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Professional fluoride treatments have long been an important part of a thorough dental health regimen for children and adolescents but, with a growing shift towards preventative dentistry, more adults are reaping the benefits of fluoride.
Fluoride is a naturally occurring mineral found in our water, air, soil, and food that, when applied to the teeth, helps prevent oral decay and disease in several ways. Cavities have a host of causes that do not discriminate based on age, but there are several risk factors for dental decay that are often unique to adults, including tobacco or alcohol use and the regular ingestion of medications that cause dry mouth.
Your dentist can help you determine whether professional fluoride applications should be a part of your individualized dental health plan by evaluating your degree of risk for tooth decay and disease. What you might not be aware of, however, is that there are safe and effective options available for you to increase your testosterone level without compromising the health and well being of the rest of your body! Testosterone is a naturally occurring steroid hormone that not only promotes bone density and muscle growth, but also produces sperm in testes. When some hear Testosterone Replacement Therapy (TRT) they automatically equate it to bodybuilding or fear that they are going to get instantly ripped as if they were “that guy” in the gym. Some of the main differences include legal distinctions, medical diagnosis, management of side-effects, and the individual’s reason for taking the drug.
Many “steroid abusers” use the same medication (testosterone cypionate) as is commonly used in TRT.
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Functionally active complement system and complement regulatory proteins are present in the normal human and rodent eye. Complement systemComplement has long been recognized as a critical component of the innate immune system [1a€“6]. CRegs can be broadly categorized into two classesa€”membrane-bound CRegs and soluble CRegs (Fig.A 1). Role of complement in the protection of the normal eyeIt is important that we discuss the role of complement and CRegs in ocular protection under normal conditions before discussing their importance in ocular pathology. Role of complement in corneal diseaseThe cornea is constantly exposed to various physical as well as immunological insults.
Role of complement in autoimmune uveitisUveitis, the inflammation of the uveal tract, can be classified anatomically as anterior, intermediate, posterior, or diffuse (panuveitis) depending on the segment of the eye that is affected. Clinical and histologic pictures of rat eye during different stages of experimental autoimmune anterior uveitis (EAAU). When considering anti-complement therapy, we cannot ignore the role of CRegs in the resolution of autoimmune uveitis. Role of complement in age-related macular degenerationAge-related macular degeneration (AMD) is the most common cause of legal blindness worldwide among the elderly over the age of 50. Using the mouse model of laser-induced CNV, we observed that the CH50 levels in the serum of lasered mice varied when compared to non-lasered mice [93, 94]. Conclusions and clinical implicationsDuring the last decade, a lot of progress has been made to understand the pathophysiology of corneal diseases, uveitis, and macular degeneration.
This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. In fact, a recent study demonstrated that a prevention based dental care plan, including fluoride treatments, reduced the need for adult fillings by over 30%. First, fluoride helps strengthen your teeth’s enamel, the hard outer layer that protects the sensitive inner layers from decay and erosion. Typically, an experienced dental hygienist will apply it with a swab or brush, or it can be placed in a tray that is held in the patient’s mouth for a few minutes. Each patient’s degree of risk is based on a number of factors, including diet, medical history, and saliva flow.
And you know that the constant fatigue you’ve been experiencing, your frustratingly-low libido, and your recurrent onslaught of sudden crankiness towards those you love the most probably have a lot to do with having low testosterone levels.
Perhaps the biggest myth is that choosing testoste­­­rone replacement therapy to increase testosterone levels will produce exactly the same side effects as abusing steroids. The difference is in the goals and purpose of therapy, and most importantly, in the way the big picture is managed. Following medically valid diagnostic tests to determine if there is indeed a deficiency in one’s testosterone level, hormone replacement therapy is then used for medical purposes – to treat a deficiency of testosterone brought about by any number of reasons. Some of these include: disease of the liver or spleen, high blood pressure, increased cholesterol, blood clots, and heart disease.
