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Article ; Online: Perfusion and Inflation of the Mouse Lung for Tumor Histology.

Davenport, Mackenzie L / Sherrill, Taylor P / Blackwell, Timothy S / Edmonds, Mick D

Journal of visualized experiments : JoVE

2020 , Issue 162

Abstract: The ability to evaluate lung histology is critical for the fields of lung cancer research and cancer metastasis. It is equally important to perform necropsies rapidly and efficiently from studies without sacrificing the quality of the tissues procured. ... ...

Abstract	The ability to evaluate lung histology is critical for the fields of lung cancer research and cancer metastasis. It is equally important to perform necropsies rapidly and efficiently from studies without sacrificing the quality of the tissues procured. The goal of this protocol is to present a method to rapidly perfuse, inflate, and fix mouse lungs for downstream histological analysis. This method does not standardize lung inflation; thus, it does not require any special procedures or equipment and instead simply instills fixative directly through the trachea following perfusion through the heart. This allows for sufficient estimation of tumor size, histology, and scoring. This also allows for the collection of frozen tissue prior to lung tissue fixation. This method is limited in that it does not allow for later morphometric quantification of the lung; however, it is more than sufficient for lung tumor analysis from genetically engineered mouse models (GEMMs), syngeneic models, as well as xenograft tumor and metastasis studies.
MeSH term(s)	Animals ; Humans ; Lung/pathology ; Lung Neoplasms/pathology ; Mice ; Perfusion ; Staining and Labeling ; Tissue Fixation ; Xenograft Model Antitumor Assays
Language	English
Publishing date	2020-08-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/60605
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Perfusion and inflation of the mouse lung for tumor histology

Davenport, Mackenzie L / Sherrill, Taylor P / Blackwell, Timothy S / Edmonds, Mick D

Journal of visualized experiments. 2020 Aug. 06, , no. 162

2020

Abstract	The ability to evaluate lung histology is critical for the fields of lung cancer research and cancer metastasis. It is equally important to perform necropsies rapidly and efficiently from studies without sacrificing the quality of the tissues procured. The goal of this protocol is to present a method to rapidly perfuse, inflate, and fix mouse lungs for downstream histological analysis. This method does not standardize lung inflation; thus, it does not require any special procedures or equipment and instead simply instills fixative directly through the trachea following perfusion through the heart. This allows for sufficient estimation of tumor size, histology, and scoring. This also allows for the collection of frozen tissue prior to lung tissue fixation. This method is limited in that it does not allow for later morphometric quantification of the lung; however, it is more than sufficient for lung tumor analysis from genetically engineered mouse models (GEMMs), syngeneic models, as well as xenograft tumor and metastasis studies.
Keywords	equipment ; genetic engineering ; heart ; histology ; inflation ; lung neoplasms ; lungs ; metastasis ; mice ; morphometry ; xenotransplantation
Language	English
Dates of publication	2020-0806
Size	p. e60605.
Publishing place	Journal of Visualized Experiments
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/60605
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Epithelial Yap/Taz are required for functional alveolar regeneration following acute lung injury.

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

JCI insight

2023 Volume 8, Issue 19

Abstract: A hallmark of idiopathic pulmonary fibrosis (IPF) and other interstitial lung diseases is dysregulated repair of the alveolar epithelium. The Hippo pathway effector transcription factors YAP and TAZ are implicated as essential for type 1 and type 2 ... ...

