studying-effects-cigarette-smoke-on-pseudomonas-infection-lung

Studying Effects of Cigarette Smoke on <em>Pseudomonas</em> Infection in Lung Epithelial Cells

Cigarette smoking is the major etiological cause for lung emphysema and chronic obstructive pulmonary disease (COPD). Cigarette smoking also promotes ...

University of Pittsburgh School of Medicine

Post-traumatic stress disorder (PTSD) is one of the most prevalent long-term psychiatric disorders among survivors of traumatic events. It is well established that social support has been related to the onset of PTSD after natural disasters. However, very little is known whether or not social support has had an influence on the recovery from the PTSD that was diagnosed after floods. This study, therefore, made a follow-up assessment of PTSD in flood victims 13-14 years after they were diagnosed with PTSD in 2000 to measure the prevalence rate of PTSD among them and identify the association between social support and their recovery from PTSD.

Association between social support and recovery from post-traumatic stress disorder after flood: a 13-14 year follow-up study in Hunan, China.

Post-traumatic stress disorder (PTSD) is a common psychological disorder caused by unusual threats or catastrophic events. Little is known about the combined incidence of PTSD after earthquakes. This study aimed at evaluating the combined incidence of PTSD among survivors after earthquakes using systematic review and meta-analysis.

The incidence of post-traumatic stress disorder among survivors after earthquakes:a systematic review and meta-analysis.

Floods are some of the most common and destructive natural disasters in the world, potentially leading to both physical injuries and psychological disorders, including post-traumatic stress disorder (PTSD). PTSD can damage functional capacity and interfere with social functioning. However, little is known about recovery from PTSD after floods. This study used 2013-2014 follow-up data on survivors of the 1998 Dongting Lake flood who were diagnosed with PTSD in 2000 to measure the prevalence rate of PTSD at follow-up and identify predictors of recovery from the PTSD diagnosis in 2000.

Predictors of recovery from post-traumatic stress disorder after the dongting lake flood in China: a 13-14 year follow-up study.

The histone acetyltransferase HBO1 (Histone acetyltransferase binding to origin recognition complex 1, Myst2/Kat7) participates in a range of life processes including DNA replication and tumorigenesis. Recent studies revealed that HBO1 is involved in gene transcriptional activation. However, the molecular behavior of HBO1 in inflammation is yet to be studied. Here we report that endotoxin lipopolysaccharide (LPS) elevates HBO1 protein level via up-regulating UPS25 (ubiquitin specific peptidase 25) and alters inflammatory gene transcription in THP-1 monocytes and in human primary macrophages. LPS protects HBO1 from ubiquitin proteasomal degradation without significantly altering its transcription. By immunoprecipitation, we identified that HBO1 associates with a deubiquitinating enzyme USP25 in THP-1 cells. LPS increases protein level of USP25 resulting in accumulation of HBO1 by suppression of HBO1 ubiquitination. Stabilized-HBO1 modulates inflammatory gene transcription in THP-1 cells. These findings indicate that USP25 promotes stability of HBO1 in bacterial infection thereby enhances HBO1-mediated inflammatory gene transcription.

LPS promotes HBO1 stability via USP25 to modulate inflammatory gene transcription in THP-1 cells.

Cigarette smoking increases susceptibility for microbial infection in respiratory system. However, the underlying molecular mechanism(s) is not fully elucidated. Here we report that cigarette smoking extract (CSE) increases bacterial load in lung epithelial cells via downregulation of the ubiquitin-specific protease 25 (USP25)/histone deacetylase 11 (HDAC11) axis. CSE treatment decreases HDAC11 at protein level in lung epithelial cells without significant changes of its transcription. Concomitantly, CSE treatment accelerates a ubiquitin-specific protease USP25 ubiquitination and degradation. Coimmunoprecipitation studies showed that USP25 associated with HDAC11. USP25 catalyzes deubiquitination of HDAC11, which regulates HDAC11 protein stability. CSE-mediated degradation of USP25 thereafter reduces HDAC11 at the protein level. Interestingly, CSE-downregulated USP25/HDAC11 axis increases the bacterial load of  in lung epithelial cells. These findings suggest that CSE-downregulated USP25 and HDAC11 may contribute to high susceptibility of bacterial infection in the cigarette smoking population.

Chen Long

Acute Lung Injury Center of Excellence,
Pulmonary,
Allergy,
Critical Care Medicine,
Department of Medicine,
Acute Lung Injury Center of Excellence, Pulmonary, Allergy, Critical Care Medicine, Department of Medicine

University of Pittsburgh School of Medicine

Studying Effects of Cigarette Smoke on Pseudomonas Infection in Lung Epithelial Cells

Chen Long

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Acute Lung Injury Center of Excellence,Pulmonary,Allergy,Critical Care Medicine,Department of Medicine,Acute Lung Injury Center of Excellence, Pulmonary, Allergy, Critical Care Medicine, Department of Medicine

University of Pittsburgh School of Medicine

Studying Effects of Cigarette Smoke on Pseudomonas Infection in Lung Epithelial Cells

Acute Lung Injury Center of Excellence,
Pulmonary,
Allergy,
Critical Care Medicine,
Department of Medicine,
Acute Lung Injury Center of Excellence, Pulmonary, Allergy, Critical Care Medicine, Department of Medicine