Interferon 5 affects the differentiation of monocytes to CD11c+ inflammatory macrophages in the colon in mice. The study, published in Science Immunology, the authors write that the discovery allows to complete the picture of pathogenesis of inflammatory bowel disease, and also reveals new aspects of inflammation as a pathological process.
Regulatory factor interferon 5 (IRF5) along with other regulatory factors in the interferon (IRF1, IRF2, IRF3, IRF4, IRF6, IRF7, IRF8 and IRF9) is involved in the regulation of the inflammatory process caused by bacteria or a virus. Each IRF is responsible for its function in protecting the body from infections. It is known that IRF5 acts as a molecular switch of macrophages, giving them the team on the differentiation, proliferation and participate in the inflammatory process. However, it was not clear on the differentiation of what cells it affects, and what is its role in the implementation of the phenotype of cells.
In the study under the leadership of Alastair Corbin (Alastair L. Corbin) from the Institute of rheumatology Kennedy of the University of Oxford described the effect of IRF5 on healthy tissue colon, what is its role in the differentiation of monocytes into macrophage system of the mucous membrane of the colon and bone marrow inflammation caused by the bacterium Helicobacter hepaticus.
First, a group of researchers studied the effect of IRF5 on the healthy tissue of the colon. The researchers compared biopsy material of colon and blind intestine of mice with a modified level of development of IRF5 and genetically modified mice, which have turned off the gene responsible for the synthesis of IRF5. Histological examination was not found (p≤0.01) morphological differences between the control and modified samples. The immune cells of the lamina propria of the mucosa (leukocytes CD45+) was counted using flow cytometry and found that the number of mice without IRF5 comparable to mice from the control group. So scientists have found that the deficiency of IRF5 has little effect on healthy intestinal mucosa. The scientists also found that nemaline and selenocysteine population of white blood cells (those leukocytes which have evolved from precursors of the connective tissue cells in the intestine) Express low levels of IRF5 compared to CD11b+ myeloid cells. Among the unmodified mice, the relative number of macrophage cells in the lamina propria was higher than in mice without IRF5 (5.1 percent and 2.9 percent, respectively). Scientists have suggested that IRF5 influences the differentiation of monocytes into macrophages in the lamina propria of the colon and that deficiency of IRF5 may protect the gut from inflammation.