Through joint research with Tokyo University of Science and Keio University, a research group led by Assistant Professor Yosuke Masamoto of the Graduate School of Medicine of the University of Tokyo has increased the proliferation of leukocytes that prevent infection by the hormone "adiponectin" secreted from fat cells. It was found to suppress the aggravation of bacterial infections caused by obesity.
Obesity is defined as having a BMI (body mass index) of 25 or higher, visceral fat obesity, and one or more obesity-related complications (2 diseases such as type 11 diabetes, hypertension, and cerebral infarction).In addition, obesity is considered to be a risk factor for influenza, pneumonia, asthma, cancer, etc., and it is said that various infectious diseases are likely to become severe, but there are many unclear points about the molecular mechanism.
This time, we discovered that the bone marrow of obese mice has decreased production of adiponectin due to abnormalities in adipocytes.Analysis shows that when adiponectin decreases, the secretion of the inflammatory cytokine TNF (a protein that promotes inflammation due to trauma, etc.) increases from bone marrow macrophages, which are a type of white blood cell.Furthermore, when hematopoietic progenitor cells (cells that differentiate into various blood types) are placed in such an environment, signal transduction of the immune system is inhibited (increased expression of the cytokine signal suppressor SOCS1).Therefore, it was found that hematopoietic progenitor cells cannot proliferate properly in response to cytokines during infection, and are aggravated by suppression of the production of granulocytes (a type of leukocyte) that prevent infection.
It was also clarified that administration of adiponectin to obese mice infected with a bacterium (Listeria monocytogenes) improved the symptoms.
From this study, it was found that the hematopoietic mechanism to prevent infection does not work well in obesity.In addition, it is clarified that hematopoietic abnormalities occur when the action of adiponectin is insufficient, which is expected to lead to the development of new therapeutic methods.
