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CUI LI, Sharon A McClellan, Ronald P Barrett, Linda D Hazlett; The role of IL-17 in resistance to Pseudomonas aeruginosa infection. Invest. Ophthalmol. Vis. Sci. 2014;55(13):6284.
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To explore the role of IL-17 as a stimulator of anti-inflammatory macrophages, phagocytosis of apoptotic PMN, and in innate immunity to Pseudomonas aeruginosa infection in resistant mice.
Normal and infected corneal IL-17 mRNA and protein levels were tested in susceptible C57BL/6 (B6) and resistant BALB/c mice. Immunohistochemistry (IHC) localized MerTk+ macrophages in both groups after infection. BALB/c mice also were injected with recombinant mouse (rm) IL-17, infected and clinical score, PMN infiltrate, and gene and protein expression of pro- and anti-inflammatory mediators tested by RT-PCR and ELISA.
IL-17 mRNA and protein were disparately upregulated in B6 (more) vs BALB/c (less) cornea after infection. Similar, but few MerTk+ cells were present in B6 and BALB/c cornea at 1 day p.i.; significantly more cells were seen in BALB/c cornea at 3 days p.i., and in B6 at 5 days p.i. rmIL-17-treated infected BALB/c mice exhibited no difference in PMN infiltrate at 3 or 5 days p.i., but mRNA levels for MIP-2, IL-1β, IL-23, MIP-1α, TNF-α, IL-6, TLR2, TLR4, NLRP3, and MMP-9 were reduced, with elevated Foxp3. Anti-inflammatory mediators, IL-10 (significantly) and ST2 (not significant), were downregulated, while SIGIRR and β-defensin-2 were upregulated (neither significantly). IL-1β protein levels did not change significantly between the two groups, but MIP-2 was decreased significantly at 5 days p.i. in rmIL-17 injected mice.
These data provide evidence that exogenous IL-17 in a resistant mouse disrupts the balance of pro- and anti-inflammatory mediators, but does not shift the disease response to susceptibility/perforation as expected.
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