AIMS microbiology · 2026
Immune evasion by Staphylococcus haemolyticus: Attenuated NET-associated responses and resistance to NET-mediated killing.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Ahmed Mohamed, Khalifa Marwa M
Аннотация
Neutrophil extracellular traps (NETs) contribute to innate immune defense by trapping and exposing microorganisms to DNA-associated antimicrobial proteins. However, some pathogens can tolerate NET-associated antimicrobial activity and persist within the host. Staphylococcus haemolyticus is an emerging multidrug-resistant coagulase-negative staphylococcal pathogen associated with healthcare-related infections, but its interaction with neutrophil-mediated defenses remains poorly understood. This study investigated whether a multidrug-resistant clinical S. haemolyticus isolate modulates neutrophil antimicrobial activity and NET-associated responses, using a clinical Staphylococcus aureus isolate as a comparator. Extracellular DNA release and NET-associated structures were assessed by fluorescence microscopy, scanning electron microscopy, fluorometric DNA quantification, microscopic enumeration, and MPO-DNA complex ELISA. The tested S. haemolyticus isolate induced extracellular DNA release and MPO-DNA complex formation; however, these responses were lower than those induced by PMA and were attenuated compared with the S. aureus comparator. S. haemolyticus also showed reduced susceptibility to neutrophil-mediated killing and greater resistance to NET-mediated killing than S. aureus. NE and MPO mRNA expression was not significantly altered following bacterial exposure. Collectively, these findings provide initial evidence that a clinical S. haemolyticus isolate can induce attenuated NET-associated responses while resisting NET-mediated antimicrobial activity, highlighting a potential immune-evasion mechanism in this emerging opportunistic pathogen.