Abstract
Introduction: bacterial keratitis caused by Pseudomonas aeruginosa is one of the causes of blindness in the world, due to pathogenicity of the bacteria that can lead to corneal perforation. Studies on the protein annexin A1 (AnxA1) point it as one of the essential mediators in homeostasis of inflammation and ocular infections. However, there are no known reports of AnxA1 in keratitis. Objetive: to investigate the expression profile of AnxA1 in the P. aeruginosainduced keratitis model in two strains of mice (susceptible and pathogen resistant).Method: for the development of experimetal keratitis, the mice had their right eyes ulcerated and immediately inoculated with 5 μl of P. aeruginosa in PBS. The animals were euthanized after 24 hours of the bacteria inoculation. The eyes were clinically evaluated and histopathologically processed for quantitative analyses of the inflammatory infiltrate and immunohistochemical studies of the expressions of the AnxA1 and the receptor for formylated peptides (fpr2).Results: our results demonstrated a higher influx of inflammatory cells, mainly neutrophils in the susceptible animals (C57BL / 6) compared to those considered resistant (BALB / c) and controls. Immunohistochemical studies indicated weak expression of AnxA1 and fpr2 in the anterior epithelium and stroma of the cornea. However, after keratitis induction, overexpression of AnxA1 and fpr2 occurred in the corneas of both mice strains. Furthermore, greater expression of AnxA1 in the anterior corneal epithelium was observed in the C57BL / 6 animals.Conclusions: AnxA1 and fpr2 may be related to infectious keratitis induced by P.aeruginosa, which stimulates further investigations on the use of AnxA1 as a possible coadjuvant therapeutic strategy in bacterial keratitis.
Highlights
Bacterial keratitis is an important cause of visual loss and is frequently associated with changes in corneal defense mechanisms
Studies of the host’s immune response against P. aeruginosa show that the condition and development of the disease is related to the production of exoenzymes and other byproducts released from the bacterial proliferation [7,8] but the production of cytokines, some eicosanoids and other molecular mediators of the host are involved in ulceration and angiogenesis, contributing to stromal necrosis and corneal edema, during bacterial keratitis [9]
After antigenic recovery with citrate buffer pH 6.0 and blockade of the endogenous peroxidase activity, the sections were incubated with the following rabbit polyclonal primary antibodies: anti-annexin A1 (AnxA1) (1: 1000) (Invitrogen, Cat No: 71-3400) and anti-FPR2 (1:2000) (Invitrogen, Cat No: 72-0293), for 12 hours
Summary
Bacterial keratitis is an important cause of visual loss and is frequently associated with changes in corneal defense mechanisms. Amongst bacterial organisms capable of inducing keratitis, Pseudomonas aeruginosa (P. aeruginosa) stands out for its rapid propagation that causes ulcerations [3,4]. Studies of the host’s immune response against P. aeruginosa show that the condition and development of the disease is related to the production of exoenzymes and other byproducts released from the bacterial proliferation [7,8] but the production of cytokines, some eicosanoids and other molecular mediators of the host are involved in ulceration and angiogenesis, contributing to stromal necrosis and corneal edema, during bacterial keratitis [9]. Immunocompromised individuals are more vulnerable to P. aeruginosa in ocular trauma, systemic and ocular diseases [11,12,13]
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