Make sure that when you choose someone to help you with your Low T symptoms, you select someone with the knowledge and expertise to improve your quality of life while ALSO keeping you safe. It’s not just about knowing which medication to use, but how to best promote overall health while optimizing testosterone levels.
Complement activation and its regulation by ocular complement regulatory proteins contribute to the pathology of various ocular diseases including keratitis, uveitis and age-related macular degeneration. It comprises of soluble and surface proteins that play a central role in host defense against infection and in the modulation of antigen-specific immune and inflammatory responses [4, 5]. Membrane-bound CRegs (Fig.A 1) include decay-accelerating factor (DAF, CD55), membrane co-factor protein (MCP, CD46), complement receptor 1 (CR1, CD35), and membrane inhibitor of reactive lysis (MIRL, CD59). As mentioned above, the eye is an immune-privileged organ [31] and is highly vulnerable to various immunological insults. Indeed the normal cornea is well equipped to protect itself from these insults and has been shown to possess functional complement activity [39a€“46]. The figure shows immunofluorescent staining for Crry (a) and CD59 (b) in the cornea of naive Lewis rat. Each year, approximately 17% of active uveitis patients experience some degree of vision loss [52].
No inflammation could be detected in the iris (I) and the ciliary body (CB) after clinical (a) and histologic (d) examination at day 8 post immunization (before the onset of EAAU).
We have demonstrated that the functionally active CRegs downregulate intraocular complement activation and are critical to protect the ocular tissues from complement-mediated damage during EAAU [63].
Laser photocoagulation results in complement activation and MAC formation in the posterior segment of the eye.
Another study demonstrated that the plasma complement C3a des Arg levels increased in AMD patients compared to controls [98].
Specifically, the studies defining the role of the complement system in ocular diseases have drawn a lot of attention. This work was supported in part by EY014623, EY016205, Research to Prevent Blindness NY, Pat & Willard Walker Eye Research Center, Jones Eye Institute and Arkansas Master Tobacco Settlement and Arkansas Biosciences Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA. In this article, we’ll provide a bit of background on fluoride and discuss how it can benefit your teeth. Fluoride also attacks the acid-producing bacteria in your mouth and makes it harder for that bad bacteria, which promotes cavities, to stick to your teeth.
Once the treatment is complete, you may be asked to avoid food and drink for thirty minutes, which will allow your teeth to fully absorb the fluoride.
That’s why routine fluoride treatments for adults, particularly those already suffering from a few dental problems, are becoming more common. To find out if your pearly whites could benefit from professional fluoride treatments, consult one of our knowledgable team members today. You should speak with your personal health care provider before making any changes in your medical treatment and follow their instructions for care.
The classical pathway can be activated by antigen-antibody complexes or by substances such a C-reactive protein.
DAF, a glycosylphosphatidylinositol (GPI)-anchored protein prevents the activation of the complement system by inhibiting the formation of C3 and C5 convertases of both the classical and alternative pathways and accelerating the decay of these convertases [9, 10]. Therefore, it is not surprising that the complement system, which represents the first line of defense, plays an important part not only in protecting the eye from immunological insults but also in maintaining the immune-privileged state of the eye. In addition, low levels of C3, C3 split products, and MAC were detected in the normal cornea [32, 39, 46].
Uveitis may be idiopathic, associated with systemic diseases such as BehA§eta€™s disease, and Vogta€“Koyanagia€“Harada disease or resulting from a variety of infectious agents.
At the peak of disease (day 19 post immunization) the anterior chamber (AC) appeared cloudy and opaque due to the presence of proteinaceous material and inflammatory cells (b). We observed that various CRegs were upregulated during the course of EAAU on the resident ocular tissue and this upregulation was not due to the infiltrating inflammatory cells because the levels of CRegs remained upregulated after the resolution of the disease when all the infiltrating cells were cleared from the anterior segment of the eye [63]. In AMD, there is a progressive destruction of the macula leading to the loss of central vision. MAC is a complex assembly of C5b to C9 components with multimers of C9 forming a pore in the cell membrane.


