Search

Your search keyword '"Sherrill, Taylor P."' showing total 145 results
Start Over Author "Sherrill, Taylor P."
145 results on '"Sherrill, Taylor P."'

1. Epithelial Yap/Taz are required for functional alveolar regeneration following acute lung injury

Author

DiGiovanni, Gianluca T., primary, Han, Wei, additional, Sherrill, Taylor P., additional, Taylor, Chase J., additional, Nichols, David S., additional, Geis, Natalie M., additional, Singha, Ujjal K., additional, Calvi, Carla L., additional, McCall, A. Scott, additional, Dixon, Molly M., additional, Liu, Yang, additional, Jang, Ji-Hoon, additional, Gutor, Sergey S., additional, Polosukhin, Vasiliy V., additional, Blackwell, Timothy S., additional, Kropski, Jonathan A., additional, and Gokey, Jason J., additional

Published
2023
Full Text
View/download PDF

2. Data from Targeting the Wnt Pathway in Synovial Sarcoma Models

Author

Barham, Whitney, primary, Frump, Andrea L., primary, Sherrill, Taylor P., primary, Garcia, Christina B., primary, Saito-Diaz, Kenyi, primary, VanSaun, Michael N., primary, Fingleton, Barbara, primary, Gleaves, Linda, primary, Orton, Darren, primary, Capecchi, Mario R., primary, Blackwell, Timothy S., primary, Lee, Ethan, primary, Yull, Fiona, primary, and Eid, Josiane E., primary

Published
2023
Full Text
View/download PDF

3. Supplementary Figures S4 - S7 from Targeting the Wnt Pathway in Synovial Sarcoma Models

Author

Barham, Whitney, primary, Frump, Andrea L., primary, Sherrill, Taylor P., primary, Garcia, Christina B., primary, Saito-Diaz, Kenyi, primary, VanSaun, Michael N., primary, Fingleton, Barbara, primary, Gleaves, Linda, primary, Orton, Darren, primary, Capecchi, Mario R., primary, Blackwell, Timothy S., primary, Lee, Ethan, primary, Yull, Fiona, primary, and Eid, Josiane E., primary

Published
2023
Full Text
View/download PDF

4. Supplementary Figure S1 from Targeting the Wnt Pathway in Synovial Sarcoma Models

Author

Barham, Whitney, primary, Frump, Andrea L., primary, Sherrill, Taylor P., primary, Garcia, Christina B., primary, Saito-Diaz, Kenyi, primary, VanSaun, Michael N., primary, Fingleton, Barbara, primary, Gleaves, Linda, primary, Orton, Darren, primary, Capecchi, Mario R., primary, Blackwell, Timothy S., primary, Lee, Ethan, primary, Yull, Fiona, primary, and Eid, Josiane E., primary

Published
2023
Full Text
View/download PDF

5. Supplementary Figure S11 and Tables S1-S3 from Targeting the Wnt Pathway in Synovial Sarcoma Models

Author

Barham, Whitney, primary, Frump, Andrea L., primary, Sherrill, Taylor P., primary, Garcia, Christina B., primary, Saito-Diaz, Kenyi, primary, VanSaun, Michael N., primary, Fingleton, Barbara, primary, Gleaves, Linda, primary, Orton, Darren, primary, Capecchi, Mario R., primary, Blackwell, Timothy S., primary, Lee, Ethan, primary, Yull, Fiona, primary, and Eid, Josiane E., primary

Published
2023
Full Text
View/download PDF

6. Supplementary Figures S2 and S3 from Targeting the Wnt Pathway in Synovial Sarcoma Models

Author

Barham, Whitney, primary, Frump, Andrea L., primary, Sherrill, Taylor P., primary, Garcia, Christina B., primary, Saito-Diaz, Kenyi, primary, VanSaun, Michael N., primary, Fingleton, Barbara, primary, Gleaves, Linda, primary, Orton, Darren, primary, Capecchi, Mario R., primary, Blackwell, Timothy S., primary, Lee, Ethan, primary, Yull, Fiona, primary, and Eid, Josiane E., primary

