea

Luan

Campanucci

Nair

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…In patients with cystic fibrosis, lack of function CFTR leads to dehydrated mucus, compromised mucociliary clearance, and, therefore, frequent bacterial infections (10,186). Though controversial, several studies suggest that the loss of CFTR leads to excessive, ENaC-mediated Na ϩ and water reabsorption (41).…”

Section: L669 Acute Lung Injury and Barrier Dysfunctionmentioning

confidence: 99%

Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction

Herold

Gabrielli

Vadász

2013

American Journal of Physiology-Lung Cellular and Molecular Phys

177

178

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Herold S, Gabrielli NM, Vadász I. Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction. Am J Physiol Lung Cell Mol Physiol 305: L665-L681, 2013. First published September 13, 2013 doi:10.1152/ajplung.00232.2013In this review we summarize recent major advances in our understanding on the molecular mechanisms, mediators, and biomarkers of acute lung injury (ALI) and alveolar-capillary barrier dysfunction, highlighting the role of immune cells, inflammatory and noninflammatory signaling events, mechanical noxae, and the affected cellular and molecular entities and functions. Furthermore, we address novel aspects of resolution and repair of ALI, as well as putative candidates for treatment of ALI, including pharmacological and cellular therapeutic means. alveolar-capillary barrier dysfunction; molecular mechanism; pharmacological and cell-based therapy; pulmonary edema; zaacute lung injury/acute respiratory distress syndrome Immune Cells and Inflammatory Signaling Pathways in ALIOne of the central concepts in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) is that an unbalanced quantity or quality of the inflammatory response aggravates epithelial or endothelial injury. This includes a dysregulated recruitment of leukocytes and/or an exaggerated activation of these cells; inappropriate expression of cytokines, lipid mediators, or reactive oxygen species; enhanced activation of death receptor signaling (97,98,140,207,240); or an uncontrolled activity of platelets or the coagulation cascade (154). In general, these responses are initiated and maintained by recognition of danger-or pathogen-associated molecular patterns

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“…Nonopsonic phagocytosis is a crucial mechanism for host control during the initial stages of infection, and mouse models indicate that this process may dictate colonization efficiency at the onset of P. aeruginosa challenge (4). Whereas recent reports and reviews have detailed various other components of P. aeruginosa respiratory disease, such as pulmonary edema, humoral immunity, and therapeutic avenues (10,16,20,31,32,46,51,61,73,88,96,102,110,122), this review will spotlight the current state of knowledge in nonopsonic phagocytic recognition and response mechanisms to P.…”

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confidence: 99%

Mechanisms of phagocytosis and host clearance ofPseudomonas aeruginosa

Lovewell

Patankar

Berwin

2014

American Journal of Physiology-Lung Cellular and Molecular Phys

145

127

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domonas aeruginosa is an opportunistic bacterial pathogen responsible for a high incidence of acute and chronic pulmonary infection. These infections are particularly prevalent in patients with chronic obstructive pulmonary disease and cystic fibrosis: much of the morbidity and pathophysiology associated with these diseases is due to a hypersusceptibility to bacterial infection. Innate immunity, primarily through inflammatory cytokine production, cellular recruitment, and phagocytic clearance by neutrophils and macrophages, is the key to endogenous control of P. aeruginosa infection. In this review, we highlight recent advances toward understanding the innate immune response to P. aeruginosa, with a focus on the role of phagocytes in control of P. aeruginosa infection. Specifically, we summarize the cellular and molecular mechanisms of phagocytic recognition and uptake of P. aeruginosa, and how current animal models of P. aeruginosa infection reflect clinical observations in the context of phagocytic clearance of the bacteria. Several notable phenotypic changes to the bacteria are consistently observed during chronic pulmonary infections, including changes to mucoidy and flagellar motility, that likely enable or reflect their ability to persist. These traits are likewise examined in the context of how the bacteria avoid phagocytic clearance, inflammation, and sterilizing immunity.

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The cytokines interleukin-1β and tumor necrosis factor-α stimulate CFTR-mediated fluid secretion by swine airway submucosal glands

Abstract: Baniak N, Luan X, Grunow A, Machen TE, Ianowski JP. The cytokines interleukin-1␤ and tumor necrosis factor-␣ stimulate CFTR-mediated fluid secretion by swine airway submucosal glands.

Cited by 25 publications

References 38 publications

Pseudomonas aeruginosa triggers CFTR-mediated airway surface liquid secretion in swine trachea

Pseudomonas aeruginosa triggers CFTR-mediated airway surface liquid secretion in swine trachea

Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction

Mechanisms of phagocytosis and host clearance ofPseudomonas aeruginosa

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