It is an exciting area for future investigations and the basic questions such as what triggers the complement activation and which specific pathway is involved in corneal diseases, uveitis and macular degeneration need to be addressed.
Saunders, Philadelphia, pp 219a€“2712.Jha P, Bora PS, Bora NS (2007) The role of complement system in ocular diseases including uveitis and macular degeneration. Finally, fluoride has healing properties that can repair teeth that are in the early stages of dental disease. The information provided by Testosterone Centers of Texas is publicly available and cannot be considered complete nor is it intended to diagnose, or direct treatment for, any medical condition. Recombinant forms of the naturally occurring complement regulatory proteins have been exploited in the animal models for treatment of these ocular diseases. The complement system can be activated by three proteolytic cascades namely, the classical, the alternative, and the lectin pathways (Fig.A 1). However, DAF does not irreversibly inactivate C3b and C4b and, after interaction with DAF, these molecules still possess cytolytic activity.
Our results and several other independent studies have demonstrated the presence of various components of the complement system in the normal eye [2, 32a€“37]. This observation further proves that low level of complement activation is taking place in the normal cornea since complement activation is necessary for the generation of these products. Inflammation resulting from uveitis may lead to conditions like cataract, glaucoma, and cystoid macular edema that may cause irreversible vision loss. Histopathologic picture of rat eye at the peak of EAAU (e) revealed severe inflammation of the iris (I) and ciliary body (CB).
Furthermore, when the function or expression of CRegs was inhibited in vivo, more severe EAAU with early onset and delayed resolution was observed. This causes increased release of growth factorsa€”VEGF, TGFI?2, and I?-FGFa€”which in turn leads to the development of CNV. Thus systemic activation of the complement system may also contribute to the pathogenesis of AMD.Currently, several different approaches are being used to treat wet AMD in humans [99].
This understanding will help us to develop better therapies for ocular diseases in the future so that blindness could be prevented.The evidence derived from the studies reviewed here supports the concept that recombinant complement regulatory proteins may be therapeutically useful in the prevention of ocular tissue damage and in the treatment of various ocular diseases.
It is hoped that in the future recombinant complement regulatory proteins will be used as novel therapeutic agents in the clinic for the treatment of keratitis, uveitis, and age-related macular degeneration. Although the initial signal for the activation of each cascade differs, complement activation via these pathways triggers a sequence of biologic reactions in which each component is activated by the upstream component [3, 5].
Activation of the alternative pathway does not require the presence of an antibody; C3, factor B, factor D, and properdin are the components of the alternative pathway. MCP a transmembrane glycoprotein regulates the complement cascade by serving as a co-factor for serine protease factor I, which irreversibly inactivates the hemolytic potential of C3b and C4b [11, 12].
We have further shown that ocular complement components are not just silent bystanders but are chronically active at a low level in normal eye [32]. Studies reported in the literature suggest that complement cascade can be aggressively activated in the cornea during an immune and inflammatory reaction [45, 46]. Heavy infiltration in the anterior chamber (AC) with spillover into the anterior vitreous was also observed at this time point. These observations demonstrate that ocular tissue can protect itself by upregulating various CRegs during uveitis and provide strong evidence for the use of recombinant CRegs as therapeutic agents in the treatment of autoimmune uveitis.Activation of the complement system has also been reported in other animal models of anterior uveitis such as endotoxin-induced uveitis (EIU) [64, 65]. In the dry type of AMD, drusena€”small yellow depositsa€”are formed between the retinal-pigmented epithelium (RPE) and Brucha€™s membrane [72]. The membrane-bound as well as recombinant-soluble (rs) CD59, bind to C9 and C8 and inhibit the polymerization of C9 which is prerequisite for MAC formation. Unfortunately, these treatment options have limitations due to their short-term and serious side effects.
