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The role of atypical bacteria in chronic rhinosinusitis
Otolaryngology– Head and Neck Surgery Volume 131 Number 2
Research Posters P189
diaphorase, in the mucosa of the maxillary and sphenoidal sinus. Most abundant was inducible NOS. Conclusion: In this small study we found lower concentrations of NO in the sphenoidal sinus than the maxillary sinus. Significance: The concentration of NO, and the abundant presence of inducible NOS in the sphenoidal sinus in these nonallergic, noninfected patients will be discussed. Support: None reported.
R120
Staphylococcus Enterotoxin A Increases Proinflammatory Cytokine Release of Nasal Epithelial Cells Michael Damm, Quante,
MD;
MD
(presenter); Jakob Rosenbohm; Gero
Roland Riekmann; Jan A Sauer,
MD;
Joseph
Califano, MD Cologne Germany; Cologne Germany; Cologne Germany;
R119 The Role of Atypical Bacteria in Chronic Rhinosinusitis Raymond E Lee,
MD
(presenter); Sarita Kaza,
MD;
Gregory V.
Plano, PhD; Roy R Casiano, MD Miami Beach FL; Miami FL; Miami FL; Miami FL
Problem: Conflicting studies exist on the microbiology of chronic rhinosinusitis (CRS), but none identify atypical bacteria, owing to these bacteria’s fastidious nature. Atypical bacteria are common causes of pneumonia. However, their role in upper respiratory disease is less clear. Recently the polymerase chain reaction has been valuable in detecting aerobic and anaerobic bacteria, fungi, and viruses implicated in chronic rhinosinusitis. This study examines the role of atypical bacterial infection in CRS by utilizing the polymerase chain reaction. Methods: Eleven patients (8 males, 3 females) with CRS were prospectively enrolled. All failed medical therapy requiring endoscopic sinus surgery (ESS). Ethmoid sinus mucosa was processed by polymerase chain reaction (PCR) to identify the presence of Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella pneumophila. Also, intra-operative routine aerobic and anaerobic cultures were processed. The control group included 6 fresh corpses (3 males, 3 females) without evident sinus disease from the Miami-Dade County Medical Examiner. Their ethmoid mucosa was also obtained endoscopically and processed by PCR. Results: Of the 17 ethmoid mucosa samples (11 patients, 6 cadaver controls), 1 cadaver control was positive by PCR for M pneumoniae. All other samples were negative for M pneumoniae, C pneumoniae, and L pneumophila. The most common organism obtained from routine culture was coagulase negative staphylococci. Conclusion: Using highly sensitive PCR techniques, chronic rhinosinusitis mucosa did not reveal DNA from M pneumoniae, C pneumoniae, or L pneumophila. Atypical bacterial infection may not play a significant role in adult CRS. Significance: This study demonstrates that PCR is highly sensitive in detecting atypical bacteria and these bacteria are not identified in patients with CRS. Support: None reported.
Problem: Staphylococcus aureus enterotoxins (SE) are discussed as etiologic factors in chronic rhinosinusitis (CRS). The aim of this study was to evaluate the effects of SE-type-A (SEA) stimulation on proinflammatory cytokine/chemokine release in a primary nasal epithelial cell culture model. Methods: Mucosa specimens of 14 subjects with CRS and 11 subjects undergoing septal surgery without CRS (controls) were used to isolate and culture nasal epithelial cells. Nasal epithelial cell cultures were stimulated under controlled conditions. Protein concentrations of interleukin-(IL)-6 and IL-8 were measured by ELISA prior (T0) and after the 24h stimulation with SEA (T1). Data were analyzed by using ANOVA for repeated measurements (within subject factor “stimulation,” for T0 vs T1; and between subject factor “group,” for CRS vs controls). Results: At T0, controls contained significant higher levels of IL-6 (56.2 pg/mL) and IL-8 (7.09 ng/mL) compared to CRS (IL-6 20.0 pg/mL; IL-8: 3.5 ng/mL; P ⬍ 0.05). After stimulation with SEA a significant increase of IL-8 (P ⫽ 0.024) and IL-6 (P ⬍ 0.1) was observed in both groups. The factor “group” had no significant effect on the cytokine release. Conclusion: Cultured nasal epithelial cells from CRS patients released significant lower levels of IL-6 and IL-8 compared to healthy controls in vitro. IL-6 (antibody production) and IL-8 (neutrophil chemotaxis) are thought to be expressed by nasal epithelial cells for mucosal protection. Transferred to the in vivo situation, our data suggest that lower releases of these IL-6 and IL-8 from epithelia in CRS may result in an impaired defense of nasal mucosa. SEA increases IL-6 and IL-8 expression significantly without statistical differences between the study groups. Therefore it seems unlikely that the pathophysiological role of SEA for CRS is mediated by epithelial cells alone. Significance: This is the first study evaluating the effects of enterotoxins on nasal epithelia. Our findings are helpful for a better understanding of the role of the most common cultured pathogen in the nose. Support: This study was supported by the Deutsche Forschungsgemeinschaft (DFG) within Collaborative Research Center 419 (SFB419) of the University of Cologne.
