{'fraction_non_alphanumeric': 0.045288531775018265, 'fraction_numerical': 0.01241782322863404, 'mean_word_length': 5.682926829268292, '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}}
Increased Mycobacterium tuberculosis growth in HIV‐1‐infected human macrophages: role of tumour necrosis factor‐α

Synergism between Mycobacterium tuberculosis (M. tuberculosis) and HIV‐1 infections was demonstrated in several in vitro models and clinical studies. Here, we investigated their reciprocal effects on growth in chronically HIV‐1‐infected promonocytic U1 cells and in acutely infected monocyte‐derived macrophages (MDM). Phagocytosis of M. tuberculosis induced HIV‐1 expression in U1 cells, together with increased TNF‐α production. M. tuberculosis growth, evaluated by competitive PCR, was greater in HIV‐1‐infected MDM compared to uninfected cells. M. tuberculosis phagocytosis induced greater TNF‐α and IL‐10 production in HIV‐1‐infected MDM than in uninfected cells. In uninfected MDM, addition of TNF‐α and IFN‐γ decreased, whereas IL‐10 increased M. tuberculosis growth. On the contrary, in HIV‐1‐infected MDM, addition of TNF‐α and IFN‐γ increased, whereas IL‐10 has no effect on M. tuberculosis growth. TNF‐α seems to play a pivotal role in the enhanced M. tuberculosis growth observed in HIV‐1‐infected MDM, being unable to exert its physiological antimycobacterial activity. Here, for the first time we demonstrated an enhanced M. tuberculosis growth in HIV‐1‐infected MDM, in line with the observed clinical synergism between the two infections.