Agents that specifically inhibit the complement system or complement activation products have been proven beneficial in the treatment of both human and experimental diseases over the past few years.
This sequential activation of complement components by all three pathways leads to the formation of membrane attack complex (MAC). We reported that both iC3b (activation product of C3) and MAC (end product of complement activation) are present in normal rat eye indicating that the complement system is continuously activated at a low level in the normal eye [32]. Unfortunately, almost all of the studies in the past three decades have focused on the role of T cells in the pathogenesis of uveitis [54, 57, 58].
The eye appeared normal both clinically (c) and histologically (f) after the resolution of EAAU (day 30 post immunization). In EIU, it was demonstrated that the complement system is critical for the development of inflammation, and there is a local activation of the complement system as evident by accumulation of complement components (C1q, C3, and C4) in various parts of the eye during inflammation [66]. In wet-type AMD, abnormal vessel growth takes place from choroid, termed choroidal neovascularization (CNV), under the retinal pigment epithelium [71, 72]. Although, photodynamic therapy (PDT) reduces the rate of vision loss in most patients, it does not lead to significant improvement in vision.
Thus, the therapy based on complement inhibition has great potential in the future for the treatment of various ocular diseases such as keratitis, uveitis, and macular degeneration. Under normal conditions, the activation of the complement system is kept under tight control by the coordinated action of soluble and membrane-associated complement regulatory proteins (CRegs). All three pathways converge on a common reaction that results in the formation of an enzymea€”C3 convertase.
In 2003, we documented that the interaction between complement activation product iC3b and its receptor is vital for the creation of immunosuppressive environment that leads to the induction and the maintenance of ocular immune privilege and protection of intraocular structures that are critical for vision [38]. In these experiments, the normal cornea from human donors was exposed to lipopolysaccharide (LPS), ribitol teichoic acid immune complex, acid (HCl), or alkali (NaOH) separately and the generation of anaphylatoxinsa€”C3a, C4a, and C5aa€”as well as MAC in the corneas was monitored. Very few laboratories have investigated the role of the complement system in the development of autoimmune uveitis [32, 58a€“66].Through our recent studies, the critical role of complement and complement regulatory proteins (CRegs) in the pathogenesis of idiopathic anterior uveitis was addressed and recognized.
Activation of the complement system was also implicated in experimental allergic uveitis [67]. Although several risk factors are associated with AMD, the exact pathogenesis still remains unknown. Furthermore, repeated PDT can cause severe damage to the posterior segment of the eye and is not cost effective. CD59 acts at the terminal step of complement activation and prevents the formation of membrane attack complex (MAC, C5b-9 complex), the final activation product of all three complement cascades by blocking the incorporation of C9 [14, 15].
The presence and expression pattern of CRegs in the normal human eye was first described by us [33]. It was reported that anaphylatoxinsa€”C3a, C4a, and C5aa€”could be generated when the cornea was injured with LPS, immune complexes, acid, or alkali. Our laboratory has used experimental autoimmune anterior uveitis (EAAU)a€”an animal model of human autoimmune anterior uveitisa€”to investigate the role of the complement system, a significant and previously neglected facet of uveitis [53, 62, 63]. Using experimental autoimmune uveoretinitis (EAU) animal model, the complement system has been reported to play an important role in the pathogenesis posterior uveitis [68].
The last few years have witnessed an amazing series of research establishing the central role of the complement system in the pathogenesis of AMD both in humans and in experimental animals. Two drugs Lucentis and Macugen are approved by Federal Drug Administration for the treatment of AMD and both drugs inhibit vascular endothelial growth factor.
