Background: Raoultella planticola, considered to be an environmental organism, is a rare cause of human infections. Although in recent years the frequency of R. planticola infections reported in the literature has increased, few cases of pneumonia caused by R. planticola have been described. Here, we investigate the clinical characteristics, management, and clinical outcomes of pneumonia caused by R. planticola. Methods: Consecutive patients with pneumonia caused by R. planticola were included. The medical records of patients with R. planticola pneumonia treated at Dankook University Hospital from January 2011 to December 2017 were collected. Results: A total of 11 adult patients with R. planticola pneumonia were diagnosed and treated [10 males and 1 female; median age, 70 years (range: 51-79 years)]; 5 patients had underlying malignant conditions (45.5%). Antibacterial susceptibility testing showed that all isolates of R. planticola were susceptible to cephalosporins, carbapenems, fluoroquinolones, aminoglycosides, and beta-lactams/beta-lactamase inhibitors. Chest imaging revealed consolidation (8/11, 72.7%), ground-glass opacity (5/11, 45.5%), pleural effusion (5/11, 45.5%), and micronodules (3/11, 27.3%). Four patients (36.4%) required mechanical ventilation; three survived but one died of multiple organ dysfunction syndrome (principally pneumonia and septic shock). Conclusions: R. planticola pneumonia occurred mainly in patients with underlying risk factors such as malignant disease, cerebral infarction or hemorrhage, and chronic obstructive pulmonary disease. The organism was sensitive to most antibiotics, and the clinical outcomes were favorable after empirical antibiotic therapy.

Background/Aims: Atopy is closely related to asthma and is a risk factor for the development and exacerbation of asthma. The aim of this study was to evaluate the association between exercise-induced asthma (EIA) and atopy in adult patients with asthma-like symptoms. Methods: Forty young male patients with asthma-like symptoms were enrolled. Skin prick, methacholine bronchial provocation, and exercise provocation tests were performed. Current and ex-smokers were excluded. Results: Exercise provocation tests were positive in 21 patients (52.5%). Airway hyperresponsiveness (AHR) to methacholine (85.7% vs. 42.1%, p = 0.007) and atopy (85.7% vs. 47.4, p = 0.017) was found more frequently in patients with EIA than in those without EIA. EIA was significantly associated with atopy score (16.5 ± 3.0 vs. 6.5 ± 2.0, p = 0.011), atopy index (2.1 ± 0.3 vs. 1.0 ± 0.3, p = 0.004), and positive responses to Dermatophagoides pteronyssinus (76.2% vs. 42.1%, p = 0.028) and Dermatophagoides farinae (76.2% vs. 36.8%, p = 0.012), but not with positive responses to pollen allergens. AHR to methacholine (odds ratio [OR]: 14.3, 95% confidence interval [CI]: 1.86-109.4) and atopy (OR: 16.9, 95% CI: 2.04-140.74) were significant risk factors for EIA. Conclusions: Atopy was a risk factor for EIA in young adult men, and sensitization to house dust mites was associated with EIA. (Korean J Med 2011;81:723-728)

The combination therapy of pegylated interferon and ribavirin is the mainstay of treatment for chronic hepatitis C patients. Anti-viral therapy is commonly associated with side effects such as headache, fever, myalgia, and arthralgia. However, anti-viral therapy can continue because these side effects are mostly mild and can be improved with supportive management. Anti-viral therapy should be stopped promptly if serious side effects, such as interstitial pneumonitis or hemolytic anemia occur, although those serious side effects are rare. There were a few case reports of interferon-related interstitial pneumonitis worldwide. In Korea, one atypical case report of interstitial pneumonitis has been reported, which followed the combination therapy of interferon-alpha and ribavirin in a patient with chronic hepatitis C. We present a case of interstitial pneumonitis and pancytopenia following the combination therapy of pegylated interferon and ribavirin in a patient with chronic hepatitis C.

Increased expression of a number of proinflammatory genes, including IL-8, is associated with inflammatory conditions such as asthma. Glucocorticoid receptor (GR)beta, one of the GR isoforms, has been suggested to be upregulated in asthma associated with glucocorticoid insensitivity and to work as a dominant negative inhibitor of wild type GRalpha. However, recent data suggest that GRbeta is not a dominant negative inhibitor of GRalpha in the transrepressive process and has its own functional role. We investigated the functional role of GRbeta expression in the suppressive effect of glucocorticoids on tumor necrosis factor (TNF)-alpha-induced IL-8 release in an airway epithelial cell line. GRbeta expression was induced by treatment of epithelial cells with either dexamethasone or TNF-alpha. GRbeta was able to inhibit glucocorticoid-induced transcriptional activation mediated by binding to glucocorticoid response elements (GREs). The suppressive effect of dexamethasone on TNF-alpha-induced IL-8 transcription was not affected by GRbeta overexpression, rather GRbeta had its own weak suppressive activity on TNF-alpha-induced IL-8 expression. Overall histone deacetylase activity and histone acetyltransferase activity were not changed by GRbeta overexpression, but TNF-alpha-induced histone H4 acetylation at the IL-8 promoter was decreased with GRbeta overexpression. This study suggests that GRbeta overexpression does not affect glucocorticoid-induced suppression of IL-8 expression in airway epithelial cells and GRbeta induces its own histone deacetylase activity around IL-8 promoter site.

Background : It is well known that the expression of Th2 cytokines are up-regulated in the atopic asthma. The study was to investigate the expression of transcription factors, such as GATA-3, c-maf, T-bet which are known to be involved in the T cell differentiation in the peripheral blood mononuclear cells (PBMCs) of atopic asthmatics. Methods : PBMCs were obtained from non-atopic controls and atopic asthmatics and cultured for 48 hours, and then 12-o-tetracanoylphorbol-13-acetate (PMA) and calcium ionophore (ionomycin) were added. mRNA of GATA-3, c-maf, T-bet, IL-4, IL-5, IL-13 and IFN- were measured by RT-PCR Results : mRNAs of Th2 cytokines, such as IL-4, IL-5 and IL-13 were expressed higher in the atopic asthmatics, and that of Th1 cytokine, IFN- was expressed higher in the non-atopic controls. GATA-3 and c-maf were expressed higher and T-bet was expressed lower in the atopic asthmatics. Expressions of GATA-3, c-maf and T-bet were not changed with the stimulation of PMA/Ionomycin. Conclusion : This study suggest that GATA-3, c-maf and T-bet participate in the Th2 type inflammation in atopic asthmatics, like GATA-3 and c-maf as stimulatory factors, and T-bet as inhibitory factor.