Published
2023
Full Text
View/download PDF

7. Supplementary Methods and Legends from Targeting the Wnt Pathway in Synovial Sarcoma Models

Author

Barham, Whitney, primary, Frump, Andrea L., primary, Sherrill, Taylor P., primary, Garcia, Christina B., primary, Saito-Diaz, Kenyi, primary, VanSaun, Michael N., primary, Fingleton, Barbara, primary, Gleaves, Linda, primary, Orton, Darren, primary, Capecchi, Mario R., primary, Blackwell, Timothy S., primary, Lee, Ethan, primary, Yull, Fiona, primary, and Eid, Josiane E., primary

Published
2023
Full Text
View/download PDF

8. Supplementary Figure Legend from Tumor Necrosis Factor-α Promotes Malignant Pleural Effusion

Author

Stathopoulos, Georgios T., primary, Kollintza, Androniki, primary, Moschos, Charalampos, primary, Psallidas, Ioannis, primary, Sherrill, Taylor P., primary, Pitsinos, Emmanuel N., primary, Vassiliou, Spyridoula, primary, Karatza, Marilena, primary, Papiris, Spyros A., primary, Graf, Daniel, primary, Orphanidou, Dora, primary, Light, Richard W., primary, Roussos, Charis, primary, Blackwell, Timothy S., primary, and Kalomenidis, Ioannis, primary

Published
2023
Full Text
View/download PDF

9. Supplementary Figure 1 from Tumor Necrosis Factor-α Promotes Malignant Pleural Effusion

Author

Stathopoulos, Georgios T., primary, Kollintza, Androniki, primary, Moschos, Charalampos, primary, Psallidas, Ioannis, primary, Sherrill, Taylor P., primary, Pitsinos, Emmanuel N., primary, Vassiliou, Spyridoula, primary, Karatza, Marilena, primary, Papiris, Spyros A., primary, Graf, Daniel, primary, Orphanidou, Dora, primary, Light, Richard W., primary, Roussos, Charis, primary, Blackwell, Timothy S., primary, and Kalomenidis, Ioannis, primary

Published
2023
Full Text
View/download PDF

10. Figure S2 from Interleukin-5 Facilitates Lung Metastasis by Modulating the Immune Microenvironment

Author

Zaynagetdinov, Rinat, primary, Sherrill, Taylor P., primary, Gleaves, Linda A., primary, McLoed, Allyson G., primary, Saxon, Jamie A., primary, Habermann, Arun C., primary, Connelly, Linda, primary, Dulek, Daniel, primary, Peebles, R. Stokes, primary, Fingleton, Barbara, primary, Yull, Fiona E., primary, Stathopoulos, Georgios T., primary, and Blackwell, Timothy S., primary

Published
2023
Full Text
View/download PDF

11. Data from Interleukin-5 Facilitates Lung Metastasis by Modulating the Immune Microenvironment

Author

Zaynagetdinov, Rinat, primary, Sherrill, Taylor P., primary, Gleaves, Linda A., primary, McLoed, Allyson G., primary, Saxon, Jamie A., primary, Habermann, Arun C., primary, Connelly, Linda, primary, Dulek, Daniel, primary, Peebles, R. Stokes, primary, Fingleton, Barbara, primary, Yull, Fiona E., primary, Stathopoulos, Georgios T., primary, and Blackwell, Timothy S., primary

Published
2023
Full Text
View/download PDF

12. Thromboxane–Prostanoid Receptor Signaling Drives Persistent Fibroblast Activation in Pulmonary Fibrosis

Author

Suzuki, Toshio, primary, Kropski, Jonathan A., additional, Chen, Jingyuan, additional, Carrier, Erica J., additional, Chen, Xinping, additional, Sherrill, Taylor P., additional, Winters, Nichelle I., additional, Camarata, Jane E., additional, Polosukhin, Vasiliy V., additional, Han, Wei, additional, Rathinasabapathy, Anandharajan, additional, Gutor, Sergey, additional, Gulleman, Peter, additional, Sabusap, Carleen, additional, Banovich, Nicholas E., additional, Tanjore, Harikrishna, additional, Freeman, Michael L., additional, Tada, Yuji, additional, Young, Lisa R., additional, Gokey, Jason J., additional, Blackwell, Timothy S., additional, and West, James D., additional

Published
2022
Full Text
View/download PDF

14. Thromboxane-Prostanoid Receptor Signaling Drives Persistent Fibroblast Activation in Pulmonary Fibrosis.

Author

Toshio Suzuki, Kropski, Jonathan A., Jingyuan Chen, Carrier, Erica J., Xinping Chen, Sherrill, Taylor P., Winters, Nichelle I., Camarata, Jane E., Polosukhin, Vasiliy V., Wei Han, Rathinasabapathy, Anandharajan, Gutor, Sergey, Gulleman, Peter, Sabusap, Carleen, Banovich, Nicholas E., Tanjore, Harikrishna, Freeman, Michael L., Yuji Tada, Young, Lisa R., and Gokey, Jason J.

