Gene expression of pro-inflammatory cytokines and chemokines in mouse eye infected with Pseudomonas aeruginosa.
Ocular infection with Pseudomonas aeruginosa triggers extensive host inflammatory response and corneal damage. The purpose of present study was to investigate the gene expression of pro-inflammatory mediators interleukin (IL)-1 beta, IL-6, tumour necrosis factor-alpha (TNF-alpha),macrophage inflammatory protein (MIP)-2 and cytokine-induced neutrophil chemoattractant (KC) in the mouse eye challenged with P. aeruginosa. Scratched mouse corneas were infected with three phenotypes of P. aeruginosa individually. Total RNA was extracted from mouse eyes at 4 h, 8 h,16 h and 24 h post-challenge. Single stranded cDNA was synthesized from total RNA by reverse transcription and then subjected to polymerase chain reaction (PCR) using specific primers for IL-1 beta, IL-6, TNF-alpha, MIP-2 and KC. Results revealed three patterns of cytokines and chemokines expression in response to ocular infection with three phenotypes of P. aeruginosa. Ocular infection with the invasive strain induced the highest levels of IL-1 beta, IL-6, MIP-2 and KC mRNA, followed by the infection with the cytotoxic strain. Ocular infection with the CLARE strain induced the lowest levels of IL-1 beta, IL-6, MIP-2 and KC mRNA. The expression of TNF-alpha mRNA was very low and irregular following P. aeruginosa challenge. These data indicate that over-expression of pro-inflammatory cytokines and chemokines may represent a vigorous immune response and therefore may contribute to corneal damage during P. aeruginosa infection.
Xue
Mei-Lang
ML
Cooperative Research Centre For Eye Research and Technology, School of Optometry, University of New South Wales, Sydney, New South Wales, Australia. Mxue@crcert.unsw.edu.au
Thakur
Archana
A
Willcox
Mark
M
D000818:Animals; D054426:Chemokine CXCL2; D018925:Chemokines / Q000096:biosynthesis / Q000235:genetics*; D003315:Cornea / Q000382:microbiology; D003320:Corneal Ulcer / Q000235:genetics* / Q000378:metabolism / Q000382:microbiology; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics*; D015818:Eye Infections, Bacterial / Q000235:genetics* / Q000378:metabolism / Q000382:microbiology; D005260:Female; D015870:Gene Expression / Q000502:physiology*; D007375:Interleukin-1 / Q000096:biosynthesis / Q000235:genetics; D015850:Interleukin-6 / Q000096:biosynthesis / Q000235:genetics; D016209:Interleukin-8 / Q000096:biosynthesis / Q000235:genetics; D051379:Mice; D008807:Mice, Inbred BALB C; D023421:Models, Animal; D015846:Monokines / Q000096:biosynthesis / Q000235:genetics; D011552:Pseudomonas Infections / Q000235:genetics* / Q000378:metabolism / Q000382:microbiology; D011550:Pseudomonas aeruginosa / Q000502:physiology; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics
D054426:Chemokine CXCL2; D018925:Chemokines; D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D015846:Monokines; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha