Activation of inflammatory cells and cytokines by peptide epitopes in vitro: a simple in-vitro screening assay for prioritizing them for in-vivo studies

Mundkur, Lakshmi; Varma, Meenakshi; Shivanandan, Hemapriya; Krishna, Dhanush; Kumar, Kiran; Lu, Xinjie; Kakkar, Vijay V.

doi:10.1007/s00011-013-0599-y

Cited by 5 publications

(3 citation statements)

References 37 publications

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“…Again, the same human ApoB (688-707) and hHSP60 peptide (153-163) were used with the aim to develop an in vitro assay to screen peptide molecules for their inflammatory properties. The results were similar to earlier studies using these peptides, with induced T cell proliferation and expansion of regulatory T cells with IL-10 and TGF-β secretion and reduction of early atherosclerotic lesion formation in mice by 32.1 and 33.5 %, respectively (Mundkur et al 2013b). It has recently been shown that resident commensal bacterial GroEL, but not mouse-derived HSP60, could cause naïve T cells to differentiate into CD4…”

Section: Hsp60 Tolerization In Atherosclerosissupporting

confidence: 91%

Tolerization against atherosclerosis using heat shock protein 60

Wick

2016

Cell Stress and Chaperones

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Section: Hsp60 Tolerization In Atherosclerosissupporting

confidence: 91%

Tolerization against atherosclerosis using heat shock protein 60

Wick

2016

Cell Stress and Chaperones

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“…When a combination of human apolipoprotein B (ApoB 688-707 ) and human HSP60 153-163 (hHSP60) peptide was used to immunize mice, an additive effect on atherosclerosis was found compared to single immunization [37] ; similar findings were reported by another study by the same group [38] . These peptides have also been successfully used orally with the aim of preventing progression of atherosclerosis [39,40] . Again, all these studies have only been performed on young animals and mbHSP65 tolerization has so far never been studied in chronic atherosclerosis of aged animals.…”

Section: Discussionmentioning

confidence: 99%

Oral Tolerization with Mycobacterial Heat Shock Protein 65 Reduces Chronic Experimental Atherosclerosis in Aged Mice

Wick

Onestingel²,

Demetz³

et al. 2017

Gerontology

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Background: Atherosclerosis is a chronic inflammatory disease of the artery wall where both innate and adaptive immunity play important roles. Modulation of the immune response against the stress protein antigen, heat shock protein (HSP) 60, by administration of mycobacterial HSP65 (mbHSP65) orally and/or nasally shows promising therapeutic results in young animals in the sense of less severe experimental atherosclerosis; however, the case of aged animals with already established atherosclerosis has so far never been investigated. Objective: To investigate if mbHSP65 immunization would further accelerate atherosclerotic progression in aged ApoE^-/- mice (18 months old) with already long-established atherosclerosis and if these mice could be orally tolerized against mbHSP65. Methods: Aged wild-type (WT) and ApoE^-/- mice (65 weeks) were immunized and/or orally treated with mbHSP65 and then either kept on normal chow or changed to high-cholesterol diet (HCD). Atherosclerosis was assessed by en face analysis and the number of CD4⁺CD25⁺FoxP3⁺ T regulatory cells (Tregs) was assessed by flow cytometry in lymph node and spleen cells. Total cholesterol and triglyceride levels were determined. Soluble mammalian HSP60 and anti-mouse HSP60 (mHSP60) and anti-mbHSP65 antibodies were detected by enzyme-linked immunosorbent assay. Results: As expected, aged WT mice had only minor lesions in the aorta, which did not change under HCD for 14 weeks. Aged ApoE^-/- mice already had large complicated plaques, which increased in size under HCD. mbHSP65 immunization led to a significant aggravation of atherosclerosis in both WT and ApoE^-/- mice irrespective of the nature of their diet. This increase was accompanied by increased titers of both anti-mHSP60 and anti-mbHSP65 antibodies in the circulation. The increased plaque formation could be significantly diminished with oral mbHSP65 tolerization. An increased number of Tregs and lower or unchanged levels of cholesterol and triglycerides were associated with the reduced size of aortal lesions. Conclusion: Oral tolerization against mbHSP65 could be used both to prevent and to treat chronic atherosclerosis in aged individuals.

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“…The efficacy of atherosclerosis prevention was assessed for peptides derived from apolipoprotein B100 (ApoB), heat shock protein 60 (HSP60), and complement cascade (peptide A). Both ApoB and HSP60 appeared to reduce early atherosclerotic lesions in mice by 32.1 and 33.5%, respectively, while the reduction with peptide A was 5.7% [ 58 ].…”

Section: Vaccinationmentioning

confidence: 99%

Vaccination against Atherosclerosis: Is It Real?

Poznyak

Bezsonov

Popkova

et al. 2022

IJMS

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Atherosclerosis has been known in medicine for several centuries. As early as 1755, the Swedish anatomist Albrecht von Haller used the term “atheroma” to describe vascular lesions. Atherosclerosis may originate from an unbalanced diet or bad habits, and is mainly found in developed countries. Clinical trials have been conducted to establish the causes of atherosclerosis, and also to develop treatments for this disease. However, prevention of the disease has always been better than treatment, so vaccination may be the key to saving thousands of lives. The creation of a vaccine may be directly related to the study of autoimmune processes occurring in the body, immunity. This review considers the issues related to the involvement of the immune response in the development of atherosclerotic lesions. Modern concepts of atherogenesis, immune inflammation in atherosclerosis, and potential vaccine targets are also discussed. There is a particular focus on experimental and clinical data supporting the development of immune therapies to reduce cardiovascular risk.

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Activation of inflammatory cells and cytokines by peptide epitopes in vitro: a simple in-vitro screening assay for prioritizing them for in-vivo studies

Cited by 5 publications

References 37 publications

Tolerization against atherosclerosis using heat shock protein 60

Tolerization against atherosclerosis using heat shock protein 60

Oral Tolerization with Mycobacterial Heat Shock Protein 65 Reduces Chronic Experimental Atherosclerosis in Aged Mice

Vaccination against Atherosclerosis: Is It Real?

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