Subjects
PROSTAGLANDINS, IDIOPATHIC pulmonary fibrosis, FIBROBLASTS, LUNGS, GROWTH factors, CELL receptors, RESEARCH funding, ARACHIDONIC acid, BLEOMYCIN, THROMBOXANES, MICE, ANIMALS, PHARMACODYNAMICS
Abstract

Rationale: Although persistent fibroblast activation is a hallmark of idiopathic pulmonary fibrosis (IPF), mechanisms regulating persistent fibroblast activation in the lungs have not been fully elucidated. Objectives: On the basis of our observation that lung fibroblasts express TBXA2R (thromboxane-prostanoid receptor) during fibrosis, we investigated the role of TBXA2R signaling in fibrotic remodeling. Methods: We identified TBXA2R expression in lungs of patients with IPF and mice and studied primary mouse and human lung fibroblasts to determine the impact of TBXA2R signaling on fibroblast activation. We used TBXA2R-deficient mice and small-molecule inhibitors to investigate TBXA2R signaling in preclinical lung fibrosis models. Measurements and Main Results: TBXA2R expression was upregulated in fibroblasts in the lungs of patients with IPF and in mouse lungs during experimental lung fibrosis. Genetic deletion of TBXA2R, but not inhibition of thromboxane synthase, protected mice from bleomycin-induced lung fibrosis, thereby suggesting that an alternative ligand activates profibrotic TBXA2R signaling. In contrast to thromboxane, F2-isoprostanes, which are nonenzymatic products of arachidonic acid induced by reactive oxygen species, were persistently elevated during fibrosis. F2-isoprostanes induced TBXA2R signaling in fibroblasts and mediated a myofibroblast activation profile due, at least in part, to potentiation of TGF-β (transforming growth factor-β) signaling. In vivo treatment with the TBXA2R antagonist ifetroban reduced profibrotic signaling in the lungs, protected mice from lung fibrosis in three preclinical models (bleomycin, Hermansky-Pudlak mice, and radiation-induced fibrosis), and markedly enhanced fibrotic resolution after bleomycin treatment. Conclusions: TBXA2R links oxidative stress to fibroblast activation during lung fibrosis. TBXA2R antagonists could have utility in treating pulmonary fibrosis. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

16. Epithelial NF-[kappa]B activation promotes urethane-induced lung carcinogenesis

Author

Stathopoulos, Georgios T., Sherrill, Taylor P., Cheng, Dong-Sheng, Scoggins, Robert M., Han, Wei, Polosukhin, Vasiliy V., Connelly, Linda, Yull, Fiona E., Fingleton, Barbara, and Blackwell, Timothy S.

Subjects
DNA binding proteins -- Health aspects, DNA binding proteins -- Physiological aspects, Lung tumors -- Risk factors, Lung tumors -- Development and progression, Epithelium -- Chemical properties, Urethanes -- Physiological aspects, Urethanes -- Health aspects, Science and technology
Abstract

Chronic inflammation is linked to carcinogenesis in several organ systems. In the lungs, NF-[kappa]B, a central effector of inflammatory responses, is frequently activated in non-small-cell lung cancer, but its role in tumor promotion has not been studied. Several lines of evidence indicate that ethyl carbamate (urethane)-induced lung tumor formation, a prototypical mouse model of multistage lung carcinogenesis, is potentiated by inflammation. We found that mouse strains susceptible to lung tumor formation (FVB, BALB/c) exhibited early NF-[kappa]B activation and inflammation in the lungs after urethane treatment. However, a resistant strain (C57B6) failed to activate NF-[kappa]B or induce lung inflammation. In FVB mice, we identified urethane-induced NF-[kappa]B activation in airway epithelium, as well as type II alveolar epithelial cells and macrophages. Using an inducible transgenic mouse model (FVB strain) to express a dominant inhibitor of NF-[kappa]B specifically in airway epithelial cells, we found that urethane-induced lung inflammation was blocked and tumor formation was reduced by >50%. Selective NF-[kappa]B inhibition resulted in increased apoptosis of airway epithelial cells at 2 weeks after urethane treatment in association with a marked reduction of Bcl-2 expression. These studies indicate that NF-[kappa] apoptosis | cancer | inflammation | airway | adenocarcinoma