Abstract	A hallmark of idiopathic pulmonary fibrosis (IPF) and other interstitial lung diseases is dysregulated repair of the alveolar epithelium. The Hippo pathway effector transcription factors YAP and TAZ are implicated as essential for type 1 and type 2 alveolar epithelial cell (AT1 and AT2) differentiation in the developing lung, yet aberrant activation of YAP/TAZ is a prominent feature of the dysregulated alveolar epithelium in IPF. In these studies, we sought to define the functional role of YAP/TAZ activity during alveolar regeneration. We demonstrated that Yap and Taz were normally activated in AT2 cells shortly after injury, and deletion of Yap/Taz in AT2 cells led to pathologic alveolar remodeling, failure of AT2-to-AT1 cell differentiation, increased collagen deposition, exaggerated neutrophilic inflammation, and increased mortality following injury induced by a single dose of bleomycin. Loss of Yap/Taz activity prior to an LPS injury prevented AT1 cell regeneration, led to intraalveolar collagen deposition, and resulted in persistent innate inflammation. These findings establish that AT2 cell Yap/Taz activity is essential for functional alveolar epithelial repair and prevention of fibrotic remodeling.
MeSH term(s)	Humans ; Acute Lung Injury ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Collagen/metabolism ; Idiopathic Pulmonary Fibrosis/pathology ; Inflammation ; Regeneration ; Signal Transduction ; YAP-Signaling Proteins/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Collagen (9007-34-5) ; YAP-Signaling Proteins ; WWTR1 protein, human
Language	English
Publishing date	2023-09-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.173374
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Article ; Online: Thromboxane-Prostanoid Receptor Signaling Drives Persistent Fibroblast Activation in Pulmonary Fibrosis.

American journal of respiratory and critical care medicine

2022 Volume 206, Issue 5, Page(s) 596–607

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Animals ; Bleomycin/pharmacology ; F2-Isoprostanes/metabolism ; Fibroblasts/metabolism ; Humans ; Idiopathic Pulmonary Fibrosis/genetics ; Lung/metabolism ; Mice ; Mice, Inbred C57BL ; Prostaglandins/metabolism ; Receptors, Thromboxane/metabolism ; Thromboxanes/metabolism ; Transforming Growth Factor beta/metabolism
Chemical Substances	F2-Isoprostanes ; Prostaglandins ; Receptors, Thromboxane ; Thromboxanes ; Transforming Growth Factor beta ; Bleomycin (11056-06-7)
Language	English
Publishing date	2022-06-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202106-1503OC
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Article ; Online: Gas6/MerTK signaling is negatively regulated by NF-κB and supports lung carcinogenesis.

Novitskiy, Sergey V / Zaynagetdinov, Rinat / Vasiukov, Georgii / Gutor, Sergey / Han, Wei / Serezani, Ana / Matafonov, Anton / Gleaves, Linda A / Sherrill, Taylor P / Polosukhin, Vasiliy V / Blackwell, Timothy S

Oncotarget

2019 Volume 10, Issue 66, Page(s) 7031–7042

Abstract: Growth arrest-specific 6 (Gas6) has been implicated in carcinogenesis through activation of its receptors, particularly MerTK. To investigate whether Gas6 plays a role in resistance to NF-κB inhibitors, which have not proven to be effective agents for ... ...

Abstract	Growth arrest-specific 6 (Gas6) has been implicated in carcinogenesis through activation of its receptors, particularly MerTK. To investigate whether Gas6 plays a role in resistance to NF-κB inhibitors, which have not proven to be effective agents for lung cancer therapy, we studied lung cancer models induced by urethane injection or expression of mutant Kras (Kras
Language	English
Publishing date	2019-12-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.27345
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Article ; Online: STAT1 Represses Cytokine-Producing Group 2 and Group 3 Innate Lymphoid Cells during Viral Infection.

Stier, Matthew T / Goleniewska, Kasia / Cephus, Jacqueline Y / Newcomb, Dawn C / Sherrill, Taylor P / Boyd, Kelli L / Bloodworth, Melissa H / Moore, Martin L / Chen, Kong / Kolls, Jay K / Peebles, R Stokes

Journal of immunology (Baltimore, Md. : 1950)

2017 Volume 199, Issue 2, Page(s) 510–519

Abstract: The appropriate orchestration of different arms of the immune response is critical during viral infection to promote efficient viral clearance while limiting immunopathology. However, the signals and mechanisms that guide this coordination are not fully ... ...

