- Email: [email protected]
Reply to comment by Kountouras et al. about article untitled “Helicobacter pylori infection and systemic sclerosis – is there a link? by Radić et al.”
Correspondence / Joint Bone Spine 78 (2011) 222–223
Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece ∗ Corresponding
author. 8 Fanariou St, Byzantio, 551 33, Thessaloniki, Macedonia, Greece. Tel.: +30 2310 892238; fax: +30 2310 992794. E-mail addresses: [email protected], [email protected] (J. Kountouras) 7 January 2011
doi:10.1016/j.jbspin.2011.01.006
Reply to comment by Kountouras et al. about article untitled “Helicobacter pylori infection and systemic sclerosis – is there a link? by Radi´c et al.” Keywords: Systemic sclerosis Multiple sclerosis Helicobacter pylori Pathogenesis
Sir, In their letter, Kountouras et al. raise some queries about possible role of Helicobacter pylori (H. pylori) infection in some autoimmune disorders such as multiple sclerosis (MS) reported in our review [1]. Recent evidence suggests that H. pylori infections play a role in the pathogenesis of a variety of autoimmune diseases. A big controversy is whether the H. pylori infection is a protective factor against conventional multiple sclerosis or not [2,3]. We agree that the serological test does not discriminate current from old infections and only current H. pylori infection induces humoral and cellular immune responses [1,4,5]. However, we performed a study to evaluate the possible association between H. pylori infection with systemic sclerosis (SSc) activity, biochemical and serological data [6]. Our preliminary results suggest that H. pylori infection is implicated in activity of SSc, especially in skin involvement of this disease. This study may indicate H. pylori infection as a possible cofactor in the development of SSc. Systematic studies examining the relationship between autoimmune entities and infection with H. pylori and documentation of the effect of H. pylori eradication are needed to complete our understanding on this topic. Gavalas et al. showed a strong association between H. pylori infection and MS in a Greek cohort [2]. Moreover, eradication of H. pylori infection may alter SSc and MS pathophysiology. Numerous infectious agents have been proposed as possible triggering factors in SSc and MS but very few infections are as rare as SSc and MS [6,7]. Therefore, development of SSc and MS is unlikely to depend exclusively on an infectious agent. Instead, it likely occurs as a result of interactions between the infectious agent and a cascade of host-
223
specific factors and events. This is not surprising because immune response to infection is highly individual. It is controlled by multiple genes, age, and the route of infection. It may even be different in the same individual from one day to the next, owing to a number of factors, including co-infections, stress, and pregnancy. In addition, polymorphisms in genes unrelated to immunity may cause an infectious agent to induce disease through molecular mimicry in one person and not another. Therefore, in a disease as varied, complex, and rare as SSc and MS, infection prevalence alone should not be expected to provide sufficient evidence for or against a pathological role in the disease. Despite intensive studies, there is no definitive evidence to conclude that SSc and MS has a viral or bacterial origin. In SSc and MS, some viral or bacterial products could synergise with other factors in the microenvironment predisposing to SSc and MS development. Conflicts of interest statement None of the authors has any conflicts of interest to declare. References [1] Radic´ M, Kaliterna DM, Radic´ J. Helicobacter pylori infection and systemic sclerosis-is there a link? Joint Bone Spine 2010. doi:10.1016/j.jbspin.2010.10.005. [2] Gavalas E, Kountouras J, Deretzi G, et al. Helicobacter pylori and multiple sclerosis. J Neuroimmunol 2007;188:187–9. [3] Li W, Minohara M, Su JJ, et al. Helicobacter pylori infection is a potential protective factor against conventional multiple sclerosis in the Japanese population. J Neuroimmunol 2007;184:227–31. [4] Deretzi G, Kountouras J, Grigoriadis N, et al. From the “little brain” gastrointestinal infection to the “big brain” neuroinflammation: a proposed fast axonal transport pathway involved in multiple sclerosis. Med Hypotheses 2009;73:781–7. [5] Randone SB, Guiducci S, Cerinic MM. Systemic sclerosis and infections. Autoimmun Rev 2008;8:36–40. [6] Radic´ M, Martinovic´ Kaliterna D, Bonacin D, et al. Correlation between Helicobacter pylori infection and systemic sclerosis activity. Rheumatology (Oxford) 2010;49:1784–5. [7] Giovannoni G, Cutter GR, Lunemann J, et al. Infectious causes of multiple sclerosis. Lancet Neurol 2006;5:887–94.
