Secretory Leukocyte Protease inhibitor (SLPI) shields the tissues against inflammatory products

in inflammation response by down-regulating the macrophage responses against bacterial

lipopolysaccharides (LPS). LPS seem to induce SLPI production by macrophages directly or by
way of interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-), IL-6, and IL-10. SLPI in
turn inhibits the downstream portion of the nuclear factor (NF-) pathway by protecting I (inhibiting factor of NF-) from degradation by the ubiquitin-proteosome pathway. SLPI is
believed to enter cells, becoming rapidly localized to the cytoplasm and nucleaus where it affects
NF- activation by binding directly to NF- binding site in a site-spesific manner. Thus,
SLPI renders macrophages unable to release proinflammatory cytokines and nitric oxide.
Sekretori Leukocyte Protease inhibitor (SLPI) melindungi jaringan terhadap produk inflamasi
pada respon keradangan melalui penurunan respon makrofag terhadap bakteri lipopolisakarida
(LPS). LPS diduga dapat menginduksi produksi SLPI oleh makrofag baik secara langsung atau
melalui interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-), IL-6, dan IL-10. SLPI dapat
menghambat jalur nuclear factor kappa B (NF-) dengan melindungi I- (faktor yang
menghambat NF-) dari degradasi melalui jalur ubiquitin-proteasome. SLIP diduga dapat
masuk ke dalam sel, dan secara cepat dilokalisasi pada sitoplasma dan nucleus, proses tersebut
kamudian dapat mempengaruhi aktivasi NF melalui pengikatan langsung ke NF- binding
site dengan cara yang spesifik. Dengan demikian, SLPI membuat makrofag tidak dapat
melepaskan sitokin proinflamasi dan oksida nitrat (Nathalie dan Michel, 2011).
Inhibitory effect of SLPI on macrophage responses may be due to its blockade of LPS transfer to
soluble CD14 (receptor of macrophages) and its interference with the uptake of LPS from LPSsoluble CD14 complexes by macrophages. SLPI attenuates macrophages' responsiveness by

inhibiting the LPS pathway through suppression of NF-B and activation of CCAAT enhancerbinding protein-transcription.
Efek penghambatan SLPI terhadap respon makrofag diduga terjadi melaui blokade transfer LPS
untuk larut ke CD14/Toll-like receptor (reseptor makrofag) dan interferensi melalui penyerapan
LPS dari kompleks CD14-LPS larut oleh makrofag. SLPI menurunkan respon makrofag dengan
menghambat jalur LPS melalui penghambatan ekspresi NF-kB dan aktivasi transkripsi CCAAT
enhancer-binding protein (Stergios et al., 2005)

Nathalie V dan Michel C, 2011, Proteases and their Receptor in inflammation. Springer Science
& Business Media. p 39
Stergios Doumas, Alexandros Kolokotronis, dan Panagiotis Stefanopoulos, 2005. AntiInflammatory and Antimicrobial Roles of Secretory Leukocyte Protease Inhibitor. Journal
List Infection Immunity v.73(3); 2005 Mar PMC106491