POSTERS
Cologne Germany; Cologne Germany; Baltimore MD
Research Posters P189
diaphorase, in the mucosa of the maxillary and sphenoidal sinus. Most abundant was inducible NOS. Conclusion: In this small study we found lower concentrations of NO in the sphenoidal sinus than the maxillary sinus. Significance: The concentration of NO, and the abundant presence of inducible NOS in the sphenoidal sinus in these nonallergic, noninfected patients will be discussed. Support: None reported.
R120
Staphylococcus Enterotoxin A Increases Proinflammatory Cytokine Release of Nasal Epithelial Cells Michael Damm, Quante,
MD;
MD
(presenter); Jakob Rosenbohm; Gero
Roland Riekmann; Jan A Sauer,
MD;
Joseph
Califano, MD Cologne Germany; Cologne Germany; Cologne Germany;
R119 The Role of Atypical Bacteria in Chronic Rhinosinusitis Raymond E Lee,
MD
(presenter); Sarita Kaza,
MD;
Gregory V.
Plano, PhD; Roy R Casiano, MD Miami Beach FL; Miami FL; Miami FL; Miami FL
Problem: Conflicting studies exist on the microbiology of chronic rhinosinusitis (CRS), but none identify atypical bacteria, owing to these bacteria’s fastidious nature. Atypical bacteria are common causes of pneumonia. However, their role in upper respiratory disease is less clear. Recently the polymerase chain reaction has been valuable in detecting aerobic and anaerobic bacteria, fungi, and viruses implicated in chronic rhinosinusitis. This study examines the role of atypical bacterial infection in CRS by utilizing the polymerase chain reaction. Methods: Eleven patients (8 males, 3 females) with CRS were prospectively enrolled. All failed medical therapy requiring endoscopic sinus surgery (ESS). Ethmoid sinus mucosa was processed by polymerase chain reaction (PCR) to identify the presence of Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella pneumophila. Also, intra-operative routine aerobic and anaerobic cultures were processed. The control group included 6 fresh corpses (3 males, 3 females) without evident sinus disease from the Miami-Dade County Medical Examiner. Their ethmoid mucosa was also obtained endoscopically and processed by PCR. Results: Of the 17 ethmoid mucosa samples (11 patients, 6 cadaver controls), 1 cadaver control was positive by PCR for M pneumoniae. All other samples were negative for M pneumoniae, C pneumoniae, and L pneumophila. The most common organism obtained from routine culture was coagulase negative staphylococci. Conclusion: Using highly sensitive PCR techniques, chronic rhinosinusitis mucosa did not reveal DNA from M pneumoniae, C pneumoniae, or L pneumophila. Atypical bacterial infection may not play a significant role in adult CRS. Significance: This study demonstrates that PCR is highly sensitive in detecting atypical bacteria and these bacteria are not identified in patients with CRS. Support: None reported.
Problem: Staphylococcus aureus enterotoxins (SE) are discussed as etiologic factors in chronic rhinosinusitis (CRS). The aim of this study was to evaluate the effects of SE-type-A (SEA) stimulation on proinflammatory cytokine/chemokine release in a primary nasal epithelial cell culture model. Methods: Mucosa specimens of 14 subjects with CRS and 11 subjects undergoing septal surgery without CRS (controls) were used to isolate and culture nasal epithelial cells. Nasal epithelial cell cultures were stimulated under controlled conditions. Protein concentrations of interleukin-(IL)-6 and IL-8 were measured by ELISA prior (T0) and after the 24h stimulation with SEA (T1). Data were analyzed by using ANOVA for repeated measurements (within subject factor “stimulation,” for T0 vs T1; and between subject factor “group,” for CRS vs controls). Results: At T0, controls contained significant higher levels of IL-6 (56.2 pg/mL) and IL-8 (7.09 ng/mL) compared to CRS (IL-6 20.0 pg/mL; IL-8: 3.5 ng/mL; P ⬍ 0.05). After stimulation with SEA a significant increase of IL-8 (P ⫽ 0.024) and IL-6 (P ⬍ 0.1) was observed in both groups. The factor “group” had no significant effect on the cytokine release. Conclusion: Cultured nasal epithelial cells from CRS patients released significant lower levels of IL-6 and IL-8 compared to healthy controls in vitro. IL-6 (antibody production) and IL-8 (neutrophil chemotaxis) are thought to be expressed by nasal epithelial cells for mucosal protection. Transferred to the in vivo situation, our data suggest that lower releases of these IL-6 and IL-8 from epithelia in CRS may result in an impaired defense of nasal mucosa. SEA increases IL-6 and IL-8 expression significantly without statistical differences between the study groups. Therefore it seems unlikely that the pathophysiological role of SEA for CRS is mediated by epithelial cells alone. Significance: This is the first study evaluating the effects of enterotoxins on nasal epithelia. Our findings are helpful for a better understanding of the role of the most common cultured pathogen in the nose. Support: This study was supported by the Deutsche Forschungsgemeinschaft (DFG) within Collaborative Research Center 419 (SFB419) of the University of Cologne.
POSTERS
Cologne Germany; Cologne Germany; Baltimore MD