The chemokine CCL18 causes maturation of cultured monocytes to macrophages in the M2 spectrum

Abstract

Summary The observation that human monocytes cultured in the presence of the chemokine CCL18 showed increased survival, led us to profile cytokine expression in CCL18‐stimulated versus control cultures. CCL18 caused significantly increased expression of chemokines (CXCL8, CCL2, CCL3 and CCL22), interleukin‐10 (IL‐10) and platelet‐derived growth factor, but no up‐regulation of M1 cytokines IL‐1β or IL‐12. CCL18‐stimulated monocytes matured into cells with morphological resemblance to IL‐4‐stimulated macrophages, and expressed the monocyte marker CD14 as well the M2 macrophage markers CD206 and 15‐lipoxygenase, but no mature dendritic cell markers (CD80, CD83 or CD86). Functionally, CCL18‐stimulated macrophages showed a high capacity for unspecific phagocytosis and for pinocytosis, which was not associated with an oxidative burst. These findings suggest that CCL18‐activated macrophages stand at the cross‐roads between inflammation and its resolution. The chemokines that are produced in response to CCL18 are angiogenic and attract various leucocyte populations, which sustain inflammation. However, the capacity of these cells to remove cellular debris without causing oxidative damage and the production of the anti‐inflammatory IL‐10 will initiate termination of the inflammatory response. In summary, CCL18 induces an M2 spectrum macrophage phenotype in the absence of IL‐4.

Reduction of eotaxin production and eosinophil recruitment by pulmonary autologous macrophage transfer in a cockroach allergen-induced asthma model

“…In this study, we have shown that exposure to CRA has a significant effect on macrophage phenotypes, increasing the number of macrophages in the lung and reducing their surface expression of CD80 and CD86, molecules, which, among others, have been previously established as useful in assessing the phenotype of macrophages (1,10,19,20,35,39,51). We have also developed a novel procedure to supplement the lung macrophage population in our outbred mouse model; to our knowledge the use of an ATM has never been investigated in the CRA-induced asthma model.…”

“…Additional studies have shown the association of low expression levels of CD80 and CD86 with the M2 phenotype (10,39,51). The purpose of this study was not to characterize the macrophage phenotype induced by CRA exposure but rather to demonstrate that CRA exposure induces a change in phenotype and that addition of naive macrophages will reduce eosinophil recruitment.…”

<b>CD14</b>^<b>+</b><b> follicular dendritic cells in lymphoid follicles may play a role in the pathogenesis of IgG4-related </b><b>disease </b>

“…Furthermore, FDCs attract Th2 cells by secreting TARC (14). M2 macrophages produce CCL18, which attracts Th2 cells and induces differentiation of monocytes into M2 macrophages (29). In addition, FDCs can be differentiated from monocytes in vitro (8).…”

In Vivo and in Vitro Studies of the Effect of Chitosan on the Bone Defect Repair Process

“…Сильный противовоспалительный эффект, который наблюдался при использовании барье-ров из ХТЗ, по всей видимости, был обусловлен способностью молекул гетерополисахарида индуцировать альтернативную активацию тка-невых макрофагов (М2), которые, как известно, нивелируют воспаление, стимулируют процессы репарации и регенерации поврежденных тканей через продукцию ряда хемокинов, ангиогенных факторов (VEGF), аргиназы-1, но не ФНОα и ИЛ-1β [9][10][11]. Поэтому в пользу ранней инициации репаративно-регенерационных процессов у кро-ликов из группы №2 свидетельствует не только крайне низкий уровень провоспалительных ци-токинов в крови на 3-и сутки, но и рост концен-трации VEGF.…”