Kari Otterdal1, Jeshina Janardhanan2, Elisabeth Astrup3, Thor Ueland4, John A J Prakash5, Tove Lekva6, O C Abraham2, Kurien Thomas7, Jan Kristian Damås8, Prasad Mathews7, Dilip Mathai7, Pål Aukrust9, George M Varghese2. 1. Research Institute for Internal Medicine, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0027 Oslo, Norway; Faculty of Medicine, University of Oslo, PO Box 1072 Blindern, 0316 Oslo, Norway. Electronic address: kari.otterdal@rr-research.no. 2. Department of Medicine and Infectious Diseases, Christian Medical College, Vellore 632 004, Tamil Nadu, India. 3. Research Institute for Internal Medicine, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0027 Oslo, Norway; Institute of Clinical Medicine, Akershus University Hospital, Sykehusveien 25, 1478 Lørenskog, Norway. 4. Research Institute for Internal Medicine, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0027 Oslo, Norway; Faculty of Medicine, University of Oslo, PO Box 1072 Blindern, 0316 Oslo, Norway. 5. Department of Microbiology, Christian Medical College, Vellore 632 004, Tamil Nadu, India. 6. Research Institute for Internal Medicine, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0027 Oslo, Norway; Section of Specialized Endocrinology, Department of Endocrinology, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0027 Oslo, Norway; Faculty of Medicine, University of Oslo, PO Box 1072 Blindern, 0316 Oslo, Norway. 7. Department of Medicine, Christian Medical College, Vellore 632 004, Tamil Nadu, India. 8. Centre of Molecular Inflammation Research, Department of Cancer Research and Molecular Medicine, St. Olavs Hospital, PO Box 3250 Sluppen, 7006 Trondheim, Norway; Norwegian University of Science and Technology, PO Box 8905, 7491 Trondheim, Norway. 9. Research Institute for Internal Medicine, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0027 Oslo, Norway; Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0027 Oslo, Norway; Faculty of Medicine, University of Oslo, PO Box 1072 Blindern, 0316 Oslo, Norway.
Abstract
OBJECTIVES: Scrub typhus is endemic in the Asia-Pacific region. Mortality is high even with treatment, and further knowledge of the immune response during this infection is needed. This study was aimed at comparing plasma levels of monocyte/macrophage and endothelial related inflammatory markers in patients and controls in South India and to explore a possible correlation to disease severity and clinical outcome. METHODS: Plasma levels of ALCAM, VCAM-1, sCD163, sCD14, YKL-40 and MIF were measured in scrub typhus patients (n = 129), healthy controls (n = 31) and in infectious disease controls (n = 31), both in the acute phase and after recovery, by enzyme immunoassays. RESULTS: Patients had markedly elevated levels of all mediators in the acute phase, differing from both healthy and infectious disease controls. During follow-up levels of ALCAM, VCAM-1, sCD14 and YKL-40 remained elevated compared to levels in healthy controls. High plasma ALCAM, VCAM-1, sCD163, sCD14, and MIF, and in particular YKL-40 were all associated with disease severity and ALCAM, sCD163, MIF and especially YKL-40, were associated with mortality. CONCLUSIONS: Our findings show that scrub typhus is characterized by elevated levels of monocyte/macrophage and endothelial related markers. These inflammatory markers, and in particular YKL-40, may contribute to disease severity and clinical outcome.
OBJECTIVES: Scrub typhus is endemic in the Asia-Pacific region. Mortality is high even with treatment, and further knowledge of the immune response during this infection is needed. This study was aimed at comparing plasma levels of monocyte/macrophage and endothelial related inflammatory markers in patients and controls in South India and to explore a possible correlation to disease severity and clinical outcome. METHODS: Plasma levels of ALCAM, VCAM-1, sCD163, sCD14, YKL-40 and MIF were measured in scrub typhus patients (n = 129), healthy controls (n = 31) and in infectious disease controls (n = 31), both in the acute phase and after recovery, by enzyme immunoassays. RESULTS:Patients had markedly elevated levels of all mediators in the acute phase, differing from both healthy and infectious disease controls. During follow-up levels of ALCAM, VCAM-1, sCD14 and YKL-40 remained elevated compared to levels in healthy controls. High plasma ALCAM, VCAM-1, sCD163, sCD14, and MIF, and in particular YKL-40 were all associated with disease severity and ALCAM, sCD163, MIF and especially YKL-40, were associated with mortality. CONCLUSIONS: Our findings show that scrub typhus is characterized by elevated levels of monocyte/macrophage and endothelial related markers. These inflammatory markers, and in particular YKL-40, may contribute to disease severity and clinical outcome.
Authors: Thor Ueland; Elisabeth Astrup; Kari Otterdal; Tove Lekva; Jeshina Janardhanan; John A J Prakash; Kurien Thomas; Annika E Michelsen; Pål Aukrust; George M Varghese; Jan K Damås Journal: PLoS Negl Trop Dis Date: 2021-04-29
Authors: Lynn Soong; Hui Wang; Thomas R Shelite; Yuejin Liang; Nicole L Mendell; Jiaren Sun; Bin Gong; Gustavo A Valbuena; Donald H Bouyer; David H Walker Journal: PLoS Negl Trop Dis Date: 2014-09-25
Authors: Tuula K Outinen; Paula Mantula; Pia Jaatinen; Mari Hämäläinen; Eeva Moilanen; Antti Vaheri; Heini Huhtala; Satu Mäkelä; Jukka Mustonen Journal: Viruses Date: 2019-08-21 Impact factor: 5.048