Filtered By:
Condition: Pneumonia

This page shows you your search results in order of relevance.

Order by Relevance | Date

Total 107 results found since Jan 2013.

Autophagy Is a Defense Mechanism Inhibiting Invasion and Inflammation During High-Virulent Haemophilus parasuis Infection in PK-15 Cells
In this study, we sought to investigate whether SH0165 (serovar 5, high-virulent strain) and HN0001 (serovar 6, non-virulent strain) infection induces autophagy and the specific role of autophagy in bacterial invasion and inflammation during H. parasuis infection. Moreover, we explored the mechanism underlying autophagy regulated inflammation through inflammatory signaling cascades during H. parasuis infection. This observation could provide useful information for further understanding the role of autophagy in H. parasuis infection and improve our knowledge of new strategies against this pathogen. Materials and Methods B...
Source: Frontiers in cellular and infection microbiology - April 15, 2019 Category: Microbiology Source Type: research

Histone Deacetylase 7 Inhibition in a Murine Model of Gram-Negative Pneumonia-Induced Acute Lung Injury
Conclusion: HDAC7 appears to play a key role in the inflammatory response that leads to ALI after gram-negative pneumonia in mice.
Source: Shock - February 12, 2020 Category: Emergency Medicine Tags: Basic Science Aspects Source Type: research

Oxidative stress associated with aging activates Protein Kinase C Epsilon, leading to cilia slowing.
Abstract Older people are four times more likely to develop pneumonia than younger people. As we age, many components of pulmonary innate immunity are impaired, including slowing of mucociliary clearance. Ciliary beat frequency (CBF) is a major determinant of mucociliary clearance, and it slows as we age. We hypothesized that CBF is slowed in aging due to increased oxidative stress, which activates PKCε signaling. We pharmacologically inhibited PKCε in ex vivo mouse models of aging. We measured a slowing of CBF with aging that was reversed with inhibition using the novel PKC inhibitor, Ro-31-8220, as well as the...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - September 13, 2018 Category: Cytology Authors: Bailey KL, Kharbanda KK, Katafiasz DM, Sisson JH, Wyatt TA Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

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

Klebsiella pneumoniae targets an EGF receptor‐dependent pathway to subvert inflammation.
Abstract The NF‐κB transcriptional factor plays a key role governing the activation of immune responses. Klebsiella pneumoniae is an important cause of community‐acquired and nosocomial pneumonia. Evidence indicates that K. pneumoniae infections are characterized by lacking an early inflammatory response. Recently, we have demonstrated that Klebsiella antagonizes the activation of NF‐κB via the deubiquitinase CYLD. In this work, by applying a high‐throughput siRNA gain‐on‐function screen interrogating the human kinome, we identified 17 kinases that when targeted by siRNA restored IL‐1β‐dependent NF‐κB...
Source: Cellular Microbiology - January 25, 2013 Category: Microbiology Authors: Christian G. Frank, Verónica Reguerio, Marion Rother, David Moranta, André P. Maeurer, Junkal Garmendia, Thomas F. Meyer, José A. Bengoechea Tags: Research Article Source Type: research

Klebsiella pneumoniae targets an EGF receptor‐dependent pathway to subvert inflammation
Summary The NF‐κB transcriptional factor plays a key role governing the activation of immune responses. Klebsiella pneumoniae is an important cause of community‐acquired and nosocomial pneumonia. Evidence indicates that K. pneumoniae infections are characterized by lacking an early inflammatory response. Recently, we have demonstrated that Klebsiella antagonizes the activation of NF‐κB via the deubiquitinase CYLD. In this work, by applying a high‐throughput siRNA gain‐of‐function screen interrogating the human kinome, we identified 17 kinases that when targeted by siRNA restored IL‐1β‐dependent NF‐κ...
Source: Cellular Microbiology - February 17, 2013 Category: Microbiology Authors: Christian G. Frank, Verónica Reguerio, Marion Rother, David Moranta, André P. Maeurer, Junkal Garmendia, Thomas F. Meyer, José A. Bengoechea 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

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

The RIPK3 Scaffold Regulates Lung Inflammation During Pseudomonas Aeruginosa Pneumonia
Am J Respir Cell Mol Biol. 2022 Sep 30. doi: 10.1165/rcmb.2021-0474OC. Online ahead of print.ABSTRACTRIPK3 kinase activity triggers cell death via necroptosis, while scaffold function supports protein binding and cytokine production. To determine if RIPK3 kinase or scaffold domains mediate pathology during Pseudomonas aeruginosa infection, control mice and those with deletion or mutation of RIPK3 and associated signaling partners were subjected to Pseudomonas pneumonia and followed for survival or sacrificed for biologic assays. Murine immune cells were studied in vitro for Pseudomonas-induced cytokine production and cell ...
Source: Am J Respir Cell Mol... - September 30, 2022 Category: Respiratory Medicine Authors: John D Lyons Pratyusha Mandal Shunsuke Otani Deena B Chihade Kristen F Easley David A Swift Eileen M Burd Zhe Liang Michael Koval Edward S Mocarski Craig M Coopersmith Source Type: research