Heat shock response: presence and effects in burn patient neutrophils

Rodeberg, David A.; Meyer, Joseph G.; Babcock, George F.

doi:10.1002/jlb.66.5.773

Cited by 16 publications

(7 citation statements)

References 59 publications

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“…TLR-4 is also involved in HSP signalling [23,24] . In addition, HSPs can be shed by the cell and circulate causing delayed apoptosis and signalling through TLR-4 [25,26] . Our results correlate with previous research showing CD11b/CD18 [26] and apoptotic downregulation following HS in neutrophils [21] .…”

Section: Discussionmentioning

confidence: 99%

“…In addition, HSPs can be shed by the cell and circulate causing delayed apoptosis and signalling through TLR-4 [25,26] . Our results correlate with previous research showing CD11b/CD18 [26] and apoptotic downregulation following HS in neutrophils [21] . Both adult and neonatal neutrophils have signifi cantly increased CD11b expression following treatment with LPS.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Heat Shock and Hypoxia on Neonatal Neutrophil Lipopolysaccharide Responses: Altered Apoptosis, Toll-Like Receptor-4 and CD11b Expression Compared with Adults

Molloy

O’Neill²,

Doyle³

et al. 2006

Neonatology

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Background: Dysfunctional inflammatory responses have been implicated in several neonatal inflammatory disorders following infection and hypoxia. Objectives: We aimed to study the effects of in vitro hypoxia and heat shock (HS) on normal adult and newborn neutrophil migration (CD11b) and persistence (apoptosis) following lipopolysaccharide (LPS) stimulation. Methods: The mechanism for altered LPS responses was assessed at the level of the LPS signalling receptors, Toll-like receptor-4 (TLR-4), TLR-2 and CD14 expression in normal neonates and adults. Results: In adults, although hypoxia delayed neutrophil apoptosis, LPS enhanced this response. In contrast, HS (42°C) increased adult apoptotic rates and abrogated the LPS responses. Both hypoxia and HS prevented the LPS-induced increase in adult CD11b although it was unaltered in neonates. Adult TLR-4 neutrophil expression was increased by LPS and hypoxia, and decreased in HS, possibly explaining their variable LPS responsiveness. In contrast, neonatal neutrophils were LPS hyporesponsive which may be mediated by failure of TLR-4 upregulation with LPS. Conclusions: Neonates do not have increased LPS responsiveness in hypoxia or heat shock in vitro, which may prevent hyperinflammation and thereby minimise tissue damage in inflammation or infection.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of Heat Shock and Hypoxia on Neonatal Neutrophil Lipopolysaccharide Responses: Altered Apoptosis, Toll-Like Receptor-4 and CD11b Expression Compared with Adults

Molloy

O’Neill²,

Doyle³

et al. 2006

Neonatology

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“…Burn injury often leads to a systemic inflammatory state, which has been attributed to the resulting exacerbated innate immune response, referred to as systemic inflammatory response syndrome (SIRS) [1], [2]. Macrophages, which upregulate Toll-like receptor 4 (TLR4) responses, are believed to be the major source of inflammatory mediators during SIRS [3], [4], [5], [6]. The adaptive immune system, by contrast, acquires a suppressive phenotype characterized by a reduced T helper (Th) 1 and cytotoxic T cell response, and heightened T regulatory (Treg) cell activity [7], [8], [9], [10], [11], [12].…”

Section: Introductionmentioning

confidence: 99%

Burn Injury Triggered Dysfunction in Dendritic Cell Response to TLR9 Activation and Resulted in Skewed T Cell Functions

et al. 2012

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Severe trauma such as burn injury is often associated with a systemic inflammatory syndrome characterized by a hyperactive innate immune response and suppressed adaptive immune function. Dendritic cells (DCs), which sense pathogens via their Toll-like receptors (TLRs), play a pivotal role in protecting the host against infections. The effect of burn injury on TLR-mediated DC function is a debated topic and the mechanism controlling the purported immunosuppressive response remains to be elucidated. Here we examined the effects of burn injury on splenic conventional DC (cDC) and plasmacytoid DC (pDC) responses to TLR9 activation. We demonstrate that, following burn trauma, splenic cDCs’ cytokine production profile in response to TLR9 activation became anti-inflammatory dominant, with high production of IL-10 (>50% increase) and low production of IL-6, TNF-α and IL-12p70 (∼25–60% reduction). CD4+ T cells activated by these cDCs were defective in producing Th1 and Th17 cytokines. Furthermore, burn injury had a more accentuated effect on pDCs than on cDCs. Following TLR9 activation, pDCs displayed an immature phenotype with an impaired ability to secrete pro-inflammatory cytokines (IFN-α, IL-6 and TNF-α) and to activate T cell proliferation. Moreover, cDCs and pDCs from burn-injured mice had low transcript levels of TLR9 and several key molecules of the TLR signaling pathway. Although hyperactive innate immune response has been associated with severe injury, our data show to the contrary that DCs, as a key player in the innate immune system, had impaired TLR9 reactivity, an anti-inflammatory phenotype, and a dysfunctional T cell-priming ability. We conclude that burn injury induced impairments in DC immunobiology resulting in suppression of adaptive immune response. Targeted DC immunotherapies to promote their ability in triggering T cell immunity may represent a strategy to improve immune defenses against infection following burn injury.

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“…The rationale for harmonic content characterization was based on the need to ensure that the system would expose cells to only one fundamental frequency throughout the exposure period. Four-hour exposure period was based on the previous stress studies requiring several hours to maintain transcription levels [Rodeberg et al, 1999].…”

Section: Measurement Of Harmonic Contentsmentioning

confidence: 99%

A single magnetic field exposure system for sequential investigation of real time and downstream cellular responses

Rao

Kisaalita

2003

Bioelectromagnetics

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To be able to correlate real time membrane potential or ion flux changes with further downstream gene transcription responses due to extremely low frequency (ELF) electromagnetic field (EMF) exposure, we devised an experimental system consisting of a pair of symmetric circular coils. This system can be used on an inverted microscope stage (real time signaling) as well as inside controlled environment incubators (gene transcription end points). The system includes a unique, custom made switch box for blinding the experimental staff and a power amplifier. We report herein the design and characterization of the system with respect to parameters considered important in in vitro ELF-EMF exposure studies, including linear magnetic field distribution, compensation for microscope objective lens interference, heating effects of the coils, and harmonic content of the signals.

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Heat shock response: presence and effects in burn patient neutrophils

Cited by 16 publications

References 59 publications

Effects of Heat Shock and Hypoxia on Neonatal Neutrophil Lipopolysaccharide Responses: Altered Apoptosis, Toll-Like Receptor-4 and CD11b Expression Compared with Adults

Effects of Heat Shock and Hypoxia on Neonatal Neutrophil Lipopolysaccharide Responses: Altered Apoptosis, Toll-Like Receptor-4 and CD11b Expression Compared with Adults

Burn Injury Triggered Dysfunction in Dendritic Cell Response to TLR9 Activation and Resulted in Skewed T Cell Functions

A single magnetic field exposure system for sequential investigation of real time and downstream cellular responses

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