Blocking triggering receptor expressed on myeloid cells-1 attenuates lipopolysaccharide-induced acute lung injury via inhibiting NLRP3 inflammasome activation.

Liu T, Zhou Y, Li P, Duan JX, Liu YP, Sun GY, Wan L, Dong L, Fang X, Jiang JX, Guan CX

Scientific reports22 Dec 2016Cited by 72 (Europe PMC)

PMID28004759PMCIDPMC5177963DOI10.1038/srep39473PepBankPUB-28004759

Summary

Acute lung injury (ALI) is associated with high mortality and uncontrolled inflammation plays a critical role in ALI. TREM-1 is an amplifier of inflammatory response, and is involved in the pathogenesis of many infectious diseases. NLRP3 inflammasome is a member of NLRs family that contributes to ALI. However, the effect of TREM-1 on NLRP3 inflammasome and ALI is still unknown. This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS. LR12 also attenuated inflammation and lung tissue damage by reducing histopathologic changes, infiltration of the macrophage and neutrophil into the lung, and production of the pro-inflammatory cytokine, and oxidative stress. LR12 decreased expression of the NLRP3, pro-caspase-1 and pro-IL-1β, and inhibited priming of the NLRP3 inflammasome by inhibiting NF-κB. LR12 also reduced the expression of NLRP3 and caspase-1 p10 protein, and secretion of the IL-1β, inhibited activation of the NLRP3 inflammasome by decreasing ROS. For the first time, these data show that TREM-1 aggravates inflammation in ALI by activating NLRP3 inflammasome, and blocking TREM-1 may be a potential therapeutic approach for ALI.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study16

16 results from studies that gave the peptide. No result from this study comes from people.

