Filtered By:
Condition: Pneumonia

This page shows you your search results in order of date. This is page number 7.

Order by Relevance | Date

Total 107 results found since Jan 2013.

H7N9 Influenza A Virus Exhibits Importin- α7–Mediated Replication in the Mammalian Respiratory Tract
The acute respiratory distress syndrome (ARDS) is the leading cause of death in influenza A virus (IAV) –infected patients. Hereby, the cellular importin-α7 gene plays a major role. It promotes viral replication in the lung, thereby increasing the risk for the development of pneumonia complicated by ARDS. Herein, we analyzed whether the recently emerged H7N9 avian IAV has already adapted to human i mportin-α7 use, which is associated with high-level virus replication in the mammalian lung. Using a cell-based viral polymerase activity assay, we could detect a decreased H7N9 IAV polymerase activity when importin-α7 was silenced by siRNA.
Source: American Journal of Pathology - February 8, 2017 Category: Pathology Authors: Stephanie Bertram, Swantje Thiele, Carola Dreier, Patricia Resa-Infante, Annette Preu ß, Debby van Riel, Chris K.P. Mok, Folker Schwalm, Joseph S.M. Peiris, Hans-Dieter Klenk, Gülsah Gabriel Tags: Regular Article Source Type: research

H7N9 Influenza A Virus Exhibits Importin- α7-Mediated Replication in the Mammalian Respiratory Tract.
H7N9 Influenza A Virus Exhibits Importin-α7-Mediated Replication in the Mammalian Respiratory Tract. Am J Pathol. 2017 Feb 08;: Authors: Bertram S, Thiele S, Dreier C, Resa-Infante P, Preuß A, van Riel D, Mok CK, Schwalm F, Peiris JS, Klenk HD, Gabriel G Abstract The acute respiratory distress syndrome (ARDS) is the leading cause of death in influenza A virus (IAV)-infected patients. Hereby, the cellular importin-α7 gene plays a major role. It promotes viral replication in the lung, thereby increasing the risk for the development of pneumonia complicated by ARDS. Herein, we analyzed whether the rec...
Source: The American Journal of Pathology - February 7, 2017 Category: Pathology Authors: Bertram S, Thiele S, Dreier C, Resa-Infante P, Preuß A, van Riel D, Mok CK, Schwalm F, Peiris JS, Klenk HD, Gabriel G Tags: Am J Pathol Source Type: research

CYP1A1 mediates the suppression of major inflammatory cytokines in pulmonary macrophage (PAM) cell lines caused by mycoplasma hyponeumoniae.
In this study, pulmonary alveolar macrophage (PAM) cell lines with CYP1A1 overexpression or siRNA-mediated CYP1A1 silencing were used to explore the biological function and regulatory mechanism of CYP1A1 gene expression changed on the inflammatory response of pigs infected with M. hyopneumoniae. The results showed that the cells overexpressing CYP1A1 infected with M. hyopneumoniae led to a rapid increase in PPAR-γ expression, which resulted in decreasing the levels of several inflammatory cytokines including IL-1β, IL-6, IL-8 and TNF-α. On the contrary, this effect was just opposite in CYP1A1-RNAi cells infected with M....
Source: Developmental and Comparative Immunology - June 30, 2016 Category: Allergy & Immunology Authors: Fang X, Zhao W, Xu J, Tu F, Wang X, Li B, Fu Y, Ren S Tags: Dev Comp Immunol Source Type: research

Targeting host calpain proteases decreases influenza A virus infection
Influenza A viruses (IAV) trigger contagious acute respiratory diseases. A better understanding of the molecular mechanisms of IAV pathogenesis and host immune responses is required for the development of more efficient treatments of severe influenza. Calpains are intracellular proteases that participate in diverse cellular responses, including inflammation. Here, we used in vitro and in vivo approaches to investigate the role of calpain signaling in IAV pathogenesis. Calpain expression and activity were found altered in IAV-infected bronchial epithelial cells. With the use of small-interfering RNA (siRNA) gene silencing, ...
Source: AJP: Lung Cellular and Molecular Physiology - March 31, 2016 Category: Respiratory Medicine Authors: Blanc, F., Furio, L., Moisy, D., Yen, H.-L., Chignard, M., Letavernier, E., Naffakh, N., Mok, C. K. P., Si-Tahar, M. Tags: ARTICLES Source Type: research

