Different patterns of cytokine regulation of phagocytosis and bacterial killing by human neutrophils

Pechkovsky, Dmitri V.; Потапнев, М. П.; Zalutskaya, Oksana M.

doi:10.1016/0924-8579(96)00007-6

Cited by 30 publications

(14 citation statements)

References 23 publications

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“…Altered human neutrophil function in response to acute psychological stress. Psychosomatic Medicine, 72, 636-640. http://dx.doi.org/10.1097/PSY.0b013e3181e7fae8 different phagocytosis and superoxide production results observed here, given that the regulation of neutrophil function is under the control of many different receptors for a variety of cytokines (27), which are also differentially affected by stress (34,35).…”

Section: Discussionmentioning

confidence: 55%

“…However, it should be noted that academic examination stress over several weeks cannot be considered to be acute psychological stress. Furthermore, studies evaluating neutrophil function and regulation have shown that phagocytosis and intracellular bacterial killing are independent activities of neutrophilmediated antibacterial defense (27,28). Accordingly, it is feasible that phagocytosis and stimulated superoxide production could be differentially affected by acute stress.…”

Section: Discussionmentioning

confidence: 99%

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Altered Human Neutrophil Function in Response to Acute Psychological Stress

Khanfer

Phillips

Lord

2010

Psychosomatic Medicine

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Objective: To examine the effects of an acute laboratory psychological stress task on neutrophil function, specifically phagocytosis of Escherichia coli and stimulated superoxide production in human neutrophils. There is mounting evidence that acute stress is associated with short-term increases in a number of immune indices. Methods:Participants were 40 (n = 20 females) university students (mean age, 25.9 ± 4.56 years). Blood samples to determine neutrophil function by flow cytometry were taken at the end of resting baseline, during an acute stress task, and during recovery. The stress task was a 10-minute timepressured mental arithmetic challenge with social evaluation. Results:There was an acute increase in phagocytic ability, p = .047, ²p = 0.076, and a reduction of superoxide production, p = .026, ²p = 0.101, associated with the stress task relative to baseline. Conclusion:These findings suggest that neutrophil bactericidal function may be sensitive to mental challenge tasks that provoke acute psychological stress. Further research is needed to replicate the observed psychological stress-induced changes in neutrophil function.Key words: acute psychological stress, neutrophil, phagocytosis, superoxide production. SBP = systolic blood pressure; DBP = diastolic blood pressure; HR = heart rate; MFI = mean fluorescent intensity; EDTA = ethylene diamine tetraacetic acid.

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Section: Discussionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Altered Human Neutrophil Function in Response to Acute Psychological Stress

Khanfer

Phillips

Lord

2010

Psychosomatic Medicine

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“…Furthermore, our data suggest a new mechanism by which IL-1␤ exerts its acute host defense function against S. aureus (23), identifying IL-6 as an important downstream mediator of IL-1 signaling. IL-6, in turn, can activate the killing capacity of neutrophils as critical early effectors against the bacteria (24), a function that may be further augmented by IL-1 (25).…”

Section: Discussionmentioning

confidence: 99%

NOD2 contributes to cutaneous defense againstStaphylococcus aureusthrough α-toxin-dependent innate immune activation

Hrúz¹,

Zinkernagel

Jeníková³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

177

184

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Staphylococcus aureus is a major cause of community-acquired and nosocomial infections including the life-threatening conditions endocarditis, necrotizing pneumonia, necrotizing fasciitis, and septicemia. Toll-like receptor (TLR)-2, a membrane-bound microbial sensor, detects staphylococcal components, but macrophages lacking TLR2 or both TLR2 and TLR4 remain S. aureus responsive, suggesting that an alternative microbial recognition receptor might be involved. The cytoplasmic sensor nucleotide-binding oligomerization domain containing (NOD) 2/caspase recruitment domain (CARD) 15 detects muramyl dipeptide from bacterial peptidoglycans and mediates cytokine responses to S. aureus in vitro, but the physiological significance of these observations is not well defined. Here we show that NOD2-deficient mice exhibit a delayed but ultimately exacerbated ulcerative response and impaired bacterial clearance after s.c. infection with S. aureus. NOD2-dependent recognition of S. aureus and muramyl dipeptide is facilitated by ␣-toxin (␣-hemolysin), a pore-forming toxin and virulence factor of the pathogen. The action of NOD2 is dependent on IL-1␤-amplified production of IL-6, which promotes rapid bacterial killing by neutrophils. These results significantly broaden the physiological importance of NOD2 in innate immunity from the recognition of bacteria that primarily enter the cytoplasm to the detection of bacteria that typically reside extracellularly and demonstrate that this microbial sensor contributes to the discrimination between commensal bacteria and bacterial pathogens that elaborate poreforming toxins.Innate immunity ͉ interleukin-1 ͉ interleukin-6 ͉ microbial pathogenesis

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“…They specifically modulate human neutrophil chemotaxis, adherence, degranulation, respiratory burst, antimicrobial activity and cytotoxicity. Two of the proinflammatory cytokines, namely TNFα and IL-8, were recognised as being especially important in the promotion of neutrophil activation and up-regulation of most functional responses of these cells (Pechlowsky et al, 1996;Bratt and Palmblad, 1997;Galligan and Coomber, 2000;McClenahan et al, 2000). TNFα is a powerful priming factor for human neutrophils; it enhances the expression of CD11b/CD18 on neutrophils, increases neutrophil adhesion to endothelium, triggers adherent neutrophils to release large amounts of reactive oxygen intermediates, and promotes neutrophil degranulation and phagocytosis (Salamone et al, 2001).…”

mentioning

confidence: 99%

The influence of TNFα and IL-8 on secretory action of neutrophils isolated from heifers in the course of bovine respiratory disease

Wessely-Szponder¹

2008

Acta Veterinaria Hungarica

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The goal of this study was to give insight into the lesser known action of neutrophils in the course of bovine respiratory disease (BRD). Neutrophils are principally involved in resistance to infection but under certain conditions these cells participate in lung injury. TNFα and IL-8, primary cytokines which play an essential role in neutrophil activation during the inflammatory process, may lead not only to host defence reaction but also to destructive responses. Neutrophil constituents, such as elastase, myeloperoxidase (MPO), alkaline phosphatase (ALKP) and superoxide among others, contribute to tissue destruction. Also, 5-oxo-eicosatetraenoic acid (5-oxo-ETE), the potent activator of neutrophil chemotaxis and degranulation, can cause lung injury. This study revealed that neutrophils under the influence of TNFα exacerbated the release of elastase, MPO, ALKP and superoxide. IL-8, in turn, triggered those neutrophils which were isolated from heifers suffering from BRD, and released elastase, ALKP and 5-oxo-ETE, but not MPO or superoxide (O 2− ). The most pronounced degranulative response was observed in the acute form of BRD and a lesser response was seen in the chronic form. The secretory action of neutrophils varied not only depending on the form and phase of the disease but it also diminished successively during recovery.

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Different patterns of cytokine regulation of phagocytosis and bacterial killing by human neutrophils

Cited by 30 publications

References 23 publications

Altered Human Neutrophil Function in Response to Acute Psychological Stress

Altered Human Neutrophil Function in Response to Acute Psychological Stress

NOD2 contributes to cutaneous defense againstStaphylococcus aureusthrough α-toxin-dependent innate immune activation

The influence of TNFα and IL-8 on secretory action of neutrophils isolated from heifers in the course of bovine respiratory disease

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