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Pro-inflammatory and anti-inflammatory types are the main phenotypes of the macrophage, which are commonly notified as M1 and M2, respectively. The alteration of macrophage phenotypes and the progression of inflammation are intimately associated; both phenotypes usually coexist throughout the whole inflammation stage, involving the transduction of intracellular signals and the secretion of extracellular cytokines. This paper aims to address the interaction of macrophages and surrounding cells and tissues with inflammation-related diseases and clarify the crosstalk of signal pathways relevant to the phenotypic metamorphosis of macrophages. On these bases, some novel therapeutic methods are proposed for regulating inflammation through monitoring the transition of macrophage phenotypes so as to prevent the negative effects of antibiotic drugs utilized in the long term in the clinic. This information will be quite beneficial for the diagnosis and treatment of inflammation-related diseases like pneumonia and other disorders involving macrophages.

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As immune checkpoint inhibitors (ICIs) are widely used, a series of immune-related adverse events (irAEs) have been reported, including immune checkpoint inhibitor-related pneumonitis (ICI-pneumonitis). The incidence of ICI-pneumonitis is higher in reality than in clinical trials. The diagnosis is challenging, mainly based on clinical and imaging features, and requires the exclusion of other causes. The data on the biological mechanisms of ICI-pneumonitis are scarce, resulting in little knowledge of the best treatment for ICI-pneumonitis. Bronchoalveolar lavage (BAL) may be helpful to identify the biological differences or find predictive biomarkers, and may in turn help to develop phenotype-specific targeted drugs to treat ICI-pneumonitis. Herein, we outline the characterization of immunomodulatory factors and cells in bronchoalveolar lavage fluid for ICI-pneumonitis. Through careful sorting and literature review, we find crosstalk between pathogenic Th17/Th1 cells (i.e., Th17.1) and pro-inflammatory monocytes, and activation of Th17(/Th1)/IL-17A (/IFN-γ) pathways may play a key role in the pathogenesis of ICI-pneumonitis. Disruption of the interaction between pathogenic Th17/Th1 cells and pro-inflammatory monocytes (such as, anti-IL-23) may be a potential treatment for ICI-pneumonitis. We first describe the possible pathophysiological mechanisms of ICI-pneumonitis, hoping to contribute to the optimization of diagnosis and treatment, as well as provide readers with research inspiration.

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Objective To study the histopathological changes and ultrastructure features of human gliomas after receiving stereotactic radiosurgery (SRS) and stereotactic radiotherapy (SRT), and observe the changes of tumor-associated factor Ki-67 level, endothelial growth factor (VEGF) level and microvessel density (MVD).Methods A comparative, retrospective study of pathological and immunohistochemical changes of 25 gliorna specimens without radiotherapy (controls) and 25 patients with glioma received with SRS and SRT (treatment group), admitted to our hospital from November 1995to July 2008, were carried out. Eight specimens from both groups, fixed with glutaraldehyde, were chosen for electron microscope observation; the ultrastructure changes in the tumor center, tumor margin and peripheral edema brain tissues in each specimen were observed. Immunohistochemical staining was employed to detect the expressions of Ki-67 and VEGF, and the MVD. And these data were statistically analyzed. Results The square and extent of tumor necrosis and liquation were positively significantly correlated with the tumor grade (r=0.649, P=0.001). Electron microscope indicated that the organdles,capillaries and blood-brain barrier in the tumor center, tumor margin and peritumoral edema cortex of the treatment group occurred different degrees of brain tissue degeneration and necrosis; while these were without damage in the controls. Immunohistochemistry showed that the protein expression of VEGF, the Ki-67 positive cells, and the MVD in the control group and treatment group were positively correlated with the glioma grade (P＜0.05). Of the glioma with the same grade, the Ki-67 protein expression and MVD in the treatment group were significantly lower than those in the control group (P＜0.05).Conclusion SRS and SRT may lead tumor cells to different degrees of degeneration, necrosis, and apoptosis, as well as the three-tier structure damage of capillaries in the blood-brain barrier, which provides a laboratory and theoretical foundation to take individualized comprehensive treatment of different gliomas.