Electronic cigarette liquid increases inflammation and virus infection in primary human airway epithelial cells.

Background/objective: The use of electronic cigarettes (e-cigarettes) is rapidly increasing in the United States, especially among young people since e-cigarettes have been perceived as a safer alternative to conventional tobacco cigarettes. However, the scientific evidence regarding the human health effects of e-cigarettes on the lung is extremely limited. The major goal of our current study is to determine if e-cigarette use alters human young subject airway epithelial functions such as inflammatory response and innate immune defense against respiratory viral (i.

Airway epithelial NF-κB activation promotes Mycoplasma pneumoniae clearance in mice.

Background/objective: Respiratory infections including atypical bacteria Mycoplasma pneumoniae (Mp) contribute to the pathobiology of asthma and chronic obstructive pulmonary disease (COPD). Mp infection mainly targets airway epithelium and activates various signaling pathways such as nuclear factor κB (NF-κB). We have shown that short palate, lung, and nasal epithelium clone 1 (SPLUNC1) serves as a novel host defense protein and is up-regulated upon Mp infection through NF-κB activation in cultured human and mouse primary airway epithelial cells.

A novel function of MUC18: amplification of lung inflammation during bacterial infection.

Bacterial infection plays a critical role in exacerbations of various lung diseases, including chronic pulmonary obstructive disease (COPD) and asthma. Excessive lung inflammation is a prominent feature in disease exacerbations, but the underlying mechanisms remain poorly understood. Cell surface glycoprotein MUC18 (alias CD146 or melanoma cell adhesion molecule) has been shown to promote metastasis in several tumors, including melanoma.

SPLUNC1 deficiency enhances airway eosinophilic inflammation in mice.

Short palate, lung and nasal epithelium clone 1 (SPLUNC1) is enriched in normal airway lining fluid, but is significantly reduced in airway epithelium exposed to a Th2 cytokine milieu. The role of SPLUNC1 in modulating airway allergic inflammation (e.g.

Heat shock factor 1 protects against lung mycoplasma pneumoniae infection in mice.

Heat shock factor 1 (HSF1) is a transcriptional factor that controls the induction of heat shock proteins (e.g. HSP70) in response to stress.

MicroRNA-21 inhibits toll-like receptor 2 agonist-induced lung inflammation in mice.

Impaired airway innate immunity (e.g., suppressed Toll-like receptor 2 [TLR2] signaling) has been reported in allergic lungs with bacterial infection.

SPLUNC1 promotes lung innate defense against Mycoplasma pneumoniae infection in mice.

Short palate, lung, and nasal epithelium clone 1 (SPLUNC1) protein is highly expressed in normal airways, but is dramatically decreased in allergic and cigarette smoke exposure settings. We have previously demonstrated SPLUNC1 in vitro antibacterial property against Mycoplasma pneumoniae (Mp). However, its in vivo biological functions remain unclear.

Cigarette smoke increases susceptibility to tuberculosis--evidence from in vivo and in vitro models.

Background: Cigarette smoke (CS) exposure is an epidemiological risk factor for tuberculosis, although the biological basis has not been elucidated.

Methods: We exposed C57BL/6 mice to CS for 14 weeks and examined their ability to control an aerosol infection of Mycobacterium tuberculosis Erdman.

Results: CS-exposed mice had more M.

In vivo function of airway epithelial TLR2 in host defense against bacterial infection.

Decreased Toll-like receptor 2 (TLR2) expression has been reported in patients with chronic obstructive pulmonary disease and in a murine asthma model, which may predispose the hosts to bacterial infections, leading to disease exacerbations. Since airway epithelial cells serve as the first line of respiratory mucosal defense, the present study aimed to reveal the role of airway epithelial TLR2 signaling to lung bacterial [i.e.

SPLUNC1 regulation in airway epithelial cells: role of Toll-like receptor 2 signaling.

Background: Respiratory infections including Mycoplasma pneumoniae (Mp) contribute to various chronic lung diseases. We have shown that mouse short palate, lung, and nasal epithelium clone 1 (SPLUNC1) protein was able to inhibit Mp growth. Further, airway epithelial cells increased SPLUNC1 expression upon Mp infection.

Roflumilast increases Clara cell secretory protein in cigarette smoke-exposed mice.

Decreased Clara cell secretory protein (CCSP) levels have been found in smokers and chronic obstructive pulmonary disease (COPD) patients, which may be related to the development of COPD. A phosphodiesterase-4 (PDE4) inhibitor, roflumilast, appears to have therapeutic value for COPD. However, its effect on CCSP in cigarette smoke (CS)-exposed lungs has not been investigated.

Impact of cigarette smoke exposure on innate immunity: a Caenorhabditis elegans model.

Background: Cigarette smoking is the major cause of chronic obstructive pulmonary disease (COPD) and lung cancer. Respiratory bacterial infections have been shown to be involved in the development of COPD along with impaired airway innate immunity.

Methodology/principal Findings: To address the in vivo impact of cigarette smoke (CS) exclusively on host innate defense mechanisms, we took advantage of Caenorhabditis elegans (C.

Cigarette smoke decreases MARCO expression in macrophages: implication in Mycoplasma pneumoniae infection.

Bacterial infections including Mycoplasma pneumoniae (Mp) are a major cause of exacerbations in chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) is the leading cause of COPD, and affects the function of alveolar macrophages that act as the first line of defense against the invading respiratory pathogens. Macrophages express a transmembrane receptor called macrophage receptor with collagenous structure (MARCO) that is involved in the clearance of microorganisms.