Spontaneous neutrophil activation in HTLV-1 infected patients

Guerreiro, Jaqueline; Porto, Murilo de Jesus; Santos, Sara; Lacerda, L.; Ho, John L.; Carvalho, Edgar M.

doi:10.1590/s1413-86702005000600010

Cited by 12 publications

(9 citation statements)

References 25 publications

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“…While adaptive immunity has been studied extensively, little is known about the host's innate immunity to HTLV‐I infection. It has been demonstrated that, despite their clinical status, the spontaneous neutrophils activation is significantly higher in HTLV‐1‐infected patients compared to healthy individuals [16]. These authors have proposed that spontaneous neutrophil activation would be another general immunological marker resulting from HTLV‐1 infection.…”

Section: Discussionmentioning

confidence: 99%

IL-10 produced by CD4+ and CD8+ T cells emerge as a putative immunoregulatory mechanism to counterbalance the monocyte-derived TNF-α and guarantee asymptomatic clinical status during chronic HTLV-I infection

Brito-Melo

Peruhype-Magalhães

Teixeira-Carvalho

et al. 2006

Clinical and Experimental Immunology

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Section: Discussionmentioning

confidence: 99%

IL-10 produced by CD4+ and CD8+ T cells emerge as a putative immunoregulatory mechanism to counterbalance the monocyte-derived TNF-α and guarantee asymptomatic clinical status during chronic HTLV-I infection

Brito-Melo

Peruhype-Magalhães

Teixeira-Carvalho

et al. 2006

Clinical and Experimental Immunology

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“…It was observed that HAM/TSP individuals display a high frequency of TNF-alpha + neutrophils and increased frequency of CD8+ IFN-gamma(+) and CD8(+) TNF-alpha(+) cells, which is a demonstration of the inflammatory microenvironment related to HAM/TSP progression [113]. Despite their clinical status, the spontaneous neutrophils activation was shown to be significantly higher in HTLV-1 infected patients as compared to healthy individuals [114]. The presence of neutrophil activation has been proposed as a possible general immunological marker resulting from HTLV-1 infection [114].…”

Section: Ham/tsp Immunopathogenesismentioning

confidence: 99%

“…Despite their clinical status, the spontaneous neutrophils activation was shown to be significantly higher in HTLV-1 infected patients as compared to healthy individuals [114]. The presence of neutrophil activation has been proposed as a possible general immunological marker resulting from HTLV-1 infection [114].…”

Section: Ham/tsp Immunopathogenesismentioning

confidence: 99%

HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) Inflammatory Network

Gonçalves¹,

Proietti²,

Barbosa-Stancioli³

et al. 2008

IADT

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| HAM/TSP patients experience impaired functional capacity. The use of categorical scales to accurately describe motor ability in these patients has been questioned. Aim: To evaluate the functional capacity of HAM/TSP patients by using the individual tests comprising the GDLAM protocol. Methods: Cross-sectional study carried out in the CHTLV, Salvador, Brazil. Functional capacity was evaluated using the tests of the GDLAM protocol (timed 10-minute walk, getting up from a sitting position, rising from a prone position, getting up from a chair, and moving around the house). Functional classifications were made by comparing patient performance to that of uninfected control individuals. Results: Twenty-four HAM/TSP and 25 healthy individuals were enrolled. Only 75% HAM/TSP patients completed the GDLAM protocol. Six patients failed to perform the RPP test. Timed measurements were significantly higher in the HAM/ TSP patients in comparison to uninfected controls. Conclusion: The use of alternative methods, such as the individual tests comprising the GDLAM protocol, may more accurately assess motor function in HAM/ TSP patients.

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“…Reports have indicated that exaggerated or reduced rates of spontaneous neutrophil activation are linked to viral [13] or autoimmune conditions [14], implying a physiological function for spontaneous neutrophil activation. Spontaneous and stimulated activation of neutrophil oxidative metabolism has been extensively documented in-vitro [15–18].…”

Section: Introductionmentioning

confidence: 99%

S100A8 and S100A9 inhibit neutrophil oxidative metabolismin-vitro: Involvement of adenosine metabolites

Sroussi

Lu²,

Zhang³

et al. 2010

Free Radical Research

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Neutrophils are short-lived granulocytic cells of the innate immune system specialized in the production of reactive oxygen species. S100A8 and S100A9 and their heterocomplex calprotectin play a role in neutrophil recruitment and represent 40% of neutrophil cytosolic protein weight. The present study was designed to test the effect of S100A8 and S100A9 on the rate of neutrophil oxidative metabolism. It is hypothesized that the two S100 proteins inhibit neutrophil associated oxidation. Granulocytes freshly isolated from healthy volunteers were tested for their ability to oxidize dichlorofluorescin-diacetate (DCFH-DA) in-vitro. The data showed that S100A8 and S100A9 inhibited spontaneous and stimulated oxidation of the DCFH-DA probe by neutrophils. The inhibition of neutrophil oxidative metabolism by S100A8 and S100A9 was markedly reduced by the enzymatic activity of adenosine deaminase. Inhibitors of the P1 adenosine receptors also reduced the anti-oxidative effect of S100A8/A9 providing further support for the involvement of adenosine metabolites in S100A8/A9 anti-oxidative effect.

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Spontaneous neutrophil activation in HTLV-1 infected patients

Cited by 12 publications

References 25 publications

IL-10 produced by CD4+ and CD8+ T cells emerge as a putative immunoregulatory mechanism to counterbalance the monocyte-derived TNF-α and guarantee asymptomatic clinical status during chronic HTLV-I infection

IL-10 produced by CD4+ and CD8+ T cells emerge as a putative immunoregulatory mechanism to counterbalance the monocyte-derived TNF-α and guarantee asymptomatic clinical status during chronic HTLV-I infection

HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) Inflammatory Network

S100A8 and S100A9 inhibit neutrophil oxidative metabolismin-vitro: Involvement of adenosine metabolites

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