Acinetobacter baumannii escape from neutrophil extracellular traps (NETs)

Kamoshida, Go; Kikuchi-Ueda, Takane; Tansho-Nagakawa, Shigeru; Nakano, Ryuichi; Nakano, Akiyo; Kikuchi, Hirotoshi; Ubagai, Tsuneyuki; Ono, Yasuo

doi:10.1016/j.jiac.2014.08.032

Cited by 30 publications

(29 citation statements)

References 34 publications

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“…In conclusion, our findings strongly indicate that all the strains tested were phagocytosed and killed by human neutrophils. This is clearly in contrast to reports by others 24, 25 . Based on the experimental methods described in these previous publications, there is no obvious indication for the discrepancies in the reported results, apart from bacteria-cell contact time 1 h 26 vs 4 h. According to our immunofluorescence, SEM, CFUs counting and live-cell and live/dead imaging experiments, neutrophils are in contact with Acinetobacter at 1 h, but further incubation time renders active phagocytosis.…”

Section: Discussioncontrasting

confidence: 99%

Human neutrophils phagocytose and kill Acinetobacter baumannii and A. pittii

Lázaro-Díez

Chapartegui-González

Redondo-Salvo

et al. 2017

Sci Rep

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Acinetobacter baumannii is a common cause of health care associated infections worldwide. A. pittii is an opportunistic pathogen also frequently isolated from Acinetobacter infections other than those from A. baumannii. Knowledge of Acinetobacter virulence factors and their role in pathogenesis is scarce. Also, there are no detailed published reports on the interactions between A. pittii and human phagocytic cells. Using confocal laser and scanning electron microscopy, immunofluorescence, and live-cell imaging, our study shows that immediately after bacteria-cell contact, neutrophils rapidly and continuously engulf and kill bacteria during at least 4 hours of infection in vitro. After 3 h of infection, neutrophils start to release neutrophil extracellular traps (NETs) against Acinetobacter. DNA in NETs colocalizes well with human histone H3 and with the specific neutrophil elastase. We have observed that human neutrophils use large filopodia as cellular tentacles to sense local environment but also to detect and retain bacteria during phagocytosis. Furthermore, co-cultivation of neutrophils with human differentiated macrophages before infections shows that human neutrophils, but not macrophages, are key immune cells to control Acinetobacter. Although macrophages were largely activated by both bacterial species, they lack the phagocytic activity demonstrated by neutrophils.

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Section: Discussioncontrasting

confidence: 99%

Human neutrophils phagocytose and kill Acinetobacter baumannii and A. pittii

Lázaro-Díez

Chapartegui-González

Redondo-Salvo

et al. 2017

Sci Rep

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“…In some studies, it has been found that the release of nets is directly proportional to the phagocytic activity of neutrophils, for example if there are no induction of nets, the phagocytosis is limited . We found something similar since the direct quantification of cell‐free DNA was higher in neutrophils which interacted with opsonized trophozoites, and consequently, there was a reduction of trophozoites (Figure ).…”

Section: Discussionsupporting

confidence: 69%

Neutrophils extracellular traps damage Naegleria fowleri trophozoites opsonized with human IgG

Carrasco-Yepez

Campos-Rodrı́guez

et al. 2016

Parasite Immunology

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Naegleria fowleri infects humans through the nasal mucosa causing a disease in the central nervous system known as primary amoebic meningoencephalitis (PAM). Polymorphonuclear cells (PMNs) play a critical role in the early phase of N. fowleri infection. Recently, a new biological defence mechanism called neutrophil extracellular traps (NETs) has been attracting attention. NETs are composed of nuclear DNA combined with histones and antibacterial proteins, and these structures are released from the cell to direct its antimicrobial attack. In this work, we evaluate the capacity of N. fowleri to induce the liberation of NETs by human PMN cells. Neutrophils were cocultured with unopsonized or IgG-opsonized N. fowleri trophozoites. DNA, histone, myeloperoxidase (MPO) and neutrophil elastase (NE) were stained, and the formation of NETs was evaluated by confocal microscopy and by quantifying the levels of extracellular DNA. Our results showed N. fowleri induce the liberation of NETs including release of MPO and NE by human PMN cells as exposure interaction time is increased, but N. fowleri trophozoites evaded killing. However, when trophozoites were opsonized, they were susceptible to the neutrophils activity. Therefore, our study suggests that antibody-mediated PMNs activation through NET formation may be crucial for antimicrobial responses against N. fowleri.

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“…At the molecular level, studies focused on the mechanisms used by neutrophils to eliminate this bacterium demonstrated a dispensable role for the nitric oxide synthase 2 and a critical requirement for the nicotinamide adenine dinucleotide phosphate phagocyte oxidase (NADPH) to kill A. baumannii , prevent replication and dissemination of the bacterium as well protection of the infected mice from death (22). Other novel defense mechanisms like neutrophil extracellular traps (NETs) are not induced in response to this bacterium (23), despite the fact that the formation of NETs can be stimulated through reactive oxygen species (24, 25). …”

Section: Neutrophils Essential Players During a Baumannii Infectionmentioning

confidence: 99%

The Immune Response against Acinetobacter baumannii, an Emerging Pathogen in Nosocomial Infections

2017

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Acinetobacter baumannii is the etiologic agent of a wide range of nosocomial infections, including pneumonia, bacteremia, and skin infections. Over the last 45 years, an alarming increase in the antibiotic resistance of this opportunistic microorganism has been reported, a situation that hinders effective treatments. In order to develop effective therapies against A. baumannii it is crucial to understand the basis of host–bacterium interactions, especially those concerning the immune response of the host. Different innate immune cells such as monocytes, macrophages, dendritic cells, and natural killer cells have been identified as important effectors in the defense against A. baumannii; among them, neutrophils represent a key immune cell indispensable for the control of the infection. Several immune strategies to combat A. baumannii have been identified such as recognition of the bacteria by immune cells through pattern recognition receptors, specifically toll-like receptors, which trigger bactericidal mechanisms including oxidative burst and cytokine and chemokine production to amplify the immune response against the pathogen. However, a complete picture of the protective immune strategies activated by this bacteria and its potential therapeutic use remains to be determined and explored.

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Acinetobacter baumannii escape from neutrophil extracellular traps (NETs)

Cited by 30 publications

References 34 publications

Human neutrophils phagocytose and kill Acinetobacter baumannii and A. pittii

Human neutrophils phagocytose and kill Acinetobacter baumannii and A. pittii

Neutrophils extracellular traps damage Naegleria fowleri trophozoites opsonized with human IgG

The Immune Response against Acinetobacter baumannii, an Emerging Pathogen in Nosocomial Infections

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