Clarithromycin Suppresses Chloride Channel Accessory 1 and Inhibits Interleukin-13-Induced Goblet Cell Hyperplasia in Human Bronchial Epithelial Cells.

Activation of the interleukin-13 (IL-13) receptor leads to signal transducer and activator of transcription 6 (STAT6) activation and subsequent induction of SAM pointed domain containing ETS transcription factor (SPDEF) and chloride channel accessory 1 (CLCA1), increasing secretion of the gel-forming mucin MUC5AC. Activation of the epidermal growth factor receptor (EGFR) also leads to MUC5AC production via extracellular signal-regulated kinase (ERK1/2). We examined the effect of clarithromycin IL-13 signaling leading to production.

Relapse of both small cell lung cancer and Lambert-Eaton myasthenic syndrome after a 13-year disease-free survival period.

Lambert-Eaton myasthenic syndrome (LEMS) is a paraneoplastic syndrome and only 3% of small cell lung carcinoma (SCLC) patients have LEMS. Moreover, the recurrence of SCLC after a disease-free survival (DFS) of more than 10 years is rare. We report a patient who had a recurrence of both SCLC and LEMS after a 13-year DFS period.

HO-1 inhibits IL-13-induced goblet cell hyperplasia associated with CLCA1 suppression in normal human bronchial epithelial cells.

Mucus hypersecretion and goblet cell hyperplasia are common features that characterize asthma. IL-13 increases mucin (MUC) 5AC, the major component of airway mucus, in airway epithelial cells. According to the literature, IL-13 receptor activation leads to STAT6 activation and consequent induction of chloride channel accessory 1 (CLCA1) gene expression, associated with the induction of MUC5AC.

High frequency of β-lactamase-negative, ampicillin-resistant strains of Haemophilus influenzae in patients with chronic bronchitis in Japan.

In Japan, the increasing incidence of β-lactum-resistant Haemophilus influenzae infections is of growing concern. We retrospectively studied whether the prevalence of β-lactamase-negative ampicillin-resistant strains of H. influenzae was influenced by chronic lung diseases.

[The preventive effect of 23-valent pneumococcal polysaccharide vaccine against drug-resistant Streptococcus pneumonia in patients with chronic respiratory disease].

Objective: To elucidate the preventive effect of 23-valent pneumococcal polysaccharide vaccine (PV) on drug-resistant Streptococcus pneumoniae.

Methodology: Participants (outpatients, over 60 years of age, and with chronic lung disease) were interviewed and divided into two groups: the PV-vaccinated group (n=722) and the non-vaccinated group (n=872). The antimicrobial susceptibility and the genotype of antibiotic-resistant genes among the isolated pneumococcal strains from sputum before and after vaccination were studied.