Published
2007

20. Opposing effects of bortezomib-induced nuclear factor-κB inhibition on chemical lung carcinogenesis

Author

Karabela, Sophia P., Psallidas, Ioannis, Sherrill, Taylor P., Kairi, Chrysoula A., Zaynagetdinov, Rinat, Cheng, Dong-Sheng, Vassiliou, Spyridoula, McMahon, Frank, Gleaves, Linda A., Han, Wei, Stathopoulos, Ioannis, Zakynthinos, Spyros G., Yull, Fiona E., Roussos, Charis, Kalomenidis, Ioannis, Blackwell, Timothy S., and Stathopoulos, Georgios T.

Published
2012
Full Text
View/download PDF

25. Specific effects of bortezomib against experimental malignant pleural effusion: a preclinical study

Author

Blackwell Timothy S, Roussos Charis, Theodoropoulou Panagiota, Magkouta Sophia, Kollintza Androniki, Sherrill Taylor P, Moschos Charalampos, Karabela Sophia P, Psallidas Ioannis, Kalomenidis Ioannis, and Stathopoulos Georgios T

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background We have previously shown that nuclear factor (NF)-κB activation of mouse Lewis lung carcinoma (LLC) specifically promotes the induction of malignant pleural effusions (MPE) by these cells. In the present studies we hypothesized that treatment of immunocompetent mice with bortezomib tailored to inhibit cancer cell NF-κB activation and not proliferation specifically inhibits MPE formation by LLC cells. Results Treatment of LLC cells with low concentrations of bortezomib (100 ng/ml) inhibited NF-κB activation and NF-κB-dependent transcription, but not cellular proliferation. Bortezomib treatment of immunocompetent C57BL/6 mice bearing LLC-induced subcutaneous tumors and MPEs significantly blocked tumor-specific NF-κB activation. However, bortezomib treatment did not impair subcutaneous LLC tumor growth, but was effective in limiting LLC-induced MPE. This specific effect was evidenced by significant reductions in effusion accumulation and the associated mortality and was observed with both preventive (beginning before MPE formation) and therapeutic (beginning after MPE establishment) bortezomib treatment. The favorable impact of bortezomib on MPE was associated with suppression of cardinal MPE-associated phenomena, such as inflammation, vascular hyperpermeability, and angiogenesis. In this regard, therapeutic bortezomib treatment had identical favorable results on MPE compared with preventive treatment, indicating that the drug specifically counteracts effusion formation. Conclusions These studies indicate that proteasome inhibition tailored to block NF-κB activation of lung adenocarcinoma specifically targets the effusion-inducing phenotype of this tumor. Although the drug has limited activity against advanced solid lung cancer, it may prove beneficial for patients with MPE.

Published
2010
Full Text
View/download PDF

26. p52 over-expression increases epithelial apoptosis, enhances lung injury, and reduces survival after LPS treatment1

Author

Saxon, Jamie A., Cheng, Dong-Sheng, Han, Wei, Polosukhin, Vasiliy V., McLoed, Allyson G., Richmond, Bradley W., Gleaves, Linda A., Tanjore, Harikrishna, Sherrill, Taylor P., Barham, Whitney, Yull, Fiona E., and Blackwell, Timothy S.

Subjects
Lipopolysaccharides, Respiratory Distress Syndrome, Blotting, Western, Apoptosis, Enzyme-Linked Immunosorbent Assay, Mice, Transgenic, Pneumonia, Respiratory Mucosa, respiratory system, Real-Time Polymerase Chain Reaction, Immunohistochemistry, Article, Up-Regulation, Disease Models, Animal, Mice, NF-kappa B p52 Subunit, parasitic diseases, Animals, Humans, Signal Transduction
Abstract