Mislav Radic´ a,∗ Duˇsanka Martinovic´ Kaliterna a Josipa Radic´ b a Department of Rheumatology, University Hospital Split, Croatia b Department of Nephrology, University Hospital Split, Croatia ∗ Corresponding
author. ´ E-mail address: [email protected] (M. Radic) 6 January 2011 doi:10.1016/j.jbspin.2011.01.002
Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece ∗ Corresponding
author. 8 Fanariou St, Byzantio, 551 33, Thessaloniki, Macedonia, Greece. Tel.: +30 2310 892238; fax: +30 2310 992794. E-mail addresses: [email protected], [email protected] (J. Kountouras) 7 January 2011
doi:10.1016/j.jbspin.2011.01.006
Reply to comment by Kountouras et al. about article untitled “Helicobacter pylori infection and systemic sclerosis – is there a link? by Radi´c et al.” Keywords: Systemic sclerosis Multiple sclerosis Helicobacter pylori Pathogenesis
Sir, In their letter, Kountouras et al. raise some queries about possible role of Helicobacter pylori (H. pylori) infection in some autoimmune disorders such as multiple sclerosis (MS) reported in our review [1]. Recent evidence suggests that H. pylori infections play a role in the pathogenesis of a variety of autoimmune diseases. A big controversy is whether the H. pylori infection is a protective factor against conventional multiple sclerosis or not [2,3]. We agree that the serological test does not discriminate current from old infections and only current H. pylori infection induces humoral and cellular immune responses [1,4,5]. However, we performed a study to evaluate the possible association between H. pylori infection with systemic sclerosis (SSc) activity, biochemical and serological data [6]. Our preliminary results suggest that H. pylori infection is implicated in activity of SSc, especially in skin involvement of this disease. This study may indicate H. pylori infection as a possible cofactor in the development of SSc. Systematic studies examining the relationship between autoimmune entities and infection with H. pylori and documentation of the effect of H. pylori eradication are needed to complete our understanding on this topic. Gavalas et al. showed a strong association between H. pylori infection and MS in a Greek cohort [2]. Moreover, eradication of H. pylori infection may alter SSc and MS pathophysiology. Numerous infectious agents have been proposed as possible triggering factors in SSc and MS but very few infections are as rare as SSc and MS [6,7]. Therefore, development of SSc and MS is unlikely to depend exclusively on an infectious agent. Instead, it likely occurs as a result of interactions between the infectious agent and a cascade of host-
223
specific factors and events. This is not surprising because immune response to infection is highly individual. It is controlled by multiple genes, age, and the route of infection. It may even be different in the same individual from one day to the next, owing to a number of factors, including co-infections, stress, and pregnancy. In addition, polymorphisms in genes unrelated to immunity may cause an infectious agent to induce disease through molecular mimicry in one person and not another. Therefore, in a disease as varied, complex, and rare as SSc and MS, infection prevalence alone should not be expected to provide sufficient evidence for or against a pathological role in the disease. Despite intensive studies, there is no definitive evidence to conclude that SSc and MS has a viral or bacterial origin. In SSc and MS, some viral or bacterial products could synergise with other factors in the microenvironment predisposing to SSc and MS development. Conflicts of interest statement None of the authors has any conflicts of interest to declare. References [1] Radic´ M, Kaliterna DM, Radic´ J. Helicobacter pylori infection and systemic sclerosis-is there a link? Joint Bone Spine 2010. doi:10.1016/j.jbspin.2010.10.005. [2] Gavalas E, Kountouras J, Deretzi G, et al. Helicobacter pylori and multiple sclerosis. J Neuroimmunol 2007;188:187–9. [3] Li W, Minohara M, Su JJ, et al. Helicobacter pylori infection is a potential protective factor against conventional multiple sclerosis in the Japanese population. J Neuroimmunol 2007;184:227–31. [4] Deretzi G, Kountouras J, Grigoriadis N, et al. From the “little brain” gastrointestinal infection to the “big brain” neuroinflammation: a proposed fast axonal transport pathway involved in multiple sclerosis. Med Hypotheses 2009;73:781–7. [5] Randone SB, Guiducci S, Cerinic MM. Systemic sclerosis and infections. Autoimmun Rev 2008;8:36–40. [6] Radic´ M, Martinovic´ Kaliterna D, Bonacin D, et al. Correlation between Helicobacter pylori infection and systemic sclerosis activity. Rheumatology (Oxford) 2010;49:1784–5. [7] Giovannoni G, Cutter GR, Lunemann J, et al. Infectious causes of multiple sclerosis. Lancet Neurol 2006;5:887–94.
Mislav Radic´ a,∗ Duˇsanka Martinovic´ Kaliterna a Josipa Radic´ b a Department of Rheumatology, University Hospital Split, Croatia b Department of Nephrology, University Hospital Split, Croatia ∗ Corresponding
author. ´ E-mail address: [email protected] (M. Radic) 6 January 2011 doi:10.1016/j.jbspin.2011.01.002