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Antibiotic Therapy in Autoimmune Disorders

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Antibiotic Therapy in Autoimmune Disorders Review Antibiotic therapy in autoimmune disorders Yossi Rosman1, Merav Lidar2,3,4 & Yehuda Shoenfeld*3,4 Practice Points Infections may trigger autoimmunity through several mechanisms most notably; ‘molecular mimicry’, ‘epitope spreading’ and ‘bystander activation’. Minocycline, macrolides and fluoroquinolones may be recommended to patients with early and mild rheumatoid arthritis. Ciprofloxacin therapy may obviate chronic reactive arthritis in HLA-B27 patients, while antichlamydia-based antibiotic regimens may enhance chronicity. Trimethoprim/sulfamothoxazole should be part of the treatment protocol of granulomatosis with polyangitis. Helicobacter pylori eradication should be offered to all carriers with chronic thrombocytopenic purpura. Empiric antibiotic treatment should be considered as a standard part of the treatment protocol in catastrophic antiphosphlipid antibody syndrome. SUMMARY: Antibiotics have been applied for the treatment of autoimmune diseases for over five decades, based on the premise that infections play a role in the initiation and propagation of these entities. The mechanisms by which an infection may trigger an autoimmune reaction include the so-called ‘molecular mimicry’, ‘epitope spreading’ or ‘bystander activation’. The association between infection and autoimmunity may be directly evident, as in cases of reactive arthritis, or in a more roundabout manner, as exemplified by the association between anaerobic bacterial infection of the gums and rheumatoid arthritis. Moreover, some antibiotics have, in addition to 1Department of Medicine D, Sheba Medical Center, Tel Hashomer, Israel 2Division of Rheumatology, Sheba Medical Center, Tel Hashomer, Israel 3Autoimmune Disease Center, Sheba Medical Center, Tel Hashomer, Israel 4Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel *Author for correspondence: [email protected] part of 10.2217/CPR.13.84 © 2014 Future Medicine Ltd Clin. Pract. (2014) 11(1), 91–103 ISSN 2044-9038 91 Review | Rosman, Lidar & Shoenfeld their antibacterial effects, anti-inflammatory and immunomodulatory properties. In this review we focus on the rationale and possible benefits of antibiotic treatment in various autoimmune diseases, including rheumatoid arthritis, reactive arthritis, granulomatosis with polyangitis, immune thrombocytopenia purpura and the antiphospholipid syndrome. Antibiotics have been applied for the treatment the association between anaerobic bacterial infec- of autoimmune diseases for over five decades, tion of the gums (periodontitis) and rheumatoid based on the premise that infections play a arthritis (RA) [5]. Epidemiological studies have role in the initiation and propagation of these shown that periodontal disease is more frequent entities. and more severe in patients with RA [6]. Also, the There are several proposed mechanisms by severity of periodontal disease was found to corre- which an infection may trigger an autoimmune late with RA severity [7], and treating periodontal reaction [1] . ‘Molecular mimicry’, in which the disease was demonstrated to improve clinical and pathogen and host share a common epitope laboratory parameters of the disease [8]. The pres- (i.e., proteins or DNA) resulting in the cross-acti- ence of peripathogenic bacteria in the synovium vation of autoreactive T or B cells by pathogen- of patients with RA suggests that joint seeding derived peptides is one of them [2,3]. The classic and localized inflammatory amplification may autoimmune disease rheumatic fever is thought initiate and propogate inflammation[9] . Nota- to be triggered by an infectious origin probably bly, the Gram-negative, anaerobic, coccobacillus via ‘molecular mimicry’ [4]. rheumatic fever is a Porphyromonas gingivalis has received consider- systemic disease, affecting the heart, joints, CNS able attention for its role in the development of and the skin, following Streptococcal infection periodontal disease and its association with RA. of the tonsils or the skin. In this disease, anti- It was shown that anti-P. gingivalis antibodies bodies against group A b-hemolytic Streptococ- were present in high titers in RA patients and cus are also active against host target, including that these antibodies were associated with the the heart and joints. Antibiotic treatment with presence of anti citrullinated cyclic peptides [10] . penicillin is known to prevent the autoimmune Moreover, in rat models, arthritis was induced by reaction when given during the acute infection, implanting killed P. gingivalis organisms subcu- or may prevent the continued deterioration when taneously, suggesting a role for molecular mim- given for a long period of time even after the icry [11] . Taken