Although numerous studies have demonstrated a critical role for canonical NF-κB signaling in inflammation and disease, the function of the noncanonical NF-κB pathway remains ill-defined. In lung tissue from patients with acute respiratory distress syndrome, we identified increased expression of the noncanonical pathway component p100/p52. To investigate the effects of p52 expression in vivo, we generated a novel transgenic mouse model with inducible expression of p52 in Clara cell secretory protein-expressing airway epithelial cells. Although p52 overexpression alone did not cause significant inflammation, p52 overexpression caused increased lung inflammation, injury, and mortality following intratracheal delivery of Escherichia coli LPS. No differences in cytokine/chemokine expression were measured between p52-overexpressing mice and controls, but increased apoptosis of Clara cell secretory protein-positive airway epithelial cells was observed in transgenic mice after LPS stimulation. In vitro studies in lung epithelial cells showed that p52 overexpression reduced cell survival and increased the expression of several proapoptotic genes during cellular stress. Collectively, these studies demonstrate a novel role for p52 in cell survival/apoptosis of airway epithelial cells and implicate noncanonical NF-κB signaling in the pathogenesis of acute respiratory distress syndrome.

Published
2016

28. Neutrophil-Derived IL-1β Impairs the Efficacy of NF-κB Inhibitors against Lung Cancer

Author

McLoed, Allyson G., primary, Sherrill, Taylor P., additional, Cheng, Dong-Sheng, additional, Han, Wei, additional, Saxon, Jamie A., additional, Gleaves, Linda A., additional, Wu, Pingsheng, additional, Polosukhin, Vasiliy V., additional, Karin, Michael, additional, Yull, Fiona E., additional, Stathopoulos, Georgios T., additional, Georgoulias, Vassilis, additional, Zaynagetdinov, Rinat, additional, and Blackwell, Timothy S., additional

Published
2016
Full Text
View/download PDF

29. Epithelial NF-κB signaling promotes EGFR-driven lung carcinogenesis via macrophage recruitment

Author

Saxon, Jamie A., primary, Sherrill, Taylor P., additional, Polosukhin, Vasiliy V., additional, Sai, Jiqing, additional, Zaynagetdinov, Rinat, additional, McLoed, Allyson G., additional, Gulleman, Peter M., additional, Barham, Whitney, additional, Cheng, Dong-Sheng, additional, Hunt, Raphael P., additional, Gleaves, Linda A., additional, Richmond, Ann, additional, Young, Lisa R., additional, Yull, Fiona E., additional, and Blackwell, Timothy S., additional

Published
2016
Full Text
View/download PDF

30. p52 Overexpression Increases Epithelial Apoptosis, Enhances Lung Injury, and Reduces Survival after Lipopolysaccharide Treatment

Author

Saxon, Jamie A., primary, Cheng, Dong-Sheng, additional, Han, Wei, additional, Polosukhin, Vasiliy V., additional, McLoed, Allyson G., additional, Richmond, Bradley W., additional, Gleaves, Linda A., additional, Tanjore, Harikrishna, additional, Sherrill, Taylor P., additional, Barham, Whitney, additional, Yull, Fiona E., additional, and Blackwell, Timothy S., additional

Published
2016
Full Text
View/download PDF

31. Chronic NF-κB activation links COPD and lung cancer through generation of an immunosuppressive microenvironment in the lungs

Author

Zaynagetdinov, Rinat, primary, Sherrill, Taylor P., additional, Gleaves, Linda A., additional, Hunt, Pierre, additional, Han, Wei, additional, McLoed, Allyson G., additional, Saxon, Jamie A., additional, Tanjore, Harikrishna, additional, Gulleman, Peter M., additional, Young, Lisa R., additional, and Blackwell, Timothy S., additional

Published
2015
Full Text
View/download PDF

32. Opposing effects of NF-KB inhibition during chemical lung carcinogenesis

Author

Zaynagetdinov, Rinat Karabela, Sophia P. Psallidas, Loannis and Sherrill, Taylor P. Kairl, Chrysoula A. Cheng, Dong-Sheng and Vassiliou, Spyridoula Gleaves, Linda A. Han, Wei and Zakynthinos, Spyros G. Yull, Fiona E. Roussos, Charis and Kalomenidis, Loannis Blackwell, Timothy S. Stathopoulos, Georgios T.