Targeting host calpain proteases decreases influenza A virus infection.
Abstract Influenza A viruses (IAV) trigger contagious acute respiratory diseases. A better understanding of the molecular mechanisms of IAV pathogenesis and host immune responses is required for the development of more efficient treatments of severe influenza. Calpains are intracellular proteases that participate to diverse cellular responses, including inflammation. Here, we used in vitro and in vivo approaches to investigate the role of calpains signalling in IAV pathogenesis. Calpain expression and activity were found altered in IAV-infected bronchial epithelial cells. Using siRNA gene silencing, specific synth...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - January 8, 2016 Category: Cytology Authors: Blanc F, Furio L, Moisy D, Yen HL, Chignard M, Letavernier E, Naffakh N, Mok CK, Si-Tahar M Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Antibacterial effect of mesenchymal stem cells against Escherichia coli is mediated by secretion of beta‐defensin‐2 via toll like receptor 4 signaling
This study was done to elucidate the mechanism underlying the antibacterial effects of MSCs. The growth of E. coli in vitro was significantly inhibited only by MSCs or their conditioned medium with bacterial preconditioning, but not by fibroblasts or their conditioned medium. Microarray analysis identified significant up‐regulation of toll like receptors (TLR)‐2 and TLR‐4, and β‐defensin 2 (BD2) in MSCs compared with fibroblasts after E. coli exposure. The increased BD2 level and the in vitro antibacterial effects of MSCs were abolished by specific antagonist or by siRNA‐mediated knockdown of TLR‐4, but not TL...
Source: Cellular Microbiology - September 1, 2015 Category: Microbiology Authors: Dong Kyung Sung, Yun Sil Chang, Se In Sung, Hye Soo Yoo, So Yoon Ahn, Won Soon Park Tags: Research article Source Type: research

Increased ectodomain shedding of cell adhesion molecule 1 as a cause of type II alveolar epithelial cell apoptosis in patients with idiopathic interstitial pneumonia
Conclusions: CADM1 α-shedding appeared to be increased in all four IIP subtypes and consequently contributed to AEC apoptosis by decreasing the full-length CADM1 level. This mechanism particularly impacted f-NSIP. The molecular mechanism causing AEC apoptosis may be similar between IIP and emphysema.
Source: Respiratory Research - August 1, 2015 Category: Respiratory Medicine Authors: Azusa YoneshigeMan HagiyamaTakao InoueTakahiro MimaeTakashi KatoMorihito OkadaEisuke EnokiAkihiko Ito Source Type: research

Synergistic Costimulatory Effect of Chlamydia pneumoniae with Carbon Nanoparticles on NLRP3 Inflammasome-Mediated Interleukin-1{beta} Secretion in Macrophages Host Response and Inflammation
This study assessed whether costimulation of C. pneumoniae with CNTs synergistically enhanced IL-1β secretion from macrophages, and determined the molecular mechanism involved. Enhanced IL-1β secretion from C. pneumoniae-infected macrophages by CNTs was dose and time dependent. Transmission electron microscopy revealed that C. pneumoniae and CNTs were engulfed concurrently by macrophages. Inhibitors of actin polymerization or caspase-1, a component of the inflammasome, significantly blocked IL-1β secretion. Gene silencing using small interfering RNA (siRNA) targeting the NLRP3 gene also abolished IL-1β ...
Source: Infection and Immunity - June 15, 2015 Category: Infectious Diseases Authors: Matsuo, J., Nakamura, S., Takeda, S., Ishida, K., Yamazaki, T., Yoshida, M., Chiba, H., Hui, S.-P., Yamaguchi, H. Tags: Host Response and Inflammation Source Type: research

Pneumococci LytA-dependent KLF4 Expression Terminates IL-8 Secretion in Lung Epithelium.
In conclusion, KLF4 acts as a counter-regulatory transcription factor in pneumococci-related pro-inflammatory activation of lung epithelial cells, thereby potentially preventing lung hyper-inflammation and subsequent organ failure. PMID: 25756955 [PubMed - as supplied by publisher]
Source: American Journal of Respiratory Cell and Molecular Biology - March 10, 2015 Category: Molecular Biology Authors: Zahlten J, Herta T, Kabus C, Steinfeldt M, Kershaw O, García P, Hocke AC, Gruber AD, Hübner RH, Steinicke R, Doehn JM, Suttorp N, Hippenstiel S Tags: Am J Respir Cell Mol Biol Source Type: research

Chlamydia pneumoniae effector chlamydial outer protein N sequesters fructose bisphosphate aldolase A, providing a benefit to bacterial growth
Conclusions: We discovered that one of the C. pneumoniae CopN targets is the glycolytic enzyme aldolase A. Sequestering aldolase A may be beneficial to bacterial growth in infected host cells.
Source: BMC Microbiology - December 21, 2014 Category: Microbiology Authors: Kasumi IshidaJunji MatsuoYoshimasa YamamotoHiroyuki Yamaguchi Source Type: research

