{'fraction_non_alphanumeric': 0.016666666666666666, 'fraction_numerical': 0.0049382716049382715, 'mean_word_length': 6.078602620087336, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
DOWN-REGULATION OF CALPONIN 2 CONTRIBUTES TO THE QUIESCENCE OF LUNG MACROPHAGES.

Calponin 2 is an actin cytoskeleton-associated regulatory protein that inhibits the activity of myosin-ATPase and cytoskeleton dynamics. Recent studies have demonstrated that deletion of calponin 2 restricts the pro-inflammatory activation of macrophages in atherosclerosis and arthritis to attenuate the disease progression in mice. Here we demonstrate that the levels of calponin 2 vary among different macrophage populations, which may reflect their adaptation to specific tissue microenvironment corresponding to specific functional states. Interestingly, lung resident macrophages express significantly lower calponin 2 than peritoneal resident macrophages, which correlates with decreased substrate adhesion, reduced expression of pro-inflammatory cytokines and pro-resolution phenotypes. Deletion of calponin 2 in peritoneal macrophages also decreased substrate adhesion and down-regulated the expression of pro-inflammatory cytokines. Providing the first line of defense against microbial invasion while receiving constant exposure to extrinsic antigens, lung macrophages need to maintain a necessary level of activity while limiting exaggerated inflammatory reaction. Therefore, their low level of calponin 2 may reflect an important physiological adaption. Down-regulation of calponin 2 in macrophages may be targeted as a cytoskeleton-based novel mechanism, possibly via ER stress altering the processing and secretion of cytokines, to regulate immune response and promote quiescence for the treatment of inflammatory diseases.