Published
2012

33. Interleukin-5 Facilitates Lung Metastasis by Modulating the Immune Microenvironment

Author

Zaynagetdinov, Rinat, primary, Sherrill, Taylor P., additional, Gleaves, Linda A., additional, McLoed, Allyson G., additional, Saxon, Jamie A., additional, Habermann, Arun C., additional, Connelly, Linda, additional, Dulek, Daniel, additional, Peebles, R. Stokes, additional, Fingleton, Barbara, additional, Yull, Fiona E., additional, Stathopoulos, Georgios T., additional, and Blackwell, Timothy S., additional

Published
2015
Full Text
View/download PDF

34. BIOLUMINESCENCE IMAGING (BLI) VISUALIZES ACTIVATION OF NF-κB IN MOUSE CARDIAC TRANSPLANTATION

Author

Ma, Lianli, Xiang, Zhidan, Sherrill, Taylor P., Wang, Lei, Blackwell, Timothy S., Williams, Philip, Chong, Anita, Chari, Ravi, and Yin, Dengping

Subjects
Mice, Inbred C57BL, Mice, Mice, Inbred BALB C, Luminescence, NF-kappa B, Animals, Heart Transplantation, Transplantation, Homologous, Mice, Transgenic, Luciferases, Adoptive Transfer, Article, Spleen
Abstract

The purpose of the current study was to evaluate the role of bioluminescence imaging (BLI) in the determination of nuclear factor (NF)-kappaB activation in cardiac allograft rejection and ischemia-reperfusion injury.To visualize NF-kappaB activation, luciferase transgenic mice under the control of a mouse NF-kappaB promoter (NF-kappaB-Luc) were used as donors or recipients of cardiac grafts. Alternatively, NF-kappaB-Luc spleen cells were adoptively transferred into Rag2 -/- mice with or without cardiac allografts. BLI was performed posttransplantation to detect luciferase activity that represents NF-kappaB activation.The results show that luciferase activity was significantly increased in the cardiac allografts when NF-kappaB-Luc mice were used as recipients as well as donors. Luciferase activity was also elevated in the wild-type cardiac allografts in Rag2 -/- mice that were transferred with NF-kappaB-Luc spleen cells. CD154 monoclonal antibody (mAb) therapy inhibited luciferase activity and induced long-term survival of cardiac allografts. toll-like receptor-9 ligand, CpG DNA, enhanced luciferase activity and abrogated tolerance induction by CD154 mAb. Luciferase activity was also increased in ischemia-reperfusion injury of the cardiac grafts.BLI using Luc-NF-kappaB mice is a noninvasive approach to visualize the activation of NF-kappaB signaling in mouse cardiac allograft rejection and ischemia-reperfusion injury. CD154 mAb can inhibit NF-kappaB activation, which is reversed by toll-like receptor engagement.

Published
2008

35. Allergic Airway Inflammation Decreases Lung Bacterial Burden following Acute Klebsiella pneumoniae Infection in a Neutrophil- and CCL8-Dependent Manner

Author

Dulek, Daniel E., primary, Newcomb, Dawn C., additional, Goleniewska, Kasia, additional, Cephus, Jaqueline, additional, Zhou, Weisong, additional, Reiss, Sara, additional, Toki, Shinji, additional, Ye, Fei, additional, Zaynagetdinov, Rinat, additional, Sherrill, Taylor P., additional, Blackwell, Timothy S., additional, Moore, Martin L., additional, Boyd, Kelli L., additional, Kolls, Jay K., additional, and Peebles, R. Stokes, additional

Published
2014
Full Text
View/download PDF

36. Targeting the Wnt Pathway in Synovial Sarcoma Models

Author

Barham, Whitney, primary, Frump, Andrea L., additional, Sherrill, Taylor P., additional, Garcia, Christina B., additional, Saito-Diaz, Kenyi, additional, VanSaun, Michael N., additional, Fingleton, Barbara, additional, Gleaves, Linda, additional, Orton, Darren, additional, Capecchi, Mario R., additional, Blackwell, Timothy S., additional, Lee, Ethan, additional, Yull, Fiona, additional, and Eid, Josiane E., additional

Published
2013
Full Text
View/download PDF

37. Targeted immunomodulation of the NF-κB pathway in airway epithelium impacts host defense against Pseudomonas aeruginosa

Author

Sadikot, Ruxana T., Zeng, Heng, Joo, Myungsoo, Everhart, M. Brett, Sherrill, Taylor P., Cheng, Dongsheng, Li, Bo, Yull, Fiona E., Christman, John William Illiam, Blackwell, Timothy S., Sadikot, Ruxana T., Zeng, Heng, Joo, Myungsoo, Everhart, M. Brett, Sherrill, Taylor P., Cheng, Dongsheng, Li, Bo, Yull, Fiona E., Christman, John William Illiam, and Blackwell, Timothy S.

