Inflammatory Response
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2021 ◽  
Vol 12 ◽  
Author(s):  
Victor Vaernewyck ◽  
Boaz Arzi ◽  
Niek N. Sanders ◽  
Eric Cox ◽  
Bert Devriendt

Approximately 9 out of 10 adults have some form of periodontal disease, an infection-induced inflammatory disease of the tooth-supporting tissues. The initial form, gingivitis, often remains asymptomatic, but this can evolve into periodontitis, which is typically associated with halitosis, oral pain or discomfort, and tooth loss. Furthermore, periodontitis may contribute to systemic disorders like cardiovascular disease and type 2 diabetes mellitus. Control options remain nonspecific, time-consuming, and costly; largely relying on the removal of dental plaque and calculus by mechanical debridement. However, while dental plaque bacteria trigger periodontal disease, it is the host-specific inflammatory response that acts as main driver of tissue destruction and disease progression. Therefore, periodontal disease control should aim to alter the host’s inflammatory response as well as to reduce the bacterial triggers. Vaccines may provide a potent adjunct to mechanical debridement for periodontal disease prevention and treatment. However, the immunopathogenic complexity and polymicrobial aspect of PD appear to complicate the development of periodontal vaccines. Moreover, a successful periodontal vaccine should induce protective immunity in the oral cavity, which proves difficult with traditional vaccination methods. Recent advances in mucosal vaccination may bridge the gap in periodontal vaccine development. In this review, we offer a comprehensive overview of mucosal vaccination strategies to induce protective immunity in the oral cavity for periodontal disease control. Furthermore, we highlight the need for additional research with appropriate and clinically relevant animal models. Finally, we discuss several opportunities in periodontal vaccine development such as multivalency, vaccine formulations, and delivery systems.


2021 ◽  
pp. jnumed.121.262301
Author(s):  
Christoph Rischpler ◽  
Tienush Rassaf ◽  
Lale Umutlu ◽  
Ken Herrmann ◽  
Thomas-Wilfried Schlosser ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Hylton E. Rodel ◽  
Isabella A. T. M. Ferreira ◽  
Carly G. K. Ziegler ◽  
Yashica Ganga ◽  
Mallory Bernstein ◽  
...  

Mycobacterium tuberculosis (Mtb) bacilli readily aggregate. We previously reported that Mtb aggregates lead to phagocyte death and subsequent efficient replication in the dead infected cells. Here, we examined the transcriptional response of human monocyte derived macrophages to phagocytosis of aggregated Mtb relative to phagocytosis of non-aggregated single or multiple bacilli. Infection with aggregated Mtb led to an early upregulation of pro-inflammatory associated genes and enhanced TNFα signaling via the NFκB pathway. These pathways were significantly more upregulated relative to infection with single or multiple non-aggregated bacilli per cell. Phagocytosis of aggregates led to a decreased phagosome acidification on a per bacillus basis and increased phagocyte cell death, which was not observed when Mtb aggregates were heat killed prior to phagocytosis. Mtb aggregates, observed in a granuloma from a patient, were found surrounding a lesion cavity. These observations suggest that TB aggregation may be a mechanism for pathogenesis. They raise the possibility that aggregated Mtb, if spread from individual to individual, could facilitate increased inflammation, Mtb growth, and macrophage cell death, potentially leading to active disease, cell necrosis, and additional cycles of transmission.


2021 ◽  
Vol 12 ◽  
Author(s):  
Qi-Ming Pang ◽  
Si-Yu Chen ◽  
Qi-Jing Xu ◽  
Sheng-Ping Fu ◽  
Yi-Chun Yang ◽  
...  

Transected axons are unable to regenerate after spinal cord injury (SCI). Glial scar is thought to be responsible for this failure. Regulating the formation of glial scar post-SCI may contribute to axonal regrow. Over the past few decades, studies have found that the interaction between immune cells at the damaged site results in a robust and persistent inflammatory response. Current therapy strategies focus primarily on the inhibition of subacute and chronic neuroinflammation after the acute inflammatory response was executed. Growing evidences have documented that mesenchymal stem cells (MSCs) engraftment can be served as a promising cell therapy for SCI. Numerous studies have shown that MSCs transplantation can inhibit the excessive glial scar formation as well as inflammatory response, thereby facilitating the anatomical and functional recovery. Here, we will review the effects of inflammatory response and glial scar formation in spinal cord injury and repair. The role of MSCs in regulating neuroinflammation and glial scar formation after SCI will be reviewed as well.