Altered Surfactant Homeostasis and Alveolar Epithelial Cell Stress in Amiodarone-Induced Lung Fibrosis
Amiodarone (AD) is a highly efficient antiarrhythmic drug with potentially serious side effects. Severe pulmonary toxicity is reported in patients receiving AD even at low doses and may cause interstitial pneumonia as well as lung fibrosis. Apoptosis of alveolar epithelial type II cells (AECII) has been suggested to play an important role in this disease. In the current study, we aimed to establish a murine model of AD-induced lung fibrosis and analyze surfactant homeostasis, lysosomal, and endoplasmic reticulum (ER) stress in this model. AD/vehicle was instilled intratracheally into C57BL/6 mice, which were sacrificed on ...
Source: Toxicological Sciences - November 10, 2014 Category: Toxicology Authors: Mahavadi, P., Henneke, I., Ruppert, C., Knudsen, L., Venkatesan, S., Liebisch, G., Chambers, R. C., Ochs, M., Schmitz, G., Vancheri, C., Seeger, W., Korfei, M., Guenther, A. Tags: Inhalation and Respiratory Source Type: research

ATF3 Confers Resistance to Pneumococcal Infection Through Positive Regulation of Cytokine Production
Conclusions. Taken together, we can conclude that ATF3 regulates innate immunity positively upon pneumococcus infection by enhancing TNF-α, IL-1β, and IFN- expression and modulating bacterial clearance.
Source: The Journal of Infectious Diseases - November 7, 2014 Category: Infectious Diseases Authors: Nguyen, C. T., Kim, E.-H., Luong, T. T., Pyo, S., Rhee, D.-K. Tags: BACTERIA Source Type: research

Longistatin in tick saliva blocks advanced glycation end-product receptor activation
Ticks are notorious hematophagous ectoparasites and vectors of many deadly pathogens. As an effective vector, ticks must break the strong barrier provided by the skin of their host during feeding, and their saliva contains a complex mixture of bioactive molecules that paralyze host defenses. The receptor for advanced glycation end products (RAGE) mediates immune cell activation at inflammatory sites and is constitutively and highly expressed in skin. Here, we demonstrate that longistatin secreted with saliva of the tick Haemaphysalis longicornis binds RAGE and modulates the host immune response. Similar to other RAGE ligan...
Source: Journal of Clinical Investigation - September 2, 2014 Category: Biomedical Science Authors: Anisuzzaman, Takeshi Hatta, Takeharu Miyoshi, Makoto Matsubayashi, M. Khyrul Islam, M. Abdul Alim, M. Abu Anas, M. Mehedi Hasan, Yasunobu Matsumoto, Yasuhiko Yamamoto, Hiroshi Yamamoto, Kozo Fujisaki, Naotoshi Tsuji Source Type: research

Linalool attenuates lung inflammation induced by Pasteurella multocida via activating Nrf-2 signaling pathway.
In this study, linalool, a natural compound of the essential oils in several aromatic plant species, elevated nuclear Nrf-2 protein translocation in the A549 lung cell line and in vivo. The P. multocida-induced pro-inflammatory cytokines expression was abrogated by Nrf-2 siRNA. Postponed treatment with linalool decreased lung neutrophil accumulation and enhanced clearance of P. multocida. Furthermore, linalool significantly increased the expression of antioxidant enzymes regulated by Nrf-2 and diminished lung tissue levels of several pro-inflammatory cytokines, including tumor necrosis factor α (TNF-α) and interleukin (I...
Source: International Immunopharmacology - June 9, 2014 Category: Allergy & Immunology Authors: Wu Q, Yu L, Qiu J, Shen B, Wang D, Soromou LW, Feng H Tags: Int Immunopharmacol Source Type: research

Host metabolism promotes growth of Chlamydia pneumoniae in a low oxygen environment.
Abstract Chlamydia pneumoniae infections of the respiratory tract are common and are associated with acute and chronic diseases such as community-acquired pneumonia (CAP) and chronic obstructive pulmonary disease (COPD). Recent studies have shown that reduced environmental oxygen availability promotes chlamydial growth in infected host cells. The underlying mechanisms remain unclear. We performed a targeted siRNA screen coupled with an automated high-throughput microscopic analysis to identify key host cell genes that play a role in promoting the hypoxic growth of C. pneumoniae. A total of 294 siRNAs - targeting 9...
Source: International Journal of Medical Microbiology - April 6, 2013 Category: Microbiology Authors: Szaszák M, Shima K, Käding N, Hannus M, Solbach W, Rupp J Tags: Int J Med Microbiol Source Type: research