ST2 deficient mice display a normal host defense against pulmonary infection with Mycobacterium tuberculosis |
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| Institution: | 1. Center of Infection and Immunity Amsterdam (CINIMA), Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands;2. Center of Experimental and Molecular Medicine (CEMM), Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands;3. Department of Pathology, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands;4. Medical Research Council, Laboratory of Molecular Biology, Cambridge CB2 0QH, UK;1. Department of Respiratory and Critical Care Medicine, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China;2. Department of Respiratory and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;3. Center of Medical Research, Beijing Institute of Respiratory Diseases, Beijing, China;1. Institute of Pulmonary Medicine, Hadassah-Hebrew University Medical Center, Jerusalem 91120, Israel;2. Institute of Chemistry, The Hebrew University of Jerusalem, Jerusalem 91904, Israel;3. Institute of Medical Research, Israel-Canada Medical School, The Hebrew University of Jerusalem, Jerusalem 91120, Israel;1. Center for Food Allergy and Asthma Research, Northwestern University Feinberg School of Medicine, Chicago, Ill;2. Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, Calif;3. Division of Allergy and Immunology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Ill;4. Ann and Robert H. Lurie Children''s Hospital of Chicago, Chicago, Ill;5. Elliot and Roslyn Jaffe Food Allergy Institute, Division of Allergy, Department of Pediatrics, Mount Sinai School of Medicine, New York, NY;1. Faculty of Medicine, Islamic University of Malang, Malang, East Java 65144 Indonesia;2. School of Medicine, Faculty of Health Science, The University of Adelaide, Adelaide, 5000 SA, Australia;3. Centre for Orthopaedics and Trauma Research, The University of Adelaide, Adelaide, 5000 SA, Australia;4. School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, 5001 SA, Australia;1. Department of Respiratory and Sleep Medicine, Women''s and Children'' Hospital, North Adelaide, South Australia, Australia;2. Murdoch Children''s Research Institute, Parkville, Victoria, Australia;3. Royal Children''s Hospital Melbourne, Parkville, Victoria, Australia;4. Department of Allergy, Immunology and Respiratory Medicine, The Alfred Hospital, Prahran, Victoria, Australia;1. Parasitology Laboratory, School of Veterinary Medicine, Faculty of Agriculture, Tottori University, 680-0945, Tottori, Japan;2. The United Graduate School of Veterinary Science, Yamaguchi University, Yamaguchi 753-8515, Japan;3. National Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention, Shanghai 200025, People’s Republic of China;4. Key Laboratory of Parasite and Vector Biology, Ministry of Health, MOH, Shanghai 200025, People’s Republic of China;5. National Center for International Research on Tropical Diseases, Shanghai 200025, People’s Republic of China;6. WHO Collaborating Center for Tropical Diseases, Shanghai 200025, People’s Republic of China;7. School of Life Science and Engineering, Foshan University, Foshan 528231, People’s Republic of China;8. Department of Infectious Disease, Hokkaido Institute of Public Health, Sapporo, Hokkaido 060-0819, Japan;9. Veterinary Epidemiologist AU-IBAR/ICPALD, African Union-Interafrican Bureau for Animal Resources, Nairobi 30786-00100, Kenya |
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| Abstract: | Tuberculosis, caused by Mycobacterium (M.) tuberculosis, is a devastating infectious disease causing many deaths world-wide every year. Successful host defense mainly depends on a strong Th type 1 response. We investigated the role of T1/ST2 (recently identified as the receptor for IL-33), a typical Th2 marker in the assumption that a shift towards a beneficial Th1 response would occur in the absence of ST2. For this, ST2 KO and WT mice were intranasally infected with a virulent strain of M. tuberculosis (150 CFU). In line with our hypothesis, ST2 KO animals displayed increased numbers of lymphocytes infiltrating the lung after 2 weeks of infection, increased IFNγ production by splenocytes in ST2 KO mice early in infection and enhanced lung IFNγ levels at the chronic phase of the disease. However, we did not detect any differences between ST2 KO and WT mice in mycobacterial loads in lungs or liver after M. tuberculosis infection. The pulmonary inflammatory response, as measured by relative lung weights, cytokine and chemokine levels as well as histopathological analysis, was similar in ST2 KO and WT mice. These data suggest that apart from inducing a modest shift towards the Th1 response, the role of ST2 during murine M. tuberculosis infection is limited. |
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