Open AccessLow-Dose Lipopolysaccharide Pretreatment Suppresses Choroidal Neovascularization via IL-10 Induction
Author(s) -
Naohiro Matsumura,
Motohiro Kamei,
Motokazu Tsujikawa,
Mihoko Suzuki,
Ping Xie,
Kohji Nishida
Publication year - 2012
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0039890
Subject(s) - choroidal neovascularization , lipopolysaccharide , macular degeneration , inflammation , medicine , immunology , pathogenesis , intraperitoneal injection , interleukin 10 , neovascularization , stat3 , cytokine , pharmacology , cancer research , biology , angiogenesis , phosphorylation , ophthalmology , biochemistry
Recent studies have suggested that some kinds of microbial infection may have a crucial role in the development of many diseases such as autoimmune diseases and certain types of cancer. It has been reported that some chronic infections, such as Chlamydia pneumoniae , and immunological dysfunctions are associated with age-related macular degeneration (AMD), a leading cause of blindness. To evaluate the association between systemic low-level inflammation induced by infection and AMD pathogenesis, we investigated whether intraperitoneal injection of lipopolysaccharide (LPS) can modulate the development of laser-induced choroidal neovascularization (CNV), a key feature of AMD. Contrary to our expectations, the sizes of CNV in mice with LPS pretreatment were approximately 65% smaller than those of the control mice. After LPS pretreatment, serum IL-10 concentration and IL-10 gene expression in peritoneal macrophages and in the posterior part of the eye increased. Peritoneal injection of anti-IL10 antibody reduced CNV suppression by LPS pretreatment. Moreover, adoptive transfer of the resident peritoneal macrophages from LPS-treated mice into control littermates resulted in an approximately 26% reduction in the size of CNV compared with PBS-treated mice. We concluded that CNV formation was suppressed by low-dose LPS pretreatment via IL-10 production by macrophages.