Chlamydia pneumoniae heat shock protein 60 is associated with apoptotic signaling pathway in human atheromatous plaques of coronary artery disease patients

Jha, Hem Chandra; Srivastava, Pragya; Vardhan, Harsh; Singh, Laishram Chandreshwor; Bhengraj, Apurb Rashmi; Prasad, Jagdish; Mittal, Aliza

doi:10.1016/j.jjcc.2011.07.010

Cited by 23 publications

(16 citation statements)

References 62 publications

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“…In both Mycoplasma pneumoniae and Mycoplasma genitalium infection, GroEL is associated with adherence, complementing adhesion proteins like HMW1 and P1. In addition, Chlamydophila pneumoniae Hsp60 was reported to have an association with the apoptotic signaling pathway, and in some patients with Hsp60-positive coronary artery disease, proapoptotic genes or proteins exhibit high expression (26). Similar results were observed in our study: GroEL of M. gallisepticum not only attached to the host cells but also upregulated the expression of apoptosis-related caspase proteins (Fig.…”

Section: Discussionsupporting

confidence: 90%

GroEL Protein (Heat Shock Protein 60) of Mycoplasma gallisepticum Induces Apoptosis in Host Cells by Interacting with Annexin A2

Zhang

Chen

et al. 2019

Infect Immun

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Mycoplasma gallisepticum is an avian respiratory and reproductive tract pathogen that has a significant economic impact on the poultry industry worldwide. Although membrane proteins of Mycoplasma spp. are thought to play crucial roles in host interactions, very few have had their biochemical function defined. In this study, we found that the GroEL protein (heat shock protein 60) of Mycoplasma gallisepticum could induce apoptosis in peripheral blood mononuclear cells, and the underlying molecular mechanism was further determined. The GroEL gene from Mycoplasma gallisepticum was cloned and expressed in Escherichia coli to facilitate the functional analysis of recombinant protein. The purified GroEL protein was shown to adhere to peripheral blood mononuclear cells (PBMCs) and DF-1 cells and cause apoptosis in PBMCs. A protein pulldown assay coupled with mass spectrometry identified that annexin A2 possibly interacted with GroEL protein. Coimmunoprecipitation assays confirmed that GroEL proteins could bind to annexin A2, and confocal analysis further demonstrated that GroEL colocolized with annexin A2 in HEK293T cells and PBMCs. Moreover, annexin A2 expression was significantly induced by a recombinant GroEL protein in PBMCs, and knocking down annexin A2 expression resulted in significantly reduced apoptosis. Taken together, these data suggest that GroEL induces apoptosis in host cells by interacting with annexin A2, a novel virulence mechanism in Mycoplasma gallisepticum. Our findings lead to a better understanding of molecular pathogenesis in Mycoplasma gallisepticum.

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Section: Discussionsupporting

confidence: 90%

GroEL Protein (Heat Shock Protein 60) of Mycoplasma gallisepticum Induces Apoptosis in Host Cells by Interacting with Annexin A2

Zhang

Chen

et al. 2019

Infect Immun

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“…30,31 Polygenetic analysis has reported that rs6734238 in the IL1F10/IL1RN locus was found to be significantly associated with coronary artery disease. 32 Additionally, in atherosclerotic plaques of patients with coronary heart disease (CAD), 33 We previously reported that circulating IL-38 was increased in STEMI patients, which indicated that IL-38 may act as a promotive role in the development of MI. 20 In this study, we observed that administration of rIL-38 in mice ameliorated ventricular remodelling via suppressing infiltration of inflammatory cells and inhibiting proinflammatory cytokines in the post-MI hearts.…”

