Interleukin-6 and Interleukin-8 Secretions by Polarized Airway Epithelial Cells Infected by Normal and Small-Colony Variant Staphylococcus aureus Strains are Similar Despite Differences in Infection Levels

Gabriel Mitchell,Myriame Lafrance,Brian G Talbot

doi:10.4172/2155-9597.1000122

Abstract

Staphylococcus aureus small-colony variants (SCVs) can efficiently infect non-professional phagocytes and are often referred to as facultative intracellular pathogens. The ability to hide and persist within host cells is likely to contribute to the development of chronic S. aureus infections such as those observed in the lungs of cystic fibrosis patients. Polarized human pulmonary Calu-3 cells were used to confirm that S. aureus small-colony variants (SCVs) persist within epithelial cells without exacerbating the innate immune response. Whereas all studied S. aureus strains significantly induced the secretion of Interleukin-6 (IL-6) and Interleukin-8 (IL-8) by Calu-3 cells 48 hours after cellular invasion, dead bacteria did not. Surprisingly, no difference in the secretion of these interleukins was detected between cells infected with normal and SCV strains despite the marked difference in infection levels. This study supports the hypothesis that despite their increased ability to persist inside epithelial cells, SCVs do not over activate the host immune response in comparison to normal strains. SCVs may thus help to perpetuate infection without exacerbation of the host immune response.

Highlights

Staphylococcus aureus small-colony variants (SCVs) can efficiently infect non-professional phagocytes and are often referred to as facultative intracellular pathogens
Strains forming pin-point colonies and called small-colony variants (SCVs) are often isolated from Staphylococcus aureus chronic infections such as those encountered in the lungs of cystic fibrosis (CF) patients and from osteomyelitis, septic arthritis and infections of orthopedic devices
The distinct virulence profile of SCVs may result from the inability of the bacteria to properly activate the accessory gene regulator quorum-sensing system and/or by a sustained activity of the alternative transcription factor sigma B [7,8,9]

Summary

Introduction

Staphylococcus aureus small-colony variants (SCVs) can efficiently infect non-professional phagocytes and are often referred to as facultative intracellular pathogens. It was demonstrated that normal S. aureus strains cause an inflammatory response in endothelial cells whereas SCVs did not [12].

Results

Conclusion