PURPOSE: Mycoplasama pneumoniae is a leading cause of pneumonia and exacerbates other respiratory conditions such as asthma. Surfactant protein A(SP-A) is involved in surfactant physiology and surfactant structure, and plays a major role in innate host defense and inflammatory processes in the lung. In this study, SP-A mediated mycoplasma cidal activity. The candidate-gene approach was used to study the association between the SP-A gene locus and Mycoplasama pneumoniae pneumonia in the genetically homogeneous Korean population. METHODS: PCR-cRFLP-based methodology was used to detect SP-A genotype. The forty nine children with Mycoplasama pneumoniae pneumonia were matched to 50 nomal neonates. RESULTS: The specific frequencies for the alleles of the SP-A1 and SP-A2 gene in the study population were:6A2=21 percent, 6A3=45 percent, 6A4=11 percent, 6A8=9 percent, 6A14=8 percent, 1A=11.3 percent, 1A0=38 percent, 1A1=12.7 percent, 1A2=9.2 percent, 1A5=15.5 percent, 1A7=2.9 percent, 1A8=4.9 percent, 1A9=2.2 percent, others=3.3 percent. The frequencies of specific genotypes such as 1A2 was higher than control group, significantly. CONCLUSION: 1A2 are susceptible factors for Mycoplasama pneumoniae pneumonia. We conclude that the SP-A gene locus(1A2) is an important determinant for predisposition to Mycoplasama pneumoniae pneumonia in children.
Alleles ; Asthma ; Child* ; Genotype ; Humans* ; Infant, Newborn ; Lung ; Mycoplasma pneumoniae* ; Mycoplasma* ; Physiology ; Pneumonia* ; Pneumonia, Mycoplasma* ; Pulmonary Surfactant-Associated Protein A

In order to investigate the effect of vitamin A (VA) on the secretion of IFN-gamma and IL-4 in Mycoplasma Pneumoniae (MP)-induced A549 cells, A549 cells were co-cultured with MP for different time lengths and then the levels of IFN-gamma and IL-4 in the cell culture supernatants were detected before and after treatment with different concentrations of VA by using the enzyme-linked immunosorbent assay (ELISA). The results showed that the level of IFN-gamma and IL-4 in the supernatants of MP-induced A549 cells was much higher than that in non-induced cells (P<0.01). After application of VA, IL-4 level was not increased until the concentration of VA was up to 0.5x10(-5) mol/L (P<0.01). However, with concentration of VA increased up to 1x10(-4) mol/L, IL-4 was significantly suppressed (P<0.01). It was concluded that MP could induce the secretion of IFN-gamma and IL-4 in A549 cells. VA could inhibit the secretion of IFN-gamma and increase the IL-4 level in MP-induced A549 cells. However, high concentration of VA had an inhibitory effect on the secretion of IL-4 as well as on the IFN-gamma. These data provided a theoretical basis for the application of VA in MP pneumonia in the clinical practice.
Cell Line, Tumor ; Coculture Techniques ; Culture Techniques ; Interferon-gamma/*secretion ; Interleukin-4/*secretion ; Lung Neoplasms/pathology ; Mycoplasma pneumoniae/growth & development ; Mycoplasma pneumoniae/*physiology ; Vitamin A/*pharmacology

OBJECTIVETo investigate the effect of annexin A2 (AnxA2) on epithelial growth factor receptor (EGFR)/nuclear factor-κB (NF-κB) signal transduction and mucin expression in human airway epithelial H292 cells treated with Mycoplasma pneumoniae (MP).

METHODSH292 cells were divided into control group, MP group, NC-siRNA+MP group, and AnxA2 siRNA+MP group. The cells in the MP group were incubated with 5 μg/mL MP antigen for 2 hours. The cells in the NC-siRNA+MP and AnxA2 siRNA+MP groups were transfected with NC-siRNA and AnxA2 siRNA for 24 hours, followed by MP antigen stimulation for 2 hours. The MTT method was used to measure cell viability; quantitative real-time PCR was used to measure the mRNA expression of AnxA2; Western blot was used to measure the protein expression of AnxA2, phosphorylated EGFR (p-EGFR), and phosphorylated p65 NF-κB (p-p65 NF-κB); ELISA was used to measure the secretion of mucin 5AC (MUC5AC) and mucin 5B (MUC5B).

RESULTSThe MP and NC-siRNA+MP groups had lower cell viability than the control group (P<0.05). The AnxA2 siRNA+MP group had higher cell viability than the MP and NC-siRNA+MP groups and lower cell viability than the control group (P<0.05). The MP and NC-siRNA+MP groups had significantly higher mRNA and protein expression of AnxA2 than the AnxA2 siRNA+MP group (P<0.05). Compared with the control group, the MP and NC-siRNA+MP groups had significant increases in the protein expression of p-EGFR, p-p65 NF-κB, MUC5AC, and MUC5B (P<0.05); the AnxA2 siRNA+MP group had lower protein expression than the MP and NC-siRNA+MP groups, but higher protein expression than the control group (P<0.05).

CONCLUSIONSAnxA2 is involved in the airway lesion induced by MP antigen via mediating EGFR/NF-κB signaling activation and mucin expression in human airway epithelial cells.

Annexin A2 ; physiology ; Bronchi ; physiology ; Cells, Cultured ; Epithelial Cells ; microbiology ; Humans ; Mucins ; analysis ; Mycoplasma pneumoniae ; pathogenicity ; NF-kappa B ; physiology ; Receptor, Epidermal Growth Factor ; physiology ; Signal Transduction ; physiology