C3b forms C5 convertase that ultimately leads to the formation of membrane attack complex (MAC). Crry (5I2 antigen) is a C3 convertase inhibitor that possesses both decay-accelerating and membrane co-factor activities and present only in rodents [16, 17]. We reported that membrane-bound CRegsa€”MCP, DAF, and CD59a€”are differentially expressed in normal human and eyes [33]. Interestingly MAC could only be generated when the cornea was exposed to LPS or immune complexes. EAAU is induced by injecting bovine melanin-associated antigen emulsified in Freunda€™s complete adjuvant, in the foot pad of Lewis rats [53]. Recently, Read and co-workers demonstrated that the transgenic mice that express soluble Crry in the retina had decreased incidence and severity of EAU [68].
Various studies in the literature have indicated a potential role for complement in drusen formation in the non-exudative form of AMD in humans [73a€“75]. One of the major drawbacks of Lucentis or Macugen is that repeated injections of these drugs are needed to treat AMD. Academic, San Diego, pp 1a€“137.Liszewski MK, Farries TC, Lublin DM, Rooney IA, Atkinson JP (1996) Control of the complement system.
The complement cascade is regulated at different check points (shown with black blocks) by CRegs. Our studies along with other independent studies that were performed later demonstrated that Crry and CD59 (membrane bound and soluble) are also present in the normal rodent eye [32, 34, 35].
Complement components, complement activation products (C3a, C5a, MAC), and complement regulatory proteins (CD46, Vitronectin) have been localized in drusen in patients with AMD [73a€“75].The discovery of allelic variants of complement factor H (CFH) as a major risk factor for AMD has become a landmark study [76a€“79].
Repeated injections can cause some serious side effects including hemorrhage of the eye membrane, eye pain, and vitreous floaters. C1INH regulates activation of the classical complement pathway by inactivating the protease function of activated C1 complex. We have further shown that ocular CRegs are functionally active and tightly regulate the activation of intraocular complement [27, 32].
The immune response mounted to LPS or immune complex is similar to that generated against infectious agents like gram-negative bacteria.
The inflammation resolves after approximately 3A weeks, and the eye returns to the normal state with no apparent sign of any tissue damage (Fig.A 3).
This may be due to relatively low levels of Crry expressed compared with the levels that are required for the complete inhibition of the complement system. The polymorphism that gives rise to this allelic variant of CFH results from a tyrosine to histidine replacement at position 402. Therefore, alternative therapeutic strategies with minimum side effects are required to better treat AMD patients.


It also prevents spontaneous activation of C1 and binding to the zymogen forms of C1r and C1s [24].
Functional inhibition of ocular CRegs using specific antibodies resulted in unregulated complement activation leading to severe intraocular inflammation in normal animals [32].
Indeed the complement system has been shown to play a critical role in protection against Pseudomonas aeruginosa infection that causes keratitis [47, 48].
Interestingly, studies from our laboratory have demonstrated that the activation of the complement system is critical for the development of EAAU [62].
It is possible that a higher dose of exogenous Crry or similar CReg may result in complete inhibition of EAU.Thus, these studies provide strong evidence that the complement system and CRegs play an important role in the pathogenesis of autoimmune uveitis and provide alternative approaches for the development of effective therapy.
We believe that the results derived from the studies reviewed above would open up the window of opportunities for the development of anti-complement therapy in the treatment of AMD.In view of important developments relative to the role of the complement system in AMD during the past several years, we believe that the next decade would be critical for such studies. Furthermore, complement inhibitory activity in normal human intraocular fluid was blocked by inhibiting the function of MCP, DAF, and CD59 [27].Thus, our results clearly established that within the normal eye the complement system seems to perform two important functions.
