_enti_e7
_enti_e8
_enti_e1
_enti_e9
_enti_e10
_enti_e4
_enti_e3
_enti_e2
_enti_e55
_enti_e53
_enti_e59
_enti_e51
_enti_e56
_enti_e54
_enti_e52
_enti_e50
_enti_e61
_enti_e57
_enti_e58
_enti_e62
_enti_e60
g2_fact_g2
g1_fact_g14
g1_fact_g1
g2_fact_g12
g2_fact_g13
p1_propro_p1
PMID: 18031251
It has long been known that many cells respond to microbial stimuli such as LPS (lipopolysaccharide), lipoproteins and flagellin by the generation of neutrophil-recruiting chemokines such as IL-8 (interleukin-8).
c1 cso30:c:InputAssociation connector
c7 cso30:c:InputAssociation connector
c4 cso30:c:OutputProcess connector
p2_propro_p2
PMID: 18031251
It has long been known that many cells respond to microbial stimuli such as LPS (lipopolysaccharide), lipoproteins and flagellin by the generation of neutrophil-recruiting chemokines such as IL-8 (interleukin-8).
c2 cso30:c:InputAssociation connector
c8 cso30:c:InputAssociation connector
c5 cso30:c:OutputProcess connector
p3_propro_p3
PMID: 18031251
It has long been known that many cells respond to microbial stimuli such as LPS (lipopolysaccharide), lipoproteins and flagellin by the generation of neutrophil-recruiting chemokines such as IL-8 (interleukin-8).
c3 cso30:c:InputAssociation connector
c9 cso30:c:InputAssociation connector
c6 cso30:c:OutputProcess connector
p4_propro_p4
PMID: 18031251, 9670975
Of these, LPS was thought to be a potent stimulator of neutrophil survival, acting again via IL-1beta [39], since it was apparent that LPS-activated neutrophils were themselves a source of IL-1beta, which was an effective stimulator of survival in an autocrine fashion.
c11 cso30:c:InputAssociation connector
c12 cso30:c:InputAssociation connector
c10 cso30:c:OutputProcess connector
p6_propro_p6
PMID: 18031251, 1993838, 7504060
Such co-culture models have been employed previously to demonstrate that monocytes amplify prothrombotic responses to LPS {via production of TF (tissue factor) from endothelial cells [36]}, and can potentially enhance recruitment of other cells through the up-regulation of adhesion molecules such as VCAM (vascular cell adhesion molecule).
c16 cso30:c:InputAssociation connector
c17 cso30:c:InputAssociation connector
c15 cso30:c:OutputProcess connector
p5_propro_p5
PMID: 18031251, 1993838, 7504060
Such co-culture models have been employed previously to demonstrate that monocytes amplify prothrombotic responses to LPS {via production of TF (tissue factor) from endothelial cells [36]}, and can potentially enhance recruitment of other cells through the up-regulation of adhesion molecules such as VCAM (vascular cell adhesion molecule).
c13 cso30:c:InputAssociation connector
c14 cso30:c:InputAssociation connector
c18 cso30:c:OutputProcess connector
p7_propro_p7
PMID: 18031251, 17138954
In part, this is because of a variety of physical defence measures, including the trapping of particulate matter in larger airways by mucus and the ability of various airway-secreted molecules such as surfactant proteins to bind and neutralize LPS.
c19 cso30:c:InputProcess connector
c20 cso30:c:InputProcess connector
c21 cso30:c:OutputProcess connector
p8_propro_p8
PMID: 18031251, 1569186
Neutrophil proteases have the ability to further modify local responses, since they can digest CD14 and decrease LPS responsiveness of some cells, but may also generate IL-8 production from epithelial cells [55] or signal via TLR4.
c23 cso30:c:InputAssociation connector
c24 cso30:c:InputAssociation connector
c22 cso30:c:OutputProcess connector
LPS_enti_MO000016882
LPS
Lp_enti_MO000017793
Lp
IL-8_enti_MO000017264
IL-8
IL8_enti_G000317
IL8
flagellin_enti_MO000022185
flagellin
VCAM-1_enti_MO000000308
VCAM-1
IL-1beta_enti_G010389
IL-1beta
IL-1beta_enti_MO000016597
IL-1beta
Tissue factor_enti_e5
Tissue factor
Tissue factor_enti_e6
Tissue factor
VCAM-1_enti_G010430
VCAM-1
Surfactant protein_enti_e11
Surfactant protein
LPS: Surfactant protein_enti_e12
LPS: Surfactant protein
Neutrophil protease_enti_e13
Neutrophil protease