Section: Discussionmentioning

confidence: 99%

Interleukin‐38 alleviates cardiac remodelling after myocardial infarction

Wei

Yin

Zhong

et al. 2019

J Cellular Molecular Medi

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Excessive immune‐mediated inflammatory reaction plays a deleterious role in ventricular remodelling after myocardial infarction (MI). Interleukin (IL)‐38 is a newly characterized cytokine of the IL‐1 family and has been reported to exert a protective effect in some autoimmune diseases. However, its role in cardiac remodelling post‐MI remains unknown. In this study, we found that the expression of IL‐38 was increased in infarcted heart after MI induced in C57BL/6 mice by permanent ligation of the left anterior descending artery. In addition, our data showed that ventricular remodelling after MI was significantly ameliorated after recombinant IL‐38 injection in mice. This amelioration was demonstrated by better cardiac function, restricted inflammatory response, attenuated myocardial injury and decreased myocardial fibrosis. Our results in vitro revealed that IL‐38 affects the phenotype of dendritic cells (DCs) and IL‐38 plus troponin I (TNI)‐treated tolerogenic DCs dampened adaptive immune response when co‐cultured with CD4+T cells. In conclusion, IL‐38 plays a protective effect in ventricular remodelling post‐MI, one possibility by influencing DCs to attenuate inflammatory response. Therefore, targeting IL‐38 may hold a new therapeutic potential in treating MI.

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“…Moreover, polymorphisms in IL-38 were associated with CRP concentrations in humans [23] and were found to be significantly associated with coronary artery disease (CAD) [24]. In addition, IL-38 mRNA was found in human atheromatous plaques of coronary artery disease patients [25]. These results suggest an important role for IL-38 in cardiovascular diseases, indicating that IL-38 might also play an important role in hyperlipidemia which contributes to cardiovascular disease development.…”

Section: Introductionmentioning

confidence: 89%

Elevated Interleukin-38 Level Associates with Clinical Response to Atorvastatin in Patients with Hyperlipidemia

Yang

Song

Dong

et al. 2018

Cell Physiol Biochem

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Background/Aims: Hyperlipidemia is a risk factor for various cardiovascular and metabolic disorders. And it is tightly related to chronic inflammation. Interleukin-38 (IL-38) represents a new member of anti-inflammatory cytokines. Thus we studied the important role of IL-38 in hyperlipidemia development and treatment. Methods: The mRNA level of IL-38 in PBMCs (peripheral blood mononuclear cells) and serum IL-38 levels in hyperlipidemia patients and healthy controls were measured by real-time polymerase chain reaction (RT-PCR) and enzyme-linked immunoassay (ELISA). The hyperlipidemia patients were further divided into two groups (Sensitive and Resistant Group) according to their clinical response to Atorvastatin therapy. Finally, the effects of IL-38 on hyperlipidemia was evaluated in the mice model. Results: Data showed that the IL-38 mRNA and serum protein levels were higher in patients with hyperlipidemia compared with healthy controls. And the IL-38 mRNA and serum protein levels were higher in patients sensitive to Atorvastatin therapy than the resistant group. In vitro, IL-38 inhibited the production of IL-6, IL-1β and CRP in PBMCs of patients with hyperlipidemia. In the mice model of hyperlipidemia, IL-38 was also elevated during the hyperlipidemia development. Furthermore, the IL-38 over-expressed by adeno-associated virus significantly inhibited the hyperlipidemia development, inflammatory factor secretion and also the atherosclerosis process. Conclusion: Thus our data showed that IL-38 might present protective effects on hyperlipidemia treatment.

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Chlamydia pneumoniae heat shock protein 60 is associated with apoptotic signaling pathway in human atheromatous plaques of coronary artery disease patients

Abstract: Genes/proteins of pre-apoptotic caspase dependent/independent pathways, chemokines, and inflammatory cytokines receptors were significantly up-regulated in human atheromatous plaques of cHSP60 positive CAD patients suggesting an association of cHSP60 with CAD.

Cited by 23 publications

References 62 publications

GroEL Protein (Heat Shock Protein 60) of Mycoplasma gallisepticum Induces Apoptosis in Host Cells by Interacting with Annexin A2

GroEL Protein (Heat Shock Protein 60) of Mycoplasma gallisepticum Induces Apoptosis in Host Cells by Interacting with Annexin A2

Interleukin‐38 alleviates cardiac remodelling after myocardial infarction

Elevated Interleukin-38 Level Associates with Clinical Response to Atorvastatin in Patients with Hyperlipidemia

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