01AnimalAnimal study (in vivo)Efficacy outcome
In mice given lethal LPS doses, LR12 significantly improved survival.
In plain wordsIn mice given lethal LPS doses, LR12 significantly improved survival.
Peptide
Nangibotide
Outcome
IncreaseSurvival
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Mortality · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475901
02AnimalAnimal study (in vivo)Efficacy outcome
In mice with LPS-induced lung injury, LR12 attenuated inflammation.
In plain wordsIn mice, LR12 reduced lung inflammation.
Peptide
Nangibotide
Outcome
DecreaseLung inflammation
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Inflammation markers · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 also attenuated inflammation and lung tissue damage by reducing histopathologic changes, infiltration of the macrophage and neutrophil into the lung, and production of the pro-inflammatory cytokine, and oxidative stress.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475902
03AnimalAnimal study (in vivo)Efficacy outcome
In mice with LPS-induced lung injury, LR12 reduced lung tissue damage and histopathologic changes.
In plain wordsIn mice, LR12 reduced lung tissue damage.
Peptide
Nangibotide
Outcome
DecreaseLung tissue damage
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Lung injury and fibrosis · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 also attenuated inflammation and lung tissue damage by reducing histopathologic changes, infiltration of the macrophage and neutrophil into the lung, and production of the pro-inflammatory cytokine, and oxidative stress.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475903
04AnimalAnimal study (in vivo)Efficacy outcome
In mice with LPS-induced lung injury, LR12 reduced macrophage infiltration into the lung.
In plain wordsIn mice, LR12 reduced macrophage infiltration into the lung.
Peptide
Nangibotide
Outcome
DecreaseMacrophage infiltration
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Inflammation markers · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 also attenuated inflammation and lung tissue damage by reducing histopathologic changes, infiltration of the macrophage and neutrophil into the lung, and production of the pro-inflammatory cytokine, and oxidative stress.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475904
05AnimalAnimal study (in vivo)Efficacy outcome
In mice with LPS-induced lung injury, LR12 reduced neutrophil infiltration into the lung.
In plain wordsIn mice, LR12 reduced neutrophil infiltration into the lung.
Peptide
Nangibotide
Outcome
DecreaseNeutrophil infiltration
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Inflammation markers · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 also attenuated inflammation and lung tissue damage by reducing histopathologic changes, infiltration of the macrophage and neutrophil into the lung, and production of the pro-inflammatory cytokine, and oxidative stress.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475905
06AnimalAnimal study (in vivo)Efficacy outcome
In mice with LPS-induced lung injury, LR12 reduced pro-inflammatory cytokine production.
In plain wordsIn mice, LR12 reduced pro-inflammatory cytokine production.
Peptide
Nangibotide
Outcome
DecreasePro-inflammatory cytokine production
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Inflammation markers · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 also attenuated inflammation and lung tissue damage by reducing histopathologic changes, infiltration of the macrophage and neutrophil into the lung, and production of the pro-inflammatory cytokine, and oxidative stress.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475906
07AnimalAnimal study (in vivo)Mechanism
In mice with LPS-induced lung injury, LR12 reduced oxidative stress.
In plain wordsIn mice, LR12 reduced oxidative stress.
Peptide
Nangibotide
Outcome
DecreaseOxidative stress
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Inflammation markers · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 also attenuated inflammation and lung tissue damage by reducing histopathologic changes, infiltration of the macrophage and neutrophil into the lung, and production of the pro-inflammatory cytokine, and oxidative stress.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475907
08AnimalAnimal study (in vivo)Mechanism
In mice with LPS-induced lung injury, LR12 decreased NLRP3 expression.
In plain wordsIn mice, LR12 decreased NLRP3 expression.
Peptide
Nangibotide
Outcome
DecreaseNLRP3 expression
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Receptor activity and mechanism · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 decreased expression of the NLRP3, pro-caspase-1 and pro-IL-1β, and inhibited priming of the NLRP3 inflammasome by inhibiting NF-κB. LR12 also reduced the expression of NLRP3 and caspase-1 p10 protein, and secretion of the IL-1β, inhibited activation of the NLRP3 inflammasome by decreasing ROS.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475908
09AnimalAnimal study (in vivo)Mechanism
In mice with LPS-induced lung injury, LR12 decreased pro-caspase-1 expression.
In plain wordsIn mice, LR12 decreased pro-caspase-1 expression.
Peptide
Nangibotide
Outcome
DecreasePro-caspase-1 expression
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Receptor activity and mechanism · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 decreased expression of the NLRP3, pro-caspase-1 and pro-IL-1β, and inhibited priming of the NLRP3 inflammasome by inhibiting NF-κB.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475909
10AnimalAnimal study (in vivo)Mechanism
In mice with LPS-induced lung injury, LR12 decreased pro-IL-1β expression.
In plain wordsIn mice, LR12 decreased pro-IL-1β expression.
Peptide
Nangibotide
Outcome
DecreasePro-IL-1β expression
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Receptor activity and mechanism · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 decreased expression of the NLRP3, pro-caspase-1 and pro-IL-1β, and inhibited priming of the NLRP3 inflammasome by inhibiting NF-κB.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475910
11AnimalAnimal study (in vivo)Mechanism
In mice with LPS-induced lung injury, LR12 inhibited NLRP3 inflammasome priming.
In plain wordsIn mice, LR12 inhibited NLRP3 inflammasome priming.
Peptide
Nangibotide
Outcome
DecreaseNLRP3 inflammasome priming
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Receptor activity and mechanism · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 decreased expression of the NLRP3, pro-caspase-1 and pro-IL-1β, and inhibited priming of the NLRP3 inflammasome by inhibiting NF-κB.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475911
12AnimalAnimal study (in vivo)Mechanism
In mice with LPS-induced lung injury, LR12 inhibited NF-κB.
In plain wordsIn mice, LR12 inhibited NF-κB.
Peptide
Nangibotide
Outcome
DecreaseNF-κB activity
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Receptor activity and mechanism · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 decreased expression of the NLRP3, pro-caspase-1 and pro-IL-1β, and inhibited priming of the NLRP3 inflammasome by inhibiting NF-κB.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475912
13AnimalAnimal study (in vivo)Mechanism
In mice with LPS-induced lung injury, LR12 reduced caspase-1 p10 protein expression.
In plain wordsIn mice, LR12 reduced caspase-1 p10 protein expression.
Peptide
Nangibotide
Outcome
DecreaseCaspase-1 p10 expression
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Receptor activity and mechanism · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 also reduced the expression of NLRP3 and caspase-1 p10 protein, and secretion of the IL-1β, inhibited activation of the NLRP3 inflammasome by decreasing ROS.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475913
14AnimalAnimal study (in vivo)Efficacy outcome
In mice with LPS-induced lung injury, LR12 reduced IL-1β secretion.
In plain wordsIn mice, LR12 reduced IL-1β secretion.
Peptide
Nangibotide
Outcome
DecreaseIL-1β secretion
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Inflammation markers · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 also reduced the expression of NLRP3 and caspase-1 p10 protein, and secretion of the IL-1β, inhibited activation of the NLRP3 inflammasome by decreasing ROS.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475914
15AnimalAnimal study (in vivo)Mechanism
In mice with LPS-induced lung injury, LR12 inhibited NLRP3 inflammasome activation.
In plain wordsIn mice, LR12 inhibited NLRP3 inflammasome activation.
Peptide
Nangibotide
Outcome
DecreaseNLRP3 inflammasome activation
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Receptor activity and mechanism · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 also reduced the expression of NLRP3 and caspase-1 p10 protein, and secretion of the IL-1β, inhibited activation of the NLRP3 inflammasome by decreasing ROS.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475915
16AnimalAnimal study (in vivo)Mechanism
In mice with LPS-induced lung injury, LR12 decreased reactive oxygen species.
In plain wordsIn mice, LR12 decreased reactive oxygen species.
Peptide
Nangibotide
Outcome
DecreaseReactive oxygen species
Study
mousen: not reported in source
LPS-induced acute lung injury
Outcome group
Inflammation markers · Respiratory
Studied dose
Dose not stated
Source sentences
Summary
LR12 also reduced the expression of NLRP3 and caspase-1 p10 protein, and secretion of the IL-1β, inhibited activation of the NLRP3 inflammasome by decreasing ROS.
1 context sentence(design, population, supporting numbers)
Summary · context
This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome. We showed that LR12, a TREM-1 antagonist peptide, significantly improved survival of mice after lethal doses of LPS.
Show in the study text Report a problemFND-2800475916

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
27 Oct 2026, 18:20 UTC
Study results updated
Version 1
27 Oct 2026, 16:32 UTC
First added · source update from Europe PMC

PepBank is a research reference. Talk to a doctor before you use any peptide.

Blocking triggering receptor expressed on myeloid cells-1 attenuates lipopolysaccharide-induced acute lung injury via inhibiting NLRP3 inflammasome activation.

Summary

Results from this study16

Version history

Subjects

Publication types

MeSH terms