scholarly journals The Complement System Plays a Critical Role in the Development of Experimental Autoimmune Anterior Uveitis

2006 ◽  
Vol 47 (3) ◽  
pp. 1030 ◽  
Author(s):  
Purushottam Jha ◽  
Jeong-Hyeon Sohn ◽  
Qin Xu ◽  
Hiroki Nishihori ◽  
Yali Wang ◽  
...  
1995 ◽  
Vol 14 (8) ◽  
pp. 703-710 ◽  
Author(s):  
Mike C. Kim ◽  
Nisreen H. Kabeer ◽  
Michael T. Tandhasetti ◽  
Henry J. Kaplan ◽  
Nalini S. Bora

2010 ◽  
Vol 248 (12) ◽  
pp. 1737-1747 ◽  
Author(s):  
Po-Ting Yeh ◽  
Feng-An Lin ◽  
Chang-Pin Lin ◽  
Chung-May Yang ◽  
Muh-Shy Chen ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
I-Mo Fang ◽  
Chang-Hao Yang ◽  
Chung-May Yang

We investigated the protective effects and mechanisms of chitosan oligosaccharides (COS) on experimental autoimmune anterior uveitis (EAAU) in rats. EAAU was induced in Lewis rats by footpad and intraperitoneal injections of melanin-associated antigen. The rats received intraperitoneal injections of low-dose (5 mg/kg) or high-dose (10 mg/kg) COS or PBS daily after the immunization. The effects of COS were evaluated by determining the clinical scores and the morphology of the iris/ciliary body (ICB). The expression of inflammatory mediators was evaluated using western blot, immunofluorescence, and ELISA. Treatment with COS significantly attenuated the clinical scores and the leukocyte infiltration in the ICB in a dose-dependent manner. COS effectively reduced the expression of inflammatory mediators (TNF-α, iNOS, MCP-1, RANTES, fractalkine, and ICAM-1). Moreover, COS decreased the IκB degradation and p65 presence in the ICB, which resulted in the inhibition of NF-κB/DNA binding activity. In an in vitro study, sensitized spleen-derived lymphocytes of the COS-treated group showed less chemotaxis toward their aqueous humor and decreased secretion of the above inflammatory mediators in the culture media. COS treated EAAU by inhibiting the activation of NF-κB and reducing the expression of inflammatory mediators. COS might be a potential treatment for acute anterior uveitis.


2021 ◽  
Vol 15 ◽  
Author(s):  
Noriko Shinjyo ◽  
Wataru Kagaya ◽  
Marcela Pekna

As part of the innate immune system, complement plays a critical role in the elimination of pathogens and mobilization of cellular immune responses. In the central nervous system (CNS), many complement proteins are locally produced and regulate nervous system development and physiological processes such as neural plasticity. However, aberrant complement activation has been implicated in neurodegeneration, including Alzheimer’s disease. There is a growing list of pathogens that have been shown to interact with the complement system in the brain but the short- and long-term consequences of infection-induced complement activation for neuronal functioning are largely elusive. Available evidence suggests that the infection-induced complement activation could be protective or harmful, depending on the context. Here we summarize how various infectious agents, including bacteria (e.g., Streptococcus spp.), viruses (e.g., HIV and measles virus), fungi (e.g., Candida spp.), parasites (e.g., Toxoplasma gondii and Plasmodium spp.), and prion proteins activate and manipulate the complement system in the CNS. We also discuss the potential mechanisms by which the interaction between the infectious agents and the complement system can play a role in neurodegeneration and dementia.


2007 ◽  
Vol 48 (11) ◽  
pp. 5091 ◽  
Author(s):  
Purushottam Jha ◽  
Bharati Matta ◽  
Valeriy Lyzogubov ◽  
Ruslana Tytarenko ◽  
Puran S. Bora ◽  
...  

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