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Condition: Pneumonia
Infectious Disease: Influenza

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Total 6 results found since Jan 2013.

Immune-Modulation by the Human Respiratory Syncytial Virus: Focus on Dendritic Cells
This study is complemented by another report that found that hRSV infection induces significant expression of three miRNAs, namely hsa-miR-4448, hsa-miR-30a-5p, and hsa-miR-4634 in human DCs (104). Interestingly, this latter study also performed comparative analyses of miRNA profiles between DCs infected with hRSV and a related virus, namely the human metapneumovirus, and found that both viruses induced the expression of elevated levels of hsa-miR-4634. Elucidating the contribution of these miRNAs in DCs in response to hRSV remains to be determined. Dendritic Cell Phenotype and Migration Upon hRSV Infection in vivo Altho...
Source: Frontiers in Immunology - April 14, 2019 Category: Allergy & Immunology Source Type: research

Molecules, Vol. 22, Pages 1754: Emodin Inhibition of Influenza A Virus Replication and Influenza Viral Pneumonia via the Nrf2, TLR4, p38/JNK and NF-kappaB Pathways
In conclusion, emodin can inhibit IAV replication and influenza viral pneumonia, at least in part, by activating Nrf2 signaling and inhibiting IAV-induced activations of the TLR4, p38/JNK MAPK and NF-κB pathways.
Source: Molecules - October 18, 2017 Category: Chemistry Authors: Jian-Ping Dai Qian-Wen Wang Yun Su Li-Ming Gu Ying Zhao Xiao-Xua Chen Cheng Chen Wei-Zhong Li Ge-Fei Wang Kang-Sheng Li Tags: Article Source Type: research

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

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