Berta N Restrepo1, Katerine Marín1, Paola Romero1, Margarita Arboleda1, Ana L Muñoz2, Irene Bosch3, Heriberto Vásquez-Serna4, Orlando A Torres5. 1. Instituto Colombiano de Medicina Tropical, Universidad CES Sabaneta, Antioquía, Colombia. 2. Science Faculty, Universidad Antonio Nariño Bogotá, Cundinamarca, Colombia. 3. Institute for Medical Engineering & Science, Massachusetts Institute of Technology Cambridge, United States. 4. Secretaría de Salud de Ibagué Ibagué, Tolima, Colombia. 5. Faculty of Veterinary Medicine, Universidad Antonio Nariño Bogotá, Cundinamarca, Colombia.
Abstract
The pathogenesis of the severity of chikungunya infection is not yet fully understood. OBJECTIVE: To assess the role of the cytokines/chemokines and system of complement in the evolution of chikungunya infection. METHODS: In both acute and chronic phases, we measured the serum levels of 12 cytokines/chemokines and two complement mediators: mannose-binding lectin (MBL) and C3a, in 83 patients with chikungunya infection and ten healthy controls. RESULTS: During the acute phase, 75.9% of the patients developed musculoskeletal disorders, and in 37.7% of them, these disorders persisted until the chronic phase. In general, patients had higher levels of cytokines than healthy controls, with significant differences for IFN-γ, IL-6, IL-8, IL-10, and MIP-1. Most cytokines exhibited a downward trend during the chronic phase. However, only IL-10, and MIP-1 levels were significantly lower in the chronic phase. Additionally, these levels never decreased to concentrations found in healthy controls. Moreover, MBL levels were significantly higher in the acute phase compared with the chronic phase. C3a levels were significantly higher in patients with musculoskeletal disorder compared with patients without it, in both acute-phase 118.2 (66.5-252.9), and chronic phase 68.5 (64.4-71.3), P < 0.001. Interestingly, C3a levels were significantly higher when patients had a severe disease version. Besides, in the acute phase, C3a levels were higher in patients that suffer arthritis as opposed to when they suffer arthralgia, 194.3 (69.5-282.2), and 70.9 (62.4-198.8), P = 0.013, respectively. CONCLUSIONS: Our results showed an immunological response that persisted until the chronic phase and the role of the complement system in the severity of the disease. AJCEI
The pathogenesis of the severity of chikungunya infection is not yet fully understood. OBJECTIVE: To assess the role of the cytokines/chemokines and system of complement in the evolution of chikungunya infection. METHODS: In both acute and chronic phases, we measured the serum levels of 12 cytokines/chemokines and two complement mediators: mannose-binding lectin (MBL) and C3a, in 83 patients with chikungunya infection and ten healthy controls. RESULTS: During the acute phase, 75.9% of the patients developed musculoskeletal disorders, and in 37.7% of them, these disorders persisted until the chronic phase. In general, patients had higher levels of cytokines than healthy controls, with significant differences for IFN-γ, IL-6, IL-8, IL-10, and MIP-1. Most cytokines exhibited a downward trend during the chronic phase. However, only IL-10, and MIP-1 levels were significantly lower in the chronic phase. Additionally, these levels never decreased to concentrations found in healthy controls. Moreover, MBL levels were significantly higher in the acute phase compared with the chronic phase. C3a levels were significantly higher in patients with musculoskeletal disorder compared with patients without it, in both acute-phase 118.2 (66.5-252.9), and chronic phase 68.5 (64.4-71.3), P < 0.001. Interestingly, C3a levels were significantly higher when patients had a severe disease version. Besides, in the acute phase, C3a levels were higher in patients that suffer arthritis as opposed to when they suffer arthralgia, 194.3 (69.5-282.2), and 70.9 (62.4-198.8), P = 0.013, respectively. CONCLUSIONS: Our results showed an immunological response that persisted until the chronic phase and the role of the complement system in the severity of the disease. AJCEI
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