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Response of corneal epithelial cells to Staphylococcus aureus.

ABSTRACT: Staphylococcus aureus is a leading cause of invasive infection. It also infects wet mucosal tissues including the cornea and conjunctiva. Conflicting evidence exists on the expression of Toll-like receptors by human corneal epithelial cells. It was therefore of interest to determine how epithelial cells from this immune privileged tissue respond to S. aureus. Further, it was of interest to determine whether cytolytic toxins, with the potential to cause ion flux or potentially permit effector molecule movement across the target cell membrane, alter the response. Microarrays were used to globally assess the response of human corneal epithelial cells to S. aureus. A large increase in abundance of transcripts encoding the antimicrobial dendritic cell chemokine, CCL20, was observed. CCL20 release into the medium was detected, and this response was found to be largely TLR2 and NOD2 independent. Corneal epithelial cells also respond to S. aureus by increasing the intracellular abundance of mRNA for inflammatory mediators, transcription factors, and genes related to MAP kinase pathways, in ways similar to other cell types. The corneal epithelial cell response was surprisingly unaffected by toxin exposure. Toxin exposure did, however, induce a stress response. Although model toxigenic and non-toxigenic strains of S. aureus were employed in the present study, the results obtained were strikingly similar to those reported for stimulation of vaginal epithelial cells by clinical toxic shock toxin expressing isolates, demonstrating that the initial epithelial cellular responses to S. aureus are largely independent of strain as well as epithelial cell tissue source.

SUBMITTER: Heimer SR

PROVIDER: S-EPMC3073294 | biostudies-literature | 2010 Jul-Aug

REPOSITORIES: biostudies-literature

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Response of corneal epithelial cells to Staphylococcus aureus.

Heimer Susan R SR Yamada Ai A Russell Hugh H Gilmore Michael M

Virulence 20100701 4

Staphylococcus aureus is a leading cause of invasive infection. It also infects wet mucosal tissues including the cornea and conjunctiva. Conflicting evidence exists on the expression of Toll-like receptors by human corneal epithelial cells. It was therefore of interest to determine how epithelial cells from this immune privileged tissue respond to S. aureus. Further, it was of interest to determine whether cytolytic toxins, with the potential to cause ion flux or potentially permit effector mol ...[more]

PMID: 21178448

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Project description:Chronic rhinosinusitis (CRS) is an inflammatory disorder of the nose and paranasal sinuses. Staphylococcus aureus is increasingly linked with CRS exacerbations. Little is known about how bacteria activate inflammatory pathways that contribute to CRS.To develop an in vitro coculture system to explore how infection with S aureus stimulates innate immune responses of sinonasal epithelial cells (SNECs).Sinonasal epithelial cells were collected from 13 patients during endoscopic sinus surgery and grown in culture at the air-liquid interface from July 2014 through December 2014.Differentiated SNECs from control individuals, patients with CRS with nasal polyps (CRSwNPs), and patients with CRS without nasal polyps (CRSsNPs) were infected with S aureus at 3 different concentrations for 24 hours.Growth of S aureus and viability of SNECs were measured. Expression of inflammatory markers and innate immune genes was measured by reverse transcription-polymerase chain reaction. Basal secretion of interleukin 8 was determined by enzyme-linked immunosorbent assay.Cultured SNECs from patients with CRSsNPs demonstrated a significant increase (P?<?.05) in expression of interleukin 8 (23-fold to 82-fold) and tumor necrosis factor (11-fold to 61-fold) at all the tested concentrations of S aureus. Control or CRSwNP SNECs demonstrated a significant increase (P?<?.05) in expression of interleukin 8 (47-fold and 50-fold, respectively) and tumor necrosis factor (106-fold and 58-fold, respectively) at the higher inoculum of S aureus. Basal secretion of inflammatory markers correlated with expression changes. No significant changes in expression were observed for the helper T cell, subtype 2, inflammatory mediators tested.In this study, we developed a model to study early innate immune-mediated changes in SNECs cocultured at an air-liquid interface with bacteria. We also demonstrated that bacterial burden can be detected by SNECs in the absence of adaptive immune-mediated responses. The CRSsNP SNECs are more sensitive to S aureus burden than control or CRSwNP SNECs. Future studies will further develop this infection model and explore the SNEC innate immune response to bacteria.

Project description:Mastitis caused by Escherichia coli and Staphylococcus aureus is a major pathology of dairy cows. To better understand the differential response of the mammary gland to these two pathogens, we stimulated bovine mammary epithelial cells (bMEC) with either E. coli crude lipopolysaccharide (LPS) or with S. aureus culture supernatant (SaS) to compare the transcriptomic profiles of the initial bMEC response. By using HEK 293 reporter cells for pattern recognition receptors, the LPS preparation was found to stimulate TLR2 and TLR4 but not TLR5, Nod1 or Nod2, whereas SaS stimulated TLR2. Biochemical analysis revealed that lipoteichoic acid, protein A and ?-hemolysin were all present in SaS, and bMEC were found to be responsive to each of these molecules. Transcriptome profiling revealed a core innate immune response partly shared by LPS and SaS. However, LPS induced expression of a significant higher number of genes and the fold changes were of greater magnitude than those induced by SaS. Microarray data analysis suggests that the activation pathways and the early chemokine and cytokine production preceded the defense and stress responses. A major differential response was the activation of the type I IFN pathway by LPS but not by SaS. The higher upregulation of chemokines (Cxcl10, Ccl2, Ccl5 and Ccl20) that target mononuclear leucocytes by LPS than by SaS is likely to be related to the differential activation of the type I IFN pathway, and could induce a different profile of the initial recruitment of leucocytes. The MEC responses to the two stimuli were different, as LPS was associated with NF-?B and Fas signaling pathways, whereas SaS was associated with AP-1 and IL-17A signaling pathways. It is noteworthy that at the protein level secretion of TNF-? and IL-1? was not induced by either stimulus. These results suggest that the response of MEC to diffusible stimuli from E. coli and S. aureus contributes to the onset of the response with differential leucocyte recruitment and distinct inflammatory and innate immune reactions of the mammary gland to infection.

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Response of corneal epithelial cells to Staphylococcus aureus.

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Response of corneal epithelial cells to Staphylococcus aureus.

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