Abstract	The appropriate orchestration of different arms of the immune response is critical during viral infection to promote efficient viral clearance while limiting immunopathology. However, the signals and mechanisms that guide this coordination are not fully understood. IFNs are produced at high levels during viral infection and have convergent signaling through STAT1. We hypothesized that STAT1 signaling during viral infection regulates the balance of innate lymphoid cells (ILC), a diverse class of lymphocytes that are poised to respond to environmental insults including viral infections with the potential for both antiviral or immunopathologic functions. During infection with respiratory syncytial virus (RSV), STAT1-deficient mice had reduced numbers of antiviral IFN-γ
MeSH term(s)	Animals ; Cytokines/biosynthesis ; Gene Expression Regulation ; Immunity, Innate ; Interferon-gamma/biosynthesis ; Interferon-gamma/genetics ; Interferon-gamma/immunology ; Interleukin-13/genetics ; Interleukin-13/immunology ; Interleukin-17/genetics ; Interleukin-17/immunology ; Interleukin-23/genetics ; Interleukin-23/immunology ; Interleukin-33/genetics ; Interleukin-33/immunology ; Interleukin-5/genetics ; Interleukin-5/immunology ; Lymphocytes/classification ; Lymphocytes/immunology ; Mice ; Respiratory Syncytial Virus Infections/immunology ; Respiratory Syncytial Virus Infections/virology ; STAT1 Transcription Factor/deficiency ; STAT1 Transcription Factor/genetics ; STAT1 Transcription Factor/metabolism ; Signal Transduction
Chemical Substances	Cytokines ; Interleukin-13 ; Interleukin-17 ; Interleukin-23 ; Interleukin-33 ; Interleukin-5 ; STAT1 Transcription Factor ; Stat1 protein, mouse ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2017--15
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1601984
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Article ; Online: Bone marrow derived mesenchymal stem cells incorporate into the prostate during regrowth.

Placencio, Veronica R / Li, Xiaohong / Sherrill, Taylor P / Fritz, Gloria / Bhowmick, Neil A

PloS one

2010 Volume 5, Issue 9, Page(s) e12920

Abstract: Background: Prostate cancer recurrence involves increased growth of cancer epithelial cells, as androgen dependent prostate cancer progresses to castrate resistant prostate cancer (CRPC) following initial therapy. Understanding CRPC prostate regrowth ... ...

Abstract	Background: Prostate cancer recurrence involves increased growth of cancer epithelial cells, as androgen dependent prostate cancer progresses to castrate resistant prostate cancer (CRPC) following initial therapy. Understanding CRPC prostate regrowth will provide opportunities for new cancer therapies to treat advanced disease. Methodology/principal findings: Elevated chemokine expression in the prostate stroma of a castrate resistant mouse model, Tgfbr2(fspKO), prompted us to look at the involvement of bone marrow derived cells (BMDCs) in prostate regrowth. We identified bone marrow cells recruited to the prostate in GFP-chimeric mice. A dramatic increase in BMDC recruitment for prostate regrowth occurred three days after exogenous testosterone implantation. Recruitment led to incorporation of BMDCs within the prostate epithelia. Immunofluorescence staining suggested BMDCs in the prostate coexpressed androgen receptor; p63, a basal epithelial marker; and cytokeratin 8, a luminal epithelial marker. A subset of the BMDC population, mesenchymal stem cells (MSCs), were specifically found to be incorporated in the prostate at its greatest time of remodeling. Rosa26 expressing MSCs injected into GFP mice supported MSC fusion with resident prostate epithelial cells through co-localization of β-galactosidase and GFP during regrowth. In a human C4-2B xenograft model of CRPC, MSCs were specifically recruited. Injection of GFP-labeled MSCs supported C4-2B tumor progression by potentiating canonical Wnt signaling. The use of MSCs as a targeted delivery vector for the exogenously expressed Wnt antagonist, secreted frizzled related protein-2 (SFRP2), reduced tumor growth, increased apoptosis and potentiated tumor necrosis. Conclusions/significance: Mesenchymal stem cells fuse with prostate epithelia during the process of prostate regrowth. MSCs recruited to the regrowing prostate can be used as a vehicle for transporting genetic information with potential therapeutic effects on castrate resistant prostate cancer, for instance by antagonizing Wnt signaling through SFRP2.
MeSH term(s)	Animals ; Bone Marrow Cells/cytology ; Bone Marrow Cells/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Disease Models, Animal ; Humans ; Male ; Mesenchymal Stem Cells/cytology ; Mesenchymal Stem Cells/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Prostate/cytology ; Prostate/growth & development ; Prostate/metabolism ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/physiopathology ; Proteins/genetics ; Proteins/metabolism ; RNA, Untranslated ; Signal Transduction ; Wnt Proteins/genetics ; Wnt Proteins/metabolism
Chemical Substances	Gt(ROSA)26Sor non-coding RNA, mouse ; Proteins ; RNA, Untranslated ; Wnt Proteins
Language	English
Publishing date	2010-09-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0012920
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Article ; Online: Identification of myeloid cell subsets in murine lungs using flow cytometry.