together, these findings suggest a infection was eliminated. pathological association between P. gingivalis and Other mechanisms by which infections may RA, hence the concept that antibiotics directed trigger an autoimmune reaction include ‘Epi- against P. gingivalis may be beneficial in the tope spreading’, where an epitope is switched treatment of RA, especially in early disease. from a dominant to a cryptic position result- Helicobacter pylori is an infectious agent note- ing in the creation of autoantibodies against worthy for its association with autoimmunity. the new epitope, is another possible initiator Anti-H. pylori antibodies have been associated of autoimmunity [1] . Additional mechanisms with antiphospholipid syndrome, giant cell arte- include ‘bystander activation’, in which tissue ritis, systemic sclerosis and primary biliary cir- damage results in the release of a new antigen, rhosis. Also, H. pylori infection has been impli- which activates autolymphocytes inducing an cated in the causation of various autoimmune auto inflammatory microenvironment, lead- diseases including immune thrombocytopenic ing in turn to the destruction of neighboring, purpura, autoimmune chronic gastritis and RA. uninfected cells [1] . The persistent presence of H. pylori in gas- The association between infection and auto- tric mucosa results in chronic immune system immunity may be directly evident, as in cases of activation with ongoing cytokine signaling, reactive arthritis (ReA), where a history of a recent infiltration of gastric mucosa by neutrophils, infection is elicited and in which bacterial prod- macrophages and lymphocytes, as well as pro- ucts may be detected in joints long after all signs duction of antibodies and effector T cells [12] . of infection have abated. Alternatively, infection Molecular mimicry between H. pylori antigen may contribute to the autoimmune cascade in and the H+/K+-ATPase (the ‘autoantigen’) leads a more roundabout manner, as exemplified by to autoimmune chronic gastritis, where the 92 Clin. Pract. (2014) 11(1) future science group Antibiotic therapy in autoimmune disorders | Review + activated CD4 T lymphocytes cross react with joint damage and disability [18]. Antibiotics have + + H /K -ATPase and H. pylori antigens [13] . been administered sporadically in the past in That being said, evidence indicates an overall RA, in an attempt to retard disease progression, downregulation of the host immune response in with minimal benefit. The newly recognized H. pylori-infected individuals [12] and this bacte- importance of periodontal disease in the patho- ria is also thought to play a protective role in the genesis of RA has sparked new interest in the development of multiple sclerosis, systemic lupus use of antibiotics in the treatment and preven- erythematosus and inflammatory bowel disease. tion of this common disease. These studies are Whether these links are epiphenomenal summarized in Table 1. or H. pylori does play a causative role in the auto immune diseases remains uncertain. The Tetracyclines negative associations could possibly support Tetracyclines are a group of broad-spectrum the notion that in susceptible individuals infec- antibiotics used in the treatment of infections tions that may protect from the development of of the respiratory tract, urinary tract and intes- auto immune diseases. tines. They were first advocated as therapeutic While these examples highlight the potential candidates in RA by scientists who presumed use of antibiotics in curtailing infections which that mycoplasma infection triggers the disease may initiate an autoimmune cascade, antibiotics and proposed prolonged antibiotic therapy with are also utilized for their anti-inflammatory and the aim of eradicating the bacteria [19] . Anec- immunomodulatory properties. Tetracyclines, dotal use of tetracyclines in the treatment of RA for instance, were shown to inhibit the activity persisted during the 1970s and early 1980s yet of antiphospholipase A2, scavenge free radicals the rheumatology community remained reserved and inhibit various matrix metalloproteinases in judging their efficacy. [14,15] as well as impair lymphocyte [16] activity In the late 1980s, the anti-inflammatory prop- and impart chondroprotective properties [17] . erties of tetracyclines were discovered leading While single infectious agents promote our to renewed interest in these drugs in the treat- understanding of autoimmunity by clarifying ment for RA. Two small, but positive studies, the basic concepts of molecular mimicry, epit- published in the early 1990s, paved the way to ope spreading and bystander activation, as noted larger trials, suggesting that the tetracycline above, ‘real-life’ autoimmune disease is more derivate – minocycline, indeed exerts substantial likely the result of exposure
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