Macrophages in diabetes mellitus (DM) and COVID-19: do they trigger DM?
- PDF / 194,887 Bytes
- 4 Pages / 595.276 x 790.866 pts Page_size
- 67 Downloads / 162 Views
COMMENTARY
Macrophages in diabetes mellitus (DM) and COVID-19: do they trigger DM? Małgorzata Kloc 1,2,3 & Rafik M. Ghobrial 1,2 & Sławomir Lewicki 4 & Jacek Z. Kubiak 4,5 Received: 28 August 2020 / Revised: 28 August 2020 / Accepted: 12 October 2020 # Springer Nature Switzerland AG 2020
Abstract Diabetes mellitus (DM) augments the risk of hospitalization and mortality resulting from viral, bacterial, or fungal pathogen infection. This has been also true for the past SARS and MERS, and current SARS-CoV-2 coronavirus epidemics. Clinical data indicate that SARS-CoV-2 infection triggers a severe course of COVID-19 more frequently in diabetic than non-diabetic patients. Here we overview the cellular and molecular mechanisms associated with this phenomenon. We focus on alterations in the immune cells, especially monocytes and macrophages, involved in innate immune response and inflammatory processes, which differ in type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). We also describe the DM-related changes in the monocyte/macrophages functions, how they could lead to the severe outcome of SARS-CoV-2 infection, and importantly, if and how they could initiate DM in DM-susceptible patients. Keywords Diabetes mellitus . Macrophages . SARS-CoV-2 . COVID-19
Pancreatic macrophages Diabetes occurs when the excess of glucose accumulates in the blood because the pancreas, an organ responsible for the homeostasis of glucose in the bloodstream, is not producing enough insulin. The pancreas is a heterocrine gland that has food digestive (exocrine) and hormonal (endocrine) function. In its exocrine capacity, the pancreas produces hormones insulin, which lowers glucose level, and glucagon, which raises
* Małgorzata Kloc [email protected] * Jacek Z. Kubiak [email protected] 1
The Houston Methodist Research Institute, 6670 Bertner Ave, Houston, TX 77030, USA
2
Department of Surgery, The Houston Methodist Hospital, Houston, TX, USA
3
Department of Genetics, The University of Texas, M.D. Anderson Cancer Center, Houston, TX, USA
4
Department of Regenerative Medicine and Cell Biology, Military Institute of Hygiene and Epidemiology (WIHE), Warsaw, Poland
5
UnivRennes, UMR 6290, CNRS, Institute of Genetics and Development of Rennes, Cell Cycle Group, Faculty of Medicine, 2 Ave. du Prof. Leon Bernard, 35043 Rennes Cedex, France
glucose level, and somatostatin, which inhibits the secretion of insulin and glucagon. There are five types of cells in the pancreatic islets: β-cells secreting insulin; alpha cells secreting glucagon, delta cells secreting somatostatin, epsilon cells secreting ghrelin (a so-called “hunger hormone” that stimulates food intake, fat deposition and growth hormone release), and pancreatic polypeptide (PP) secreting cells, which regulate endocrine and exocrine secretory functions of the pancreas. In addition, the pancreatic islets contain a population of resident islet macrophages. The islet macrophages are self-renewed and are rarely, if not at all, replenished by the bone
Data Loading...
