Bacteriological study on adult chronic sinusitis operated after endoscopic sinus surgery / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To explore the bacteria isolated from middle nasal meatus, maxillary sinus, ethmoid sinus and postoperative cavity of patients with chronic rhinosinusitis and their characteristics of antibiotic resistance.</p><p><b>METHODS</b>Eighty-seven patients with chronic rhinosinusitis were operated on by ESS to obtain the pus specimen for bacterial culture and antibiotic susceptibility test, before and 1 month, 3 months and 6 months after operation.</p><p><b>RESULTS</b>Totally 645 strains (26 species) of bacteria were detected in 464 specimens [total positive rate was 78.9% (366/464)], in which aerobic bacteria was 95.3% (615/645). Gram negative bacteria and gram positive bacteria were 51.2% (330/645) and 48.8% (315/645), respectively. There was supernumerary tendency in detectable rate of gram negative bacteria isolated from postoperative groups. The main pathogens of postoperative patients were gram negative bacteria, with Enterobacter aerogenes, Pseudomonas aeruginosa and Hemophilus influenza occupying the first 3 places. The detectable rate of multiple drug resistance bacteria in postoperative group was much higher than preoperative groups, in which gram negative bacteria was the most, especially for Pseudomonas aeruginosa. There was significant difference in beta-lactamase detectable rate of the bacteria isolated from the delayed recovery group and the preoperative group (chi2 = 4.85, P < 0.05), Enterobacteriaceae occupied the first place among the beta-lactamase detectable bacteria isolated from the delayed recovery group. There was no significant difference in detectable rate of kinds of bacteria isolated from recovery group and control group.</p><p><b>CONCLUSIONS</b>The main pathogens of patients with chronic rhinosinusitis are multiple drug resistance gram negative bacteria after operation, in which Pseudomonas aeruginosa occupies the first place. Gram negative bacteria are becoming the main opportunity pathogenic bacteria, which shows antibiotic resistance. microbial population of postoperative cavity from recovery group are becoming balanced.</p>

Correlation of cyclooxygenase 2 with upstream mitogen-activated protein kinase, nuclear factor kappa B signal transduction pathway in middle turbinate mucosa of chronic rhinosinusitis / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To detect the expression and correlation of cyclooxygenase 2 (COX-2)and key enzymes both of mitogen activated protein kinase (MAPK) and nuclear factor-kappa B( NF-KB) pathways in middle turbinate mucosa of chronic rhinosinusitis (CRS) and to investigate their roles in CRS pathogenesis.</p><p><b>METHODS</b>Twenty-four lateral mucosa of CRS middle turbinates were equally divided into 3 groups according to FESS-97 Haikou criterion (CRS type I stage 2 in group 1, type II stage 2 in group 2, and type III in group 3), and 8 normal mucosa were enrolled as control. Immunohistochemistry and fluorescent real time quantitative polymerase chain reaction (FQ-RT-PCR) were performed to detect the expression of COX-2, ERK, p38MAPK, JNK and NF-kappaB subunits. The correlations between cox-2 and MAPK, NF-kappaB pathway were statistically treated by Pearson test.</p><p><b>RESULTS</b>Positive expressions of COX-2, ERK, p38MAPK and NF-kappaB subunits were detected in CRS groups, which were stronger than those in control group, by immunohistochemistry and FQ-RT-PCR (P < 0.05). Statistic difference was not found among CRS groups (P > 0.05). Negative expression of JNK was detected in all groups. Significantly positive correlation between protein and RNA expression of COX-2,ERK,p38MAPK and NF-kappaB subunits in each CRS group was confirmed by Pearson correlation treatment (P < 0.05). Significantly positive correlation of protein and RNA expression between COX-2 and ERK, p38MAPK in same CRS group was also founded (P < 0.05). The expression of COX-2 and the nucleic expression of NF-kappaB subunits in same CRS group was proved to be positively correlated (P < 0.05).</p><p><b>CONCLUSIONS</b>Upregulated expression of COX-2 is correlated with upstream ERK, p38MAPK and NF-kappaB pathway in CRS. It indicates the involvement of ERK, p38MAPK and NF-kappaB signal transduction pathway in regulation of COX-2 in CRS.</p>

Expression and significance of toll like receptor 4 mRNA and nuclear factor-kappaB p50 mRNA in human normal nasal mucosa after stimulation by lipopolysaccharide / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To investigate the expression and significance of Toll like receptor (TLR)4 mRNA and nuclear factor (NF)-kappaB p50 mRNA in human normal nasal mucosal cell before and after stimulation by LPS.</p><p><b>METHODS</b>The tissue was obtained from 15 normal middle turbinates (without rhinosinusitis). Every tissue was cultured in vitro, divided into 2 specimens. LPS was added into 15 specimens as LPS group and not added into other 15 specimens as control group. The pathomorphological characters of nasal mucosal cells were observed under optical microscope after stimulation by LPS. The expression of TLR4 mRNA and NF-kappaB p50 mRNA in normal human nasal mucosal cells were evaluated by in situ hybridization.</p><p><b>RESULTS</b>Normal mucociliary agglutinated and mucosal cells were enlarged after stimulation by LPS; The expression of TLR4 mRNA in LPS group was higher than control group obviously. Their average density of light was 1.283 +/- 0.027 in LPS group while 0.538 +/- 0.038 in control group, and there was statistical significance between the two groups (t = 1.761, P < 0.05). The expression of NF-kappaB p50 mRNA was higher than control group obviously, and expressed in cellular nucleus predominantly. Their average density of light was 1. 668 +/- 0.037 in LPS group while 0. 372 +/- 0.052 in control group, and there was statistical significance between the two groups (t = 2. 624, P < 0. 01).</p><p><b>CONCLUSIONS</b>LPS can activate the NF-kappaB p50 of human nasal mucosal cells through TLR4, and it may play some roles in stimulating and damage effect induced by LPS in nasal mucosal cells.</p>