Additionally, complement activation is believed to play an important role in ulceration of human cornea induced by gram-negative bacteria [49].The aforementioned observations have important clinical implications. During EAAU, the complement system is activated (detected by Western blot analysis for iC3b) in the eye, and the kinetics of complement activation follows a pattern that is similar to the clinical course of the disease. More research in the future will present us enough information to develop anti-complement therapy for uveitis. CFH consists of 20 short consensus repeats (SCRs) and the polymorphic site 402 resides in SCR7. We hope that the interest will continue to grow in the future so that an alternative therapy could be developed by inhibiting complement activation. CFH inhibits C3 activation by binding to C3b and acting as a co-factor for factor I-mediated cleavage of C3b and also has decay-accelerating activity for the alternative pathway C3 convertase, C3bBb. First, the chronic low level of complement activation serves as a primary defense mechanism of the eye against pathogenic infection and is finely regulated by the soluble and membrane-bound intraocular complement regulatory proteins. If in future anti-complement agents were to be considered for the treatment of corneal pathology, anaphylatoxins would be an ideal target for the patient presenting with chemical injury such as exposure to acid or alkali.
Furthermore, depletion of the complement system of the host resulted in complete inhibition of EAAU. Hopefully, in the future, complement inhibitors might be used as novel anti-uveitic agents in the clinic for the treatment of this important form of human ocular disease. SCR7 contains the binding site for C3b, glycosaminoglycans (GAG) and C-reactive protein (CRP). Since untreated CNV leads to the irreversible loss of central vision, it is important for the pharmaceutical companies to utilize the knowledge available to them from different research laboratories and should make every effort to transfer this knowledge to develop new drugs and therapies for AMD patients.
This enables destruction of the putative pathogen without inadvertent damage of ocular tissue, which is vital for the maintenance of vision. On the other hand, in the case of bacterial infection both anti-anaphylatoxin and anti-MAC therapy should be considered. In complement-depleted rats, the levels of IFN-I?, IP-10, ICAM-1, and LECAM-1 were extremely low compared to the complement-sufficient rats during EAAU. The polymorphism at position 402 in SCR7 reduces the binding affinity to CRP [80] and GAG [81].
Second, complement activation products (such as iC3b) generated as a result of the low level of complement activation results in the selective suppression of harmful T cell responses. Although as discussed below the cornea possesses the ability to express different CRegs to protect itself from complement-mediated damage, it may not be able to upregulate various CRegs to an appropriate level during an acute episode of complement activation as observed during chemical insults or acute bacterial infection. Our observations suggest that the activation of the local complement system plays a critical role in the development of inflammation during EAAU and suppression of intraocular complement system, thus may provide a successful strategy for uveitis therapy.
Binding of CFH to CRP and GAG plays an important role in the regulation of the alternative pathway. Soluble forms of MCP, DAF, CR1, CD59, and Crry have been reported to be present in various biological fluids in both humans and rodents [27a€“30].
In this role complement protects the eye from innocent bystander destruction associated with the T cell response to the invading pathogens.
In such cases, topical application of recombinant CRegs could be beneficial and serve as a better alternative for intervention.Enhanced complement activation can cause damage to the autologous corneal tissue during an infection or inflammation. At present, the exact mechanism and pathways involved in local complement activation during uveitis are not known. Thus the polymorphic form of CFH with histidine at position 402 may have reduced ability to regulate the activation of the alternative pathway. Complement components and CRegs present in normal tears have also been reported to be functionally active and have been proposed to serve as first line of defense in protecting the eye [36]. It is also not known if the increase in complement components in the anterior segment of the eye is due to the upregulation of their synthesis by resident ocular cells or is a result of spillover from the systemic complement system.
This may lead to uncontrolled activation of alternative pathway which may result in the development of AMD.
The eye is an immunologically privileged site and ocular immune privilege does not refer to the absence of immune system but, rather its fine regulation [31]. However, additional studies are required to determine the role of the complement system in normal tears. Interestingly, compared to corneal stroma and corneal endothelium, various CRegs are very strongly expressed on the corneal epithelium [33] (Fig.
Previous studies from our laboratory established that a functionally active complement system is present in the anterior segment of the eye because when a well-known activator of complement such as zymosan was injected in the anterior chamber, severe anterior uveitis was induced. The loss of regulatory activity of CFH due to polymorphism can have a direct effect on the predisposition of the eye to AMD as it has been shown recently that CFH is expressed locally in the optic nerve, retina, and retinal pigment epithelium [82]. The studies discussed in this article highlight the role of complement activation and regulation in the protection of the normal eye.
