Progression of clinical tuberculosis is associated with a Th2 immune response signature in combination with elevated levels of SOCS3 |
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| Authors: | Senait Ashenafi Getachew Aderaye Amsalu Bekele Martha Zewdie Getachew Aseffa Anh Thu Nguyen Hoang Berit Carow Meseret Habtamu Maria Wijkander Martin Rottenberg Abraham Aseffa Jan Andersson Mattias Svensson Susanna Brighenti |
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| Affiliation: | 1. Karolinska Institutet, Center for Infectious Medicine (CIM), F59, Department of Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden;2. Black Lion University Hospital and Addis Ababa University, Department of Pathology, Faculty of Medicine, Addis Ababa, Ethiopia;3. Black Lion University Hospital and Addis Ababa University, Department of Internal Medicine, Faculty of Medicine, Addis Ababa, Ethiopia;4. Armauer Hansen Research Institute (AHRI), Addis Ababa, Ethiopia;5. Black Lion University Hospital and Addis Ababa University, Department of Radiology, Faculty of Medicine, Addis Ababa, Ethiopia;6. Karolinska Institutet, Department of Microbiology, Tumor and Cell Biology (MTC), Stockholm, Sweden;g Karolinska University Hospital Huddinge, Department of Medicine, Division of Infectious Diseases, Stockholm, Sweden |
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| Abstract: | In this study, we explored the local cytokine/chemokine profiles in patients with active pulmonary or pleural tuberculosis (TB) using multiplex protein analysis of bronchoalveolar lavage and pleural fluid samples. Despite increased pro-inflammation compared to the uninfected controls; there was no up-regulation of IFN-γ or the T cell chemoattractant CCL5 in the lung of patients with pulmonary TB. Instead, elevated levels of IL-4 and CCL4 were associated with high mycobacteria-specific IgG titres as well as SOCS3 (suppressors of cytokine signaling) mRNA and progression of moderate-to-severe disease. Contrary, IL-4, CCL4 and SOCS3 remained low in patients with extrapulmonary pleural TB, while IFN-γ, CCL5 and SOCS1 were up-regulated. Both SOCS molecules were induced in human macrophages infected with Mycobacterium tuberculosis in vitro. The Th2 immune response signature found in patients with progressive pulmonary TB could result from inappropriate cytokine/chemokine responses and excessive SOCS3 expression that may represent potential targets for clinical TB management. |
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