Zaynagetdinov, Rinat / Sherrill, Taylor P / Kendall, Peggy L / Segal, Brahm H / Weller, Kevin P / Tighe, Robert M / Blackwell, Timothy S

American journal of respiratory cell and molecular biology

2013 Volume 49, Issue 2, Page(s) 180–189

Abstract: Although the antibody-based recognition of cell-surface markers has been widely used for the identification of immune cells, overlap in the expression of markers by different cell types and the inconsistent use of antibody panels have resulted in a lack ... ...

Abstract	Although the antibody-based recognition of cell-surface markers has been widely used for the identification of immune cells, overlap in the expression of markers by different cell types and the inconsistent use of antibody panels have resulted in a lack of clearly defined signatures for myeloid cell subsets. We developed a 10-fluorochrome flow cytometry panel for the identification and quantitation of myeloid cells in the lungs, including pulmonary monocytes, myeloid dendritic cells, alveolar and interstitial macrophages, and neutrophils. After the initial sorting of viable CD45(+) leukocytes, we detected three leukocyte subpopulations based on CD68 expression: CD68(-), CD68(low), and CD68(hi). Further characterization of the CD68(hi) population revealed CD45(+)/CD68(hi)/F4/80(+)/CD11b(-)/CD11c(+)/Gr1(-) alveolar macrophages and CD45(+)/CD68(hi)/F4/80(-)/CD11c(+)/Gr1(-)/CD103(+)/major histocompatibility complex (MHC) class II(hi) dendritic cells. The CD68(low) population contained primarily CD45(+)/CD68(low)/F4/80(+)/CD11b(+)/CD11c(+)/Gr1(-)/CD14(low) interstitial macrophages and CD45(+)/CD68(low)/F4/80(+)/CD11b(+)/CD11c(-)/Gr1(low)/CD14(hi) monocytes, whereas the CD68(-) population contained neutrophils (CD45(+)/CD68(-)/F4/80(-)/CD11b(+)/Gr1(hi)). The validity of cellular signatures was confirmed by a morphological analysis of FACS-sorted cells, functional studies, and the depletion of specific macrophage subpopulations using liposomal clodronate. We believe our approach provides an accurate and reproducible method for the isolation, quantification, and characterization of myeloid cell subsets in the lungs, which may be useful for studying the roles of myeloid cells during various pathological processes.
MeSH term(s)	Animals ; Bone Density Conservation Agents/pharmacology ; Clodronic Acid/pharmacology ; Dendritic Cells/cytology ; Dendritic Cells/metabolism ; Flow Cytometry ; Histocompatibility Antigens Class II/metabolism ; Lung/cytology ; Lung/metabolism ; Macrophage Activation/drug effects ; Macrophage Activation/physiology ; Macrophages, Alveolar/cytology ; Macrophages, Alveolar/metabolism ; Mice ; Mice, Transgenic ; Monocytes/cytology ; Monocytes/metabolism
Chemical Substances	Bone Density Conservation Agents ; Histocompatibility Antigens Class II ; Clodronic Acid (0813BZ6866)
Language	English
Publishing date	2013-03-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2012-0366MA
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Article ; Online: Chronic NF-κB activation links COPD and lung cancer through generation of an immunosuppressive microenvironment in the lungs.

