Tobacco Smoke Mediated Induction of Sinonasal - Copy

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Tobacco Smoke Mediated

Induction of SinonasalMicrobial Biofilms

Natalia Goldstein-Daruech, Emily K. Cope, et all.

Department of Otorhinolaryngology, Head and Neck

Surgery, University of Pennsylvania, Philadelphia,

Pennsylvania, United States of America

Emanuel Yan Daniel

(08-063)

Rossy Apriani

(09-061)

Djuwita

(08-061)


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Abstract

Cigarette smokers and those exposed to second hand

smoke are more susceptible to life threatening infection

than nonsmokers.

Epidemiologic studies demonstrate a correlation

between tobacco smoke exposure and rhinosinusitis.

Although a common cause of CRS has not been defined,

bacterial presence within the nasal and paranasalsinuses is assumed to be contributory.


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Abstract

Bacteria isolated from patients with tobacco smokeexposure demonstrate robust in vitro biofilm

formation when challenged with tobacco smoke

compared to those isolated from smoke nave

patients.


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Introduction

Chronic rhinosinusitis (CRS) represents a spectrum of

inflammatory and infectious processes concurrently

affecting the nose and paranasal sinuses. (NataliaGoldstein-Daruech;2011)

CRS patients may have significant decrements in quality

of life.

Patients requiring sinus surgery demonstrate worsescores for physical pain and social functioning than those

suffering from chronic obstructive pulmonary

disease,congestive heart failure, back pain, or angina.


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Introduction

Inherent mucociliary defects such as found inpatients with cystic fibrosis or primary ciliary

dyskinesia, abnormal innate immunity, paranasal

sinus anatomic variations, environmental exposure,

allergy, and microbial colonization have all beenassociated with CRS. (Ke-Qing Zhao et all, 2011)


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Introduction

Biofilm-forming bacteria are thought to begin asindependent, planktonic bacteria which become

sessile and initiate biofilm formation by adhering to a

surface and forming microcolonies.

we report that repetitive in vitro exposure to whole

tobacco smoke induces biofilm formation in bacteria

isolated from the sinonasal cavities of patients with

CRS.


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Materials and Methods

Specimen collectionAdult patients (over 18 yo. Male and female) who

met the objective and subjective guidelines for CRS.

Patients were stratified based on past or present

tobacco use, and whether or not each lived with asmoker.

Sinonasal cultures were obtained from CRS patients

with mucopurulent sinonasal secretions.


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Materials and Methods

In vitro smoke exposureFreshly diluted cultures were placed with the lid offinto an airtight box (20 cm (l)620 cm (w)615 cm (h))with an inflow port at the top center, and a diffusermidway between the inflow port and the 96-well

plate.

Biofilm formation in the absence or presence ofexogenous tobacco smoke

To evaluate the degree to which tobacco smokeimpacts biofilm formation, bacterial cultures wereobtained from CRS patients, with and without

tobacco exposure


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Result

1. Biofilm formation in presence of tobacco smoke

2. Biofilm formation in 2 groups (comparison) :

a. Non-smoker isolated bacteria with tobacco

exposure

b. Smoker isolated bacteria without tobacco exposure


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Result


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Result

Ex vivo smoke exposure of bacteria obtained fromsmokers sinuses resulted in significantly more

induction of biofilm formation (ratio of 1.7560.31)

than that seen in bacteria from nonsmokers sinuses


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Tobacco Biofilm Index


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Discussion

Recent work has demonstrated that cigarettesmokers and those exposed to second handsmoke are more susceptible to life-threateninginfection than non-smokers and that smoking isan independent risk factor for pneumococcal

pneumonia, Legionnaires disease, periodontaldisease, and meningococcal disease, among others

Biofilm formation after repetitive smoke exposure.

Because a single smoke exposure resulted in

opposite effects on biofilm formation in bacteriaisolated from smoke nave patients vs. smoke-exposed patients, we hypothesized that chronic orrepetitive smoke exposure would alter the biofilmforming capacity of bacteria.


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Conclusion

In contrast to the data presented clinical isolatesfrom smokers had significant cigarette smoke

inhibition of biofilm formation after growth in the

absence of smoke for several days

Because a single smoke exposure resulted inopposite effects on biofilm formation in bacteria

isolated from smoke nave patients vs. smoke-

exposed patients, we hypothesized that chronic or

repetitive smoke exposure wouldalter the biofilmforming capacity of bacteria.


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