The aim of this study was to investigate the pathogenesis of Mycoplasma pneumoniae (MP) infection and its association with cardiac and hepatic damage. Between March 2013 and March 2014, 59 children with MP pneumonia (MPP) and 30 healthy children were enrolled. Serum titers of TLR4, T cell immunoglobulin and mucin-domain (TIM) 3, IL-10, TNF-a, and IFN-g were measured both in children with MPP and healthy children. Additionally, MP-specific antibody titer and creatine kinase-MB (CK-MB), and alanine transaminase (ALT) titers were measured in patients with MPP. There were significant differences between the MPP patients and healthy controls in titers of TIM1 (P < 0.01), TLR2 (P ¼ 0.028), TLR4 (P ¼ 0.019), IL-10 (P < 0.01), TNF-a (P < 0.01) and IFN-g (P < 0.01); however, no significant difference was found in TIM3 titers (P ¼ 0.8181). TIM1 was correlated with CK-MB (P ¼ 0.025), whereas both TIM1 and TLR2 titers were correlated with MP-specific antibody titers (P < 0.001; P ¼ 0.003, respectively). Additionally, there were correlations between ALT, TIM3, and TLR2 titers (P ¼ 0.025; P ¼ 0.037, respectively). The titers of TIM1 were significantly higher in patients with cardiac damage (P ¼ 0.007) than in those without it, whereas the titers of TLR2 were significantly higher in patients with hepatic damage (P ¼ 0.026) than in those without it. TLR2, TLR4 and TIM1 may be involved in the process of MP infection. Additionally, TLR2, TLR4, TIM1 and TIM3 may play particular roles in the pathogenesis of MPP-associated cardiac and hepatic damage.Key words cardiac and hepatic damages, Mycoplasma pneumoniae.Mycoplasma pneumoniae is the smallest self-replicating agent that can cause disease and has no cell wall in any circumstances (1-3). It is a leading cause of upper and lower respiratory tract infections that can result in largescale pulmonary and extra-pulmonary events (4, 5). MPP may be responsible for 10-40% of community acquired pneumonia in children, about 18% of whom require hospitalization (6-8). Although pneumonia is the most common clinical manifestation of MP infection, extrapulmonary complications reportedly occur in up to 25% of individuals infected with MP (7). Extrapulmonary complications may occur at any time during MP infection, even in subjects who are asymptomatic. Autoimmune reactions are the main reason for the extrapulmonary complications of MP infection (9). Occurrence of cardiac and hepatic complications associated with MPP has been well established (10)(11)(12)(13)(14). However, the exact pathomechanism of MP infection-induced cardiac and hepatic complications remains unclear.Mycoplasma pneumoniae releases multiple metabolic products that participate in destruction of the mucosal epithelium (15). In addition, multiple organ and endothelium cell damage in children with MP infection is associated with changes in various pro-inflammatory cytokines (16). TLRs serve as important pattern recognition receptors in the host innate defense that induce innate immunity. TLRs can identify molecular

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