Abstract

We investigated the impact of inflammatory signaling in airway epithelial cells on host defense against Pseudomonas aeruginosa, a major cause of nosocomial pneumonia. In mice, airway instillation of P. aeruginosa resulted in NF-κB activation in the lungs that was primarily localized to the bronchial epithelium at 4 h, but was present in a variety of cell types by 24 h. We modulated NF-κB activity in airway epithelium by intratracheal delivery of adenoviral vectors expressing RelA (AdRelA) or a dominant inhibitor of NF-κB before P. aeruginosa infection. Bacterial clearance was enhanced by up-regulation of NF-κB activity following AdRelA administration and was impaired by treatment with a dominant inhibitor of NF-κB. The TNF-α concentration in lung lavage was increased by AdRelA treatment and beneficial effects of NF-κB up-regulation were abrogated in TNF-α-deficient mice. In contrast, NF-κB inhibition reduced MIP-2 expression and neutrophil influx following P. aeruginosa infection. Therefore, inflammatory signaling through the NF-κB pathway in airway epithelial cells critically regulates the innate immune response to P. aeruginosa. Copyright © 2006 by The American Association of Immunologists, Inc.

Published
2006

38. Abstract 2873: Opposing effects of NF-κB inhibition during chemical lung carcinogenesis

Author

Zaynagetdinov, Rinat, primary, Karabela, Sophia P., additional, Psallidas, Ioannis, additional, Sherrill, Taylor P., additional, Kairi, Chrysoula A., additional, Cheng, Dong-Sheng, additional, Vassiliou, Spyridoula, additional, Gleaves, Linda A., additional, Han, Wei, additional, Zakynthinos, Spyros G., additional, Yull, Fiona E., additional, Roussos, Charis, additional, Kalomenidis, Ioannis, additional, Blackwell, Timothy S., additional, and Stathopoulos, Georgios T., additional

Published
2012
Full Text
View/download PDF

39. A Critical Role for Macrophages in Promotion of Urethane-Induced Lung Carcinogenesis

Author

Zaynagetdinov, Rinat, primary, Sherrill, Taylor P., additional, Polosukhin, Vasiliy V., additional, Han, Wei, additional, Ausborn, Jamie A., additional, McLoed, Allyson G., additional, McMahon, Frank B., additional, Gleaves, Linda A., additional, Degryse, Amber L., additional, Stathopoulos, Georgios T., additional, Yull, Fiona E., additional, and Blackwell, Timothy S., additional

Published
2011
Full Text
View/download PDF

41. Differential Pathogenesis of Respiratory Syncytial Virus Clinical Isolates in BALB/c Mice

Author

Stokes, Kate L., primary, Chi, Michael H., additional, Sakamoto, Kaori, additional, Newcomb, Dawn C., additional, Currier, Michael G., additional, Huckabee, Matthew M., additional, Lee, Sujin, additional, Goleniewska, Kasia, additional, Pretto, Carla, additional, Williams, John V., additional, Hotard, Anne, additional, Sherrill, Taylor P., additional, Peebles, R. Stokes, additional, and Moore, Martin L., additional

Published
2011
Full Text
View/download PDF

42. TGFβ signaling in lung epithelium regulates bleomycin-induced alveolar injury and fibroblast recruitment

Author

Degryse, Amber L., primary, Tanjore, Harikrishna, additional, Xu, Xiaochuan C., additional, Polosukhin, Vasiliy V., additional, Jones, Brittany R., additional, Boomershine, Chad S., additional, Ortiz, Camila, additional, Sherrill, Taylor P., additional, McMahon, Frank B., additional, Gleaves, Linda A., additional, Blackwell, Timothy S., additional, and Lawson, William E., additional

Published
2011
Full Text
View/download PDF

47. Specific effects of bortezomib against experimental malignant pleural effusion: a preclinical study

Author

Psallidas, Ioannis, primary, Karabela, Sophia P, additional, Moschos, Charalampos, additional, Sherrill, Taylor P, additional, Kollintza, Androniki, additional, Magkouta, Sophia, additional, Theodoropoulou, Panagiota, additional, Roussos, Charis, additional, Blackwell, Timothy S, additional, Kalomenidis, Ioannis, additional, and Stathopoulos, Georgios T, additional

Published
2010
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results