Intracellular recognition of self and non-self -nucleic acids can result in the initiation of effective pro-inflammatory and anti-tumorigenic responses. We hypothesized that macrophages can be activated by tumor-derived nucleic acids to induce inflammasome activation in the tumor microenvironment. We show that tumor conditioned media (CM) can induce IL-1β production, indicative of inflammasome activation in primed macrophages. This could be partially dependent on caspase 1/11, AIM2 and NLRP3. IL-1β enhances tumor cell proliferation, migration and invasion while coculture of tumor cells with macrophages enhances the proliferation of tumor cells, which is AIM2 and caspase 1/11 dependent. Furthermore, we have identified that DNA-RNA hybrids could be the nucleic acid form which activates AIM2 inflammasome at a higher sensitivity as compared to dsDNA. Taken together, the tumor-secretome stimulates an innate immune pathway in macrophages which promotes paracrine cancer growth and may be a key tumorigenic pathway in cancer. Broader understanding on the mechanisms of nucleic acid recognition and interaction with innate immune signaling pathway will help us to better appreciate its potential application in diagnostic and therapeutic benefit in cancer.
Introduction: An estimated 80% of consequential medical oversights originate from communication errors during patient hand-offs between clinical providers during inter-facility transfer. During the transfer, patients are at risk of receiving low quality, fragmented care plagued with inadequate communication and coordination across settings. Effective and efficient inter-establishment transfers are thus pivotal to safeguard the quality of care received by patients, thereby optimizing patient outcomes. Methods: To inform the limited literature on the barriers to an effective and efficient intra-and inter-establishment transfer of elderly patients in health care, a scoping review specific to the geriatric context was undertaken. Searches of three electronic databases (MEDLINE, CINAHL, and Scopus) were conducted between 15th September to 1st November 2021. 18 peer-reviewed English-written articles published between 2011 and 2021 were included in this review. The Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) Checklist and Arksey and O'Malley's (2005) methodological approach for scoping reviews informed the writing of this review.Results: This review identified a total of 18 articles that discussed barriers to an effective and efficient inter-establishment transfer of elderly patients in healthcare. Three categories of barriers: individual-level, healthcare provider-level, and organizational-level were identified. Discussion: In the current literature, most studies pertain to the transition of older patients from hospital to home, there is a dearth in research elucidating the barriers related to intra-and inter-facility transfer of elderly patients. Of the barriers that we found, communication barriers were present in all three levels: individual, healthcare provider, and organizational. Limitations are presented. Conclusion: This review found several areas that should be improved for safer care transitions of elderly patients between facilities. The efficient and effective intra-and inter-establishment transfer of elderly patients in health care is impeded by a range of barriers, most importantly a lack of communication, which is found in every three levels of barriers. By categorizing the barriers to an efficient and effective transition of elderly patients into three levels: individual, health professional, and organizational, this scoping review hopes to present current research in a structured way for future research.
Introduction: Globally, Myocardial Ischemia or Ischemic Heart Disease (IHD) inflicts 126 million individuals, totaling an estimated nine million deaths annually. IHD injury and healing are characterized by recruitment of several immune cell types to the cardiac tissue. In addition, atherosclerosis, a common causative factor of IHD, is initiated by mediators of innate and adaptive immunity, thus providing the rationale for studying the role of immune cell types in myocardial ischemia. Clarifying the functions and interactions among these cell types will inform drug targeting studies and ultimately facilitate development of IHD treatment and prevention approaches. Methods: This systematic review highlights and summarizes pertinent studies evidencing the function and interaction of macrophages, monocytes, lymphocytes, platelets, and endothelial cells in IHD pathology. Electronic databases searched consist of Ovid, PubMed, Google Scholar, Web of Science, and ScienceDirect. Keywords include: “immune cells”, “innate immunity”, “inflammation”, “cardiac macrophages”, “adaptive immunity”, “lymphocytes”, “B cells”, “T cells”, “T-regulatory cells”, “myocardial infarction”, “reperfusion”, and additional related keywords. Results: Macrophages, monocytes, lymphocytes, platelets, and endothelial cells interact under innate and adaptive immune responses to initiate and sustain inflammation in cardiac tissue. Sustained inflammation signals for the recruitment of associated molecules to the site of ischemic heart damage which instigate injury and healing processes. Discussion: Building a comprehensive picture of interacting cell types enables the identification of druggable targets and potential treatment and prevention options. Here, we propose several steps of IHD pathology during which further studies with agonist and inhibitor molecules may yield fruitful treatment directions. Lastly, we discuss study limitations and future research avenues. Conclusions: Overall, explicating the immune cell type function and interactions will build a connective understanding of IHD pathology. In turn, elucidating the molecular and cell-specific mechanisms of the inflammatory immune response in cardiomyopathies will aid in the modelling of IHD disease progression as well as facilitate the identification of potential biomarkers and druggable targets to alleviate heart failure disease burden.
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