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

Oncotarget

2016 Volume 7, Issue 5, Page(s) 5470–5482

Abstract: Nuclear Factor (NF)-κB is positioned to provide the interface between COPD and carcinogenesis through regulation of chronic inflammation in the lungs. Using a tetracycline-inducible transgenic mouse model that conditionally expresses activated IκB kinase ...

Abstract	Nuclear Factor (NF)-κB is positioned to provide the interface between COPD and carcinogenesis through regulation of chronic inflammation in the lungs. Using a tetracycline-inducible transgenic mouse model that conditionally expresses activated IκB kinase β (IKKβ) in airway epithelium (IKTA), we found that sustained NF-κB signaling results in chronic inflammation and emphysema by 4 months. By 11 months of transgene activation, IKTA mice develop lung adenomas. Investigation of lung inflammation in IKTA mice revealed a substantial increase in M2-polarized macrophages and CD4+/CD25+/FoxP3+ regulatory T lymphocytes (Tregs). Depletion of alveolar macrophages in IKTA mice reduced Tregs, increased lung CD8+ lymphocytes, and reduced tumor numbers following treatment with the carcinogen urethane. Alveolar macrophages from IKTA mice supported increased generation of inducible Foxp3+ Tregs ex vivo through expression of TGFβ and IL-10. Targeting of TGFβ and IL-10 reduced the ability of alveolar macrophages from IKTA mice to induce Foxp3 expression on T cells. These studies indicate that sustained activation of NF-κB pathway links COPD and lung cancer through generation and maintenance of a pro-tumorigenic inflammatory environment consisting of alternatively activated macrophages and regulatory T cells.
MeSH term(s)	Animals ; Blotting, Western ; CD8-Positive T-Lymphocytes/immunology ; Cells, Cultured ; Epithelium/immunology ; Female ; Flow Cytometry ; Humans ; I-kappa B Kinase/physiology ; Immunosuppressive Agents/immunology ; Inflammation/immunology ; Interleukin-10/genetics ; Interleukin-10/metabolism ; Lung/immunology ; Lung/metabolism ; Lung/pathology ; Lung Neoplasms/immunology ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Macrophages, Alveolar/immunology ; Male ; Mice ; Mice, Transgenic ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Pulmonary Disease, Chronic Obstructive/immunology ; Pulmonary Disease, Chronic Obstructive/metabolism ; Pulmonary Disease, Chronic Obstructive/pathology ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; T-Lymphocytes, Regulatory/immunology ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism
Chemical Substances	Immunosuppressive Agents ; NF-kappa B ; RNA, Messenger ; Transforming Growth Factor beta ; Interleukin-10 (130068-27-8) ; I-kappa B Kinase (EC 2.7.11.10)
Language	English
Publishing date	2016-02-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.6562
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Article ; Online: p52 Overexpression Increases Epithelial Apoptosis, Enhances Lung Injury, and Reduces Survival after Lipopolysaccharide Treatment.

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 / Blackwell, Timothy S

Journal of immunology (Baltimore, Md. : 1950)

2016 Volume 196, Issue 4, Page(s) 1891–1899

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 ... ...

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.
MeSH term(s)	Animals ; Apoptosis/immunology ; Blotting, Western ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; Humans ; Immunohistochemistry ; Lipopolysaccharides/toxicity ; Mice ; Mice, Transgenic ; NF-kappa B p52 Subunit/biosynthesis ; NF-kappa B p52 Subunit/immunology ; Pneumonia/immunology ; Pneumonia/pathology ; Real-Time Polymerase Chain Reaction ; Respiratory Distress Syndrome/immunology ; Respiratory Distress Syndrome/pathology ; Respiratory Mucosa/immunology ; Respiratory Mucosa/pathology ; Signal Transduction/immunology ; Up-Regulation
Chemical Substances	Lipopolysaccharides ; NF-kappa B p52 Subunit
Language	English
Publishing date	2016-01-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1501555
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