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  • In contrast with the above results in our GC

    2022-08-13

    In CGP 53353 with the above results, in our GC model system, FPR1-, but not FPR2-knockout, enhanced tumour formation. However, it should be noted that the prominent role of mFPR2 with respect to mFPR1 in the mouse colon might be due to the significantly higher expression of mFPR2 than mFPR1 in this tissue. Furthermore, although mFPR1 is the orthologue of human FPR1, its putative ligand-binding domain contains structural features resembling those of FPR2/ALX. Moreover, in contrast with human FPR system, both mFPR1 and mFPR2 display low affinity for formylated peptides. Overall, the human FPRs have better defined and more specialized ligand-binding properties than the mouse receptors [3], and this could explain the discrepancy between data obtained in humans and those obtained in mouse models of gastrointestinal cancer.
    Summary and perspectives We would like to suggest that modulation of FPR activation and signalling could provide novel therapeutic approaches in different pathologic conditions. Inhibitory anti-angiogenic strategies targeting FPR could be exploited in chronic and persistent infectious/inflammatory situations. Furthermore, inhibitory strategies targeting FPR1 could be used to inhibit tumour angiogenesis in glioblastoma. On the contrary, stimulation of FPR activity could offer a potential therapeutic strategy in other cancer models such as gastric cancer, colorectal carcinoma, melanoma, and hepatocarcinoma. The great variety of FPR agonists exerting pro- or anti-inflammatory/angiogenic responses, and the plethora of specific antagonists (Table 1, Table 2, Table 3) may provide multiple therapeutic possibilities for several pathologic conditions.
    Conflict of interest
    Acknowledgements We are grateful for the design of the graphical abstract. This work was supported by grants from Regione Campania CISI-Lab Project, CRÈME Project, and TIMING Project.
    Molecular imaging as a technique is epitome of observing both microscopic and macroscopic events in spatial temporal manner. However, due to inherent limitation imposed by individual modality, it is usually difficult to correlate the macroscopic in vivo imaging with cellular level microscopic observation. Therefore using molecular imaging in a single mode to understand complex dynamic biological process becomes highly challenging., This is especially true in the case of inflammation imaging., Inflammation imaging is one of the most sought after areas of research in the medical field because of its wide spread application in numerous pathophysiological conditions., Inflammation is considered as root cause of many disorders and diseases, especially in the acute inflammatory conditions such as myocardial infarction (cardiovascular disease—heart attack) or brain ischemic injury such as stroke. In other cases such as arthritis pain in joints as aseptic symptoms is results of, inflammation. Septic microbial infections lead to inflammatory response such as pneumonia and tuberculosis in the lungs. Therefore inflammatory biological condition is defined as a highly intricate dynamic phenomenon wherein variety of cells from innate immune system as well as local resident cells coordinates a response for self defense. The protection and healing of the injured cells/tissue from the abnormal stimulation caused by a physical, chemical, or biologic agent, including the local reactions is required for regular physiological functioning and survival. In response to these abnormal stress stimuli morphological changes in cells/tissue are ensued leading to cytokine release which results in making blood vessels leaky to have better supply of necessary ingredients for repair and removal of damaged cells from inflamed foci. In the process cellular infiltration of innate immune cells from circulation ensues in the affected areas with an ultimate aim for rescue, repair and healing. The swelling, redness and generation of heat—raising local temperature are generally observed symptoms for inflammation. The whole process is well orchestrated, however, the controlled response from immune cells may turn into revolting situation only when persistent and sustained stress signal remains because of more damaged cells and debris leading to organ dysfunction. Thus inflammation is double edged sword and intricate response from many cellular components/cells makes it difficult to define and monitor the inflammatory dysfunction with high degree of specificity and selectivity from other physiologically active functions, and therefore defining and visualizing inflamed focal areas in vivo is not an easy task.