Author(s):  
Yuyao Shen ◽  
Senwei Zhao ◽  
Minglei Hua

Acute lung injury (ALI) induced by bacteria LPS is characterized by the upregulation of the apoptosis rate of tissue cells and aggravation of inflammatory response. Although many studies have focused on the pathogenesis of this disease, its mechanism remains unknown. This study examined the regulatory role of long non-coding RNA (lncRNA) LINC01194 in the progression of ALI through various bioinformatics analyses and experimental work, including ELISA assay, dual-luciferase reporter assay, biotinylated RNA pull-down assay, and western blot analysis. The result showed that the LINC01194 was overexpressed in the ALI-induced mice model. We observed a significant upregulation of LINC01194 in LPS-treated Mouse lung epithelial type II cells (MLE-12 cells) after 24 hrs of induction. Bioinformatics analysis, Elisa assay, qRT-PCR analysis, Biotinylated RNA pull-down assay, apoptosis test, and western blot analysis demonstrated that the LINC01194 could act as a miR-203a-3p sponge to activate the inflammatory response in LPS-induced ALI model through post-transcriptional upregulation of MIP-2. We showed that LINC01194 regulates the inflammatory response and apoptosis of LPS-induced mice and MLE-12 cells via the miR-203a-3p/MIP-2 axis. LINC01194 could be a potential biomarker for early diagnosis and the treatment of ALI.


2021 ◽  
Author(s):  
Yuqi Ma ◽  
Peixia Fan ◽  
Rui Zhao ◽  
Yinghua Zhang ◽  
Xianwei Wang ◽  
...  

Abstract BackgroundThe inflammatory response caused by microglia in the central nervous system plays an important role in Alzheimer's disease. Neuregulin-1 (NRG1) is a member of the neuregulin family and has been demonstrated to have anti-inflammatory properties. The relationship between NRG1, microglia phenotype and neuroinflammation remains unclear.Materials and MethodsBV2 cells were used to examine the mechanism of NRG1 in regulating microglia polarization. Neuronal apoptosis, inflammatory factors TNF-α and iNOS, microglia polarization, ErbB4 and NF-κB p65 expression were assessed.ResultsWe found that exogenous NRG1 treatment or overexpression improved microglial activity and reduced the secretion of the inflammatory factors TNF-α and iNOS in vitro. The expression of Bax in SH-SY5Y neuron cells incubated with medium collected from the NRG1 treatment group decreased. Additionally, our study showed that NRG1 treatment reduced the levels of the M1 microglia markers CD120 and iNOS and increased the levels of the M2 microglia markers CD206 and Arg-1. Furthermore, we observed that NRG1 treatment attenuated Aβ-induced NF-κB activation and promoted the expression of p-ErbB4 and that knockdown of ErbB4 abrogated the effects of NRG1 on NF-κB, Bax levels and M2 microglial polarization. ConclusionNRG1 inhibits the release of inflammatory factors in microglia and regulates the switching of the M1/M2 microglia phenotype, most likely via ErbB4-dependent inhibition of the NF-κB pathway.


2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Wei Li ◽  
Jiang Wu ◽  
Mingjin Guo ◽  
Jing Shang

Chronic inflammation can stimulate the formation and progression of atherosclerotic plaques and increase the vulnerability of plaques. However, there are few studies on the changes of carotid inflammatory plaques during treatment. Our study attempted to investigate the use of superparamagnetic iron oxide nanoparticle (SPION) ultrasound imaging to detect the expression of vascular cell adhesion molecule-1 (VCAM-1) in patients with carotid plaques and analyze the effects of SPION ultrasound imaging in inflammatory plaque visualization effect. SPION microbubble contrast agents have good imaging effects both in vivo and in vitro. We conjugated the VCAM-1 protein to the microbubbles wrapped in SPIONs to form SPIONs carrying VCAM-1 antibodies. Observe the signal intensity of SPIONs carrying VCAM-1 antibody to arteritis plaque. The results showed that the SPION contrast agent carrying VCAM-1 antibody had higher peak gray-scale video intensity than the other two groups of contrast agents not carrying VCAM-1 antibody. It shows that SPIONs have excellent imaging effects in ultrasound imaging, can evaluate the inflammatory response of arterial plaque lesions, and are of great significance for the study of carotid inflammatory plaque changes.


2021 ◽  
Vol 12 ◽  
Author(s):  
Flavia Tramontana ◽  
Sofia Battisti ◽  
Nicola Napoli ◽  
Rocky Strollo

Epidemiological evidence shows clear gender disparities in the Coronavirus 2019 Disease (COVID-19) severity and fatality. This may reflect the contribution of gender-related factors, such as sex hormones, to COVID-19 pathogenesis. However, the mechanism linking gender disparities to COVID-19 severity is still poorly understood. In this review, we will pinpoint several elements involved in COVID-19 pathogenesis that are regulated by the two main sex hormones, estrogen and androgen. These include tissue specific gene regulation of SARS-CoV2 entry factors, innate and adaptive immune responses to infection, immunometabolism, and susceptibility to tissue injury by cytopathic effect or hyper-inflammatory response. We will discuss the mechanistic link between sex hormone regulation of COVID-19 pathogenetic factors and disease severity. Finally, we will summarize current evidence from clinical studies and trials targeting sex hormones and their signalling in COVID-19. A better understanding of the role of sex hormones in COVID-19 may identify targets for therapeutic intervention and allow optimization of treatment outcomes towards gender-based personalised medicine.


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