Anti-Inflammatory and Antimicrobial Roles of Secretory Leukocyte Protease Inhibitor

Doumas, Stergios; Kolokotronis, Alexandros; Stefanopoulos, Panagiotis K.

doi:10.1128/iai.73.3.1271-1274.2005

Cited by 189 publications

(183 citation statements)

References 59 publications

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“…All of these data and our study are in line with the characteristics of SLPI as an acute phase inflammation-responsive gene inducible by cytokines such as TNF-␣ (23, 24) and promoting tumor formation. SLPI also exhibits anti-inflammatory properties, for instance, by inhibiting activation of the inflammatory mediator NF-B (25). SLPI might therefore be expected to inhibit inflammation-induced tumor progression.…”

Section: Discussionmentioning

confidence: 99%

The Tumor-Promoting Effect of TNF-α Involves the Induction of Secretory Leukocyte Protease Inhibitor

Devoogdt

Revets

Kindt

et al. 2006

The Journal of Immunology

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According to the cancer immunoediting concept, inflammatory mediators play not only a critical role in promoting host protection against cancer but also contribute to cancer cell growth and survival. TNF-α is a critical factor in this network. However, the mechanisms underlying the tumor-promoting effect of TNF-α have not been fully elucidated yet. We previously reported that in vitro culture of Lewis lung carcinoma 3LL cells with TNF-α-producing macrophages resulted in enhanced resistance toward TNF-α-mediated lysis and increased malignancy of the 3LL cells. In this study, we analyzed the effects of endogenous TNF-α on TNF-α resistance and malignant behavior in vivo of low-malignant/TNF-α-sensitive 3LL-S cells and cancer cells derived from 3LL-S tumors that developed in wild-type or TNF-α−/− mice. Interestingly, 3LL-S cells acquired a malignant phenotype in vivo depending on the presence of host TNF-α, whereas acquisition of TNF-α resistance was TNF-α-independent. This result suggested that malignancy-promoting characteristics of 3LL-S cells other than TNF-α resistance are influenced in vivo by TNF-α. We previously identified the malignancy-promoting genes, secretory leukocyte protease inhibitor (SLPI) and S100A4, as being up-regulated in 3LL-S cells upon their s.c. growth in wild-type mice. In this study, we show that SLPI, but not S100A4, was induced in 3LL-S cells both in vitro and in vivo by TNF-α, and that silencing of in vivo induced 3LL-S SLPI expression using RNA interference abrogated in vivo progression but did not influence TNF-α resistance. These data indicate that SLPI induction may be one mechanism whereby TNF-α acts as an endogenous tumor promoter.

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Section: Discussionmentioning

confidence: 99%

The Tumor-Promoting Effect of TNF-α Involves the Induction of Secretory Leukocyte Protease Inhibitor

Devoogdt

Revets

Kindt

et al. 2006

The Journal of Immunology

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“…7B); however, it was absent in white matter microglia of control animals. Secretory leukocyte peptidase inhibitor (Slpi) or ALP has been implicated in the resolution of inflammation and wound healing (Ashcroft et al, 2000;Doumas et al, 2005;Odaka et al, 2003). ALP immunoreactivity in microglia was only detectable at 5WD in the corpus callosum (Fig.…”

Section: Confirmation Of Gene Expression Analysis Findings In Situ Atmentioning

confidence: 99%

Identification of a microglia phenotype supportive of remyelination

Olah

Amor

Brouwer

et al. 2011

Glia

319

270

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In multiple sclerosis, endogenous oligodendrocyte precursor cells (OPCs) attempt to remyelinate areas of myelin damage. During disease progression, however, these attempts fail. It has been suggested that modulating the inflammatory environment of the lesion might provide a promising therapeutic approach to promote endogenous remyelination. Microglia are known to play a central role in neuroinflammatory processes. To investigate the microglia phenotype that supports remyelination, we performed genome-wide gene expression analysis of microglia from the corpus callosum during demyelination and remyelination in the mouse cuprizone model, in which remyelination spontaneously occurs after an episode of toxin-induced primary demyelination. We provide evidence for the existence of a microglia phenotype that supports remyelination already at the onset of demyelination and persists throughout the remyelination process. Our data show that microglia are involved in the phagocytosis of myelin debris and apoptotic cells during demyelination. Furthermore, they express a cytokine and chemokine repertoire enabling them to activate and recruit endogenous OPCs to the lesion site and deliver trophic support during remyelination. This study not only provides a detailed transcriptomic analysis of the remyelinationsupportive microglia phenotype but also reinforces the notion that the primary function of microglia is the maintenance of tissue homeostasis and the support of regeneration already at the earliest stages in the development of demyelinating lesions. V

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“…Recently, experimental evidence confirming HE4 to be a across-class protease inhibitor for serine, aspartyl, and cysteine proteases in the human seminal fluid has been published [74]. It was believed that these protease inhibitors are involved in host defense against proteolytic enzymes secreted by glandular epithelial cell during inflammation [75,76]. Little data regarding the influence on serum HE4 levels by gynecological inflammatory diseases are available.…”

Section: Inflammatory Diseasementioning

confidence: 99%

Physiopathological factors affecting the diagnostic value of serum HE4-test for gynecologic malignancies

Duan

et al. 2016

Expert Review of Molecular Diagnostics

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Anti-Inflammatory and Antimicrobial Roles of Secretory Leukocyte Protease Inhibitor

Cited by 189 publications

References 59 publications

The Tumor-Promoting Effect of TNF-α Involves the Induction of Secretory Leukocyte Protease Inhibitor

The Tumor-Promoting Effect of TNF-α Involves the Induction of Secretory Leukocyte Protease Inhibitor

Identification of a microglia phenotype supportive of remyelination

Physiopathological factors affecting the diagnostic value of serum HE4-test for gynecologic malignancies

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