This zymosan-induced uveitis was due to the activation of the complement system because anterior uveitis was completely inhibited when the complement system of the host was depleted [32]. In addition, the studies discussed below demonstrate the importance of interplay between complement activation and complement regulation in the development of vision-threatening complications such as keratitis, uveitis, and macular degeneration. This high expression of CRegs on the corneal epithelium is crucial for the protection of the cornea because the cornea is continually exposed to various pathogens including bacteria. Furthermore, we and others have reported the presence of various complement components in aqueous humor as well as other parts of the normal eye [32, 39, 41, 59, 61].
These bacteria produce phospholipase and other enzymes which can remove GPI-anchored DAF and CD59 from the corneal surface [51]. Thus, in the absence of a very high expression of CRegs on the corneal epithelium, bacterially induced loss of DAF and CD59 could be deleterious to the cornea and lead to vision loss after the putative pathogen has been destroyed by the complement system. To investigate if a deficiency or abnormality in the expression of CRegs may play a role in ocular surface disease, systemic examination of corneal tissue from patients with different diseases such as pseudophakic bullous keratopathy, HSV-1 keratitis, and herpes zoster scleritis is needed.
In this report, the investigators identified high risk allele and two protective alleles for CFB and C2 that were associated with AMD.
An independent study further established a similar association between CFB, C2, and AMD [85].
More recently, investigators compared 847 patients with AMD with 701 unaffected people and observed that a variant in the complement C3 gene affected the risk of developing AMD [86].The aforementioned studies establish that the polymorphism in the genes of certain complement components and regulators genetically predisposes some individuals to AMD. However, we should also pay attention to the fact that other risk factors for AMD such as alcohol consumption and smoking nicotine can directly affect the level of complement activation and CRegs.
For instance, chronic ethanol consumption upregulates CFB but downregulates CFH in mice [87]. Thus, association of alcohol consumption with AMD may be due to its direct effect on the complement system. Indeed we have reported that chronic alcohol consumption increases the size of CNV complex in rat model of laser-induced CNV [88]. Similarly, cigarette smoking has been shown to decrease the affinity of CFH for C3 and activate the complement system [89].In our laboratory, we use a mouse model of laser-induced CNV to study the role of complement in the pathogenesis of wet-type AMD. A reliable way to produce CNV in animals is to rupture Brucha€™s membrane with laser photocoagulation [90a€“92]. We and others have found that choroidal neovascularization induced in rodents by laser photocoagulation is useful to gain insights into the pathogenesis of new vessel growth from the choroid [90a€“96]. In 2005, we demonstrated for the first time using this animal model that complement activation and generation of MAC is critical for the development of laser-induced CNV.
As mentioned above, the importance of C3 in the pathogenesis of AMD was recently confirmed by Yates et al., who established an association of C3 polymorphism with AMD [86].
We further observed that in the absence of MAC deposition, release of angiogenic factors such as vascular endothelial growth factor (VEGF), TGF-I?2, and I?-FGF was inhibited. This is a crucial observation as it suggests that the complement system is a potential therapeutic target for the treatment of CNV.
Subsequently, we reported that the activation of complement by alternative pathway is responsible for MAC formation in laser-induced CNV.
In a separate study, we used recombinant-soluble CD59-Fc chimeric protein to inhibit the formation of MAC after laser photocoagulation [95].
Thus, our studies suggest that the recombinant forms of CD59 could be used as a potential drug in the future to treat CNV. It was reported that C3a and C5a are present not only in human drusen but are also localized in the choroid of mice with laser-induced CNV [97].
Experimental autoimmune uveitis: mechanisms of disease and clinical therapeutic indications.



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