Idioma:

Nontypeable Haemophilus influenzae –Promoted Proliferation of KRas-Induced Early Adenomatous Lesions Is Completely Dependent on Toll-Like Receptor Signaling

Jungnickel, Christopher ; Schnabel, Philipp A ; Bohle, Rainer ; Wiewrodt, Rainer ; Herr, Christian ; Bals, Robert ; Beisswenger, Christoph

The American journal of pathology, 2017-05, Vol.187 (5), p.973-979 [Periódico revisado por pares]

United States: Elsevier Inc

Texto completo disponível

Citações Citado por

Enviar para

Título:
Nontypeable Haemophilus influenzae –Promoted Proliferation of KRas-Induced Early Adenomatous Lesions Is Completely Dependent on Toll-Like Receptor Signaling
Autor: Jungnickel, Christopher ; Schnabel, Philipp A ; Bohle, Rainer ; Wiewrodt, Rainer ; Herr, Christian ; Bals, Robert ; Beisswenger, Christoph
Assuntos: Adenocarcinoma - physiopathology ; Animals ; Cell Proliferation - physiology ; Genes, ras - physiology ; Haemophilus Infections - physiopathology ; Haemophilus influenzae - physiology ; Lung Neoplasms - physiopathology ; Mice ; Neutrophils - physiology ; Pathology ; Pulmonary Disease, Chronic Obstructive - physiopathology ; Pulmonary Disease, Chronic Obstructive - virology ; ras Proteins - metabolism ; Signal Transduction - physiology ; Toll-Like Receptor 2 - deficiency ; Toll-Like Receptor 2 - physiology ; Toll-Like Receptor 4 - deficiency ; Toll-Like Receptor 4 - physiology
É parte de: The American journal of pathology, 2017-05, Vol.187 (5), p.973-979
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Descrição: Chronic obstructive pulmonary disease is a risk factor for lung cancer. COPD is characterized by chronic airway inflammation and lung infections. The airways of patients with COPD are frequently colonized with bacteria [eg, nontypeable Haemophilus influenzae (NTHi)] that cause pulmonary inflammation and exacerbations. Pulmonary adenocarcinomas are frequently associated with an activating mutation in the KRAS gene. We determined the function of Toll-like receptor (TLR) signaling on the progression of KRas-induced early adenomatous lesions in the lung. Wild-type (WT) mice and mice doubly deficient in Tlr-2 and -4 ( Tlr2/4 −/− ), both with an oncogenic Kras allele in lung epithelium, were exposed to NTHi for 4 weeks. Exposure to NTHi resulted in increased tumor proliferation and growth in WT mice, but not in Tlr2/4−/− mice. Alveolar adenomatous hyperplasia and adenocarcinoma were significantly increased in WT mice compared with Tlr2/4−/− mice. The mean size of tumors was significantly larger in WT mice, whereas there was no difference in the number of alveolar lesions between WT and Tlr2/4−/− mice. NTHi-induced pulmonary neutrophilic inflammation and tumor-associated neutrophils were reduced in Tlr2/4−/− mice. Thus, subsequent to a driver mutation, NTHi-induced inflammation promotes proliferation of early adenomatous lesions in a TLR-dependent manner.
Editor: United States: Elsevier Inc
Idioma: Inglês

Links

View this record in MEDLINE/PubMed

Voltar para lista de resultados

Realização: Logos de Redes Sociais:

Nontypeable Haemophilus influenzae –Promoted Proliferation of KRas-Induced Early Adenomatous Lesions Is Completely Dependent on Toll-Like Receptor Signaling

Jungnickel, Christopher ; Schnabel, Philipp A ; Bohle, Rainer ; Wiewrodt, Rainer ; Herr, Christian ; Bals, Robert ; Beisswenger, Christoph

United States: Elsevier Inc

Buscando em bases de dados remotas. Favor aguardar.