Takayasu's arteritis: role of Mycobacterium tuberculosis and its 65 kDa heat shock protein

1996 ◽  
Vol 55 (1) ◽  
pp. 49-55 ◽  
Author(s):  
A. Aggarwal ◽  
M. Chag ◽  
N. Sinha ◽  
S. Naik
Inflammation ◽  
2019 ◽  
Vol 43 (2) ◽  
pp. 487-506 ◽  
Author(s):  
Yanhao Zhang ◽  
Shanshan Li ◽  
Qianyi Liu ◽  
Ruiying Long ◽  
Jihong Feng ◽  
...  

Abstract Mycobacterium tuberculosis, the pathogen of tuberculosis (TB), can survive in host macrophages and induce macrophages to M2 phenotype might result in latent MTB infection. During the latent phase, the expression of MTB heat-shock protein 16.3 (Hsp16.3) is markedly increased among most of bacterial proteins, but the role of Hsp16.3 in macrophage M2 polarization is not clear. In this work, we found that macrophages incubated with 100 ng/ml MTB Hsp16.3 increased the production of Arg-1, IL-10, TGF-beta, and CD206. These results showed that MTB Hsp16.3 may induce macrophage M2 phenotype. And the interaction of Hsp16.3 with macrophages was found to depend on chemokine receptors CCRL2 and CX3CR1. Additionally, we used overexpression and silencing techniques to further verify the effect of CCRL2 and CX3CR1 on MTB Hsp16.3-induced M2 polarization macrophages. Furthermore, we explored the downstream signaling molecules of CCRL2 and CX3CR1 and we found MTB Hsp16.3 altered the signal transduction of the AKT/ERK/p38-MAPK. Taken together, this study provides evidence that MTB Hsp16.3 promotes macrophages to M2 phenotype and explores its underlying mechanism.


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 539.3-539
Author(s):  
T. Khan ◽  
N. Cleaton ◽  
T. Sheeran

Background:Takayasu’s arteritis (TA) is a large vessel vasculitis that principally affects the aorta and its main branches. The incidence has been reported at between 1.2 – 2.3 cases per million per year, more commonly in the Asian population. The age of onset is typically between tenth and fourth decade; between 80 and 90 percent of the cases are female.The relationship between Mycobacterium Tuberculosis (mTB) and TA has long been considered; both demonstrate chronic inflammatory changes on histological examination and some granuloma formation in arterial walls. There is increasing evidence implicating mTB in the pathogenesis of TA through molecular mimicry between the mycobacterium heat shock protein -65 (mHSP-65) and the human homologue HSP -60 (hHSP-60). However, no definitive link between the two diseases has been explained.Objectives:Case presentation.Results:A 23-year-old lady was referred to our outpatient rheumatology clinic with a twelve-month history of persistently enlarged cervical lymph nodes on the left side for which she had received six months of anti-Tuberculosis medication. She had been referred to the respiratory physicians who had diagnosed presumed Tuberculous Lymphadenitis, with caseating granulomas demonstrated on biopsy, positive acid-fast bacilli smear but a negative culture. The patient had been initiated six months of anti-Tuberculosis medication; however, her lymphadenopathy showed no improvement. More recently she described a five-month history of weakness, paraesthesia and claudication symptoms in her left upper limb with episodes of dizziness and blurred vision, episodes occurring 2-3 times per day and lasting between a few minutes to a few hours.Her examination at this presentation revealed an unrecordable blood pressure in the left upper limb and 104/67mmHg in the right. There was significant tender lymphadenopathy of the left cervical lymph nodes and diminished pulses in the left upper limb. Right sided pulses were normal. The rest of her examination was normal.Investigations at presentation revealed elevated inflammatory markers with C- reactive protein (CRP) of 116mg/dL and erythrocyte sedimentation rate (ESR) of 128mm/h. Complete blood count (CBC) found her to be anaemic with a haemoglobin of 100g/L, with a mean cell volume of 71.3fl, and have elevated platelet count of 649x 109/L. Recent computerized tomography scan with contrast of the thorax demonstrated features consistent with Takayasu Arteritis. Marked left subclavian stenosis was found on magnetic resonance imaging. High dose prednisolone at 60mg once daily along with Azathioprine 2mg/kg/day was started with a follow up appointment in two weeks.Conclusion:There is increasing evidence implicating mTB in the development of TA and a few cases recognising this link have been reported. We report a case of TA in a patient recently diagnosed and treated for Tuberculous lymphadenitis who then developed symptoms of TA. There should be a low threshold for suspecting a diagnosis of Takayasu’s arteritis in patients previously or actively infected with Mycobacterium Tuberculosis. Further research exploring the relationship between mTB and TA is required.References:[1]Espinoza JL, Ai S, Matsumura I. New Insights on the Pathogenesis of Takayasu Arteritis: Revisiting the Microbial Theory. Pathogens. 2018;7(3):73.[2]Aggarwal A, Chag M, Sinha N, et al. Takayasu’s arteritis: role of Mycobacterium tuberculosis and its 65 kDa heat shock protein. International Journal of Cardiology. 1996; 55: 49–55.[3]Reshkova V, Kalinova D, Rashkov R. Takayasu’s Arteritis associated with Tuberculosis Infections. Journal of Neurology and Neuroscience. 2016; 3:114.[4]Moritz K, Jansson Hilte F, Antje Kangowski, Christian Kneitz, Emil C. Reisinger. Tuberculosis and Takayasu arteritis: case-based review Rheumatology International 2019 39:345–351[5]D Misra, A Wakhlu, V Agarwal, D Danda. Recent advances in the management of Takayasu arteritis International Journal of Rheumatic Diseases 2019; 22: 60–68Disclosure of Interests:None declared


2004 ◽  
Vol 32 (6) ◽  
pp. 1425-1426 ◽  
Author(s):  
Martin Westphal ◽  
Perenlei Enkhbaatar ◽  
Daniel L. Traber

2015 ◽  
Vol 158 (3) ◽  
pp. 377-379 ◽  
Author(s):  
N. V. Ryazantseva ◽  
E. A. Stepovaya ◽  
O. L. Nosareva ◽  
E. V. Konovalova ◽  
D. S. Orlov ◽  
...  

Autoimmunity ◽  
2009 ◽  
Vol 42 (6) ◽  
pp. 475-483 ◽  
Author(s):  
Qiyan Xiong ◽  
Liang Jin ◽  
Jianping Li ◽  
Hao Fan ◽  
Rongyue Cao ◽  
...  

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