TREM1 Antibodies

Triggering receptor expressed on myeloid cells 1 (TREM1)

Stimulates neutrophil and monocyte-mediated inflammatory reactions. Triggers launch of pro-inflammatory chemokines and cytokines, as well as enhanced surface expression of cell activation markers.

Amplifier of inflammatory reactions that are triggered by bacterial and fungal infections and is a critical mediator of septic shock. .

Gene Information

Human
Gene Name:	TREM1
Uniprot:	Q9NP99
Entrez:	54210

Family

Belongs to:
No superfamily

Alternative Names

CD354 antigen; CD354; TREM1; TREM-1; TREM-1Triggering receptor expressed on monocytes 1; triggering receptor expressed on myeloid cells 1; triggering-receptor TREM1

Molecular Weight

Mass (kDA):
26.387 kDA

Genomic Context

Human
Location:	6p21.1
Sequence:	6; NC_000006.12 (41267385..41286745, complement)

Tissue Specificity

Highly expressed in adult liver, lung and spleen than in corresponding fetal tissue. Also expressed in the lymph node, placenta, spinal cord and heart tissues. Expression is more elevated in peripheral blood leukocytes than in the bone marrow and in normal cells than malignant cells. Expressed at low levels in the early development of the hematopoietic system and in the promonocytic stage and at high levels in mature monocytes. Strongly expressed in acute inflammatory lesions caused by bacteria and fungi. Isoform 2 was detected in the lung, liver and mature monocytes.

Subcellular Localizations

[Isoform 1]: Cell membrane; Single-pass type I membrane protein.; [Isoform 2]: Secreted.

Diseases

• Systemic Infection
• Inflammation
• Inflammatory Response
• Pneumonia
• Infective Disorder
• Septic Shock
• Bacterial Infections
• Severe Sepsis
• Pneumonia, Bacterial
• Systemic Inflammatory Response Syndrome
• Pneumonia, Ventilator-associated
• Porphyria Cutanea Tarda
• Community-acquired Infections

• Pleural Effusion Disorder
• Innate Immune Response
• Lung Diseases
• Dementia
• Malignant Neoplasms
• Arthritis
• Tuberculosis

Pathways

• Inflammatory Response
• Secretion
• Pathogenesis
• Immune Response
• Phagocytosis
• Cytokine Production
• Innate Immune Response
• Cell Activation
• Acute Inflammatory Response
• Neutrophil Degranulation
• Cell Maturation
• Osteoclast Differentiation
• Leukocyte Activation

• Cell Proliferation
• Respiratory Burst
• Neutrophil Activation
• Macrophage Activation
• Bone Resorption
• Rna Interference
• Cell Adhesion

PTMs

• Phosphorylation
• Carboxylation

• Biotinylation
• Cleavage

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/TREM1

Best Uses of the TREM1 Marker

You may have heard about the TREM1 marker and wonder what it's purpose is. It stimulates phagocytosis, blocks the proinflammatory subtype transformation of microglia, and is involved in neuronal synapses. This powerful marker will help you understand its function and how to utilize it effectively. We will discuss some of its most effective uses in this article.

sTREM-1, an extremely potent proinflammatory cytokine that is readily available

The levels of sTREM-1 found in plasma were found to be significantly greater in patients suffering from thrombotic PAPS than in the control group. This suggests that plasma sTREM-1 could serve as a biomarker for the development of thrombosis in this condition. Further research is required to establish the role STREM-1 has in thrombosis.

One study revealed that the sTREM-1 level positively correlated with age in a controlled group, however, not in PAPS patients and asymptomatic carriers. This could be due to the effect that sTREM-1 levels decrease with age, which could be due to an impairment in renal function. A study conducted in PAPS patients found no association between sTREM-1 and eGFR. This suggests that the significance of the clinical relationship between sTREM-1 levels and age is not clear.

This is the case in both rheumatoid-related and systemic Lupus Erythematosus. The level of sTREM-1 in plasma could be used as a biomarker for TLR-4-mediated innate immune activation. This research highlights the importance of sTREM-1 for the management and development of inflammation-related conditions.

Increased expression of sTREM-1 has been linked to an increase of inflammation markers in the intestinal tract. It is not clear what role sTREM-1 plays in the destruction of tissues. TREM-1 is believed to be one of the mediators in intestinal inflammation. Yet, despite this discovery, it is still unclear whether sTREM-1's presence is crucial to determine if the disease is diagnosed.

Studies on cross-sections were conducted to determine the sTREM-1 levels in healthy controls as well as patients suffering from PAPS. ELISA was used to measure sTREM-1 levels in plasma. In this case the plasma sTREM-1 levels were significantly higher than those of healthy subjects. The limitations of this study's design and size of the sample limit its value in clinical practice.

It promotes the process of phagocytosis.

The role of TREM1 in phagocytosis is largely not understood, but a few recent studies have suggested that it may be involved. This study demonstrates that a-TREM1 promotes phagocytosis cooperation between neutrophils and intestinal cells. It also revealed that a-TREM1 increases the expression of IL-22, TNFA, and CD177 in neutrophils of patients suffering from IBD.

sTREM-1 is a reliable biomarker for infectious diseases, because it indicates that the TREM-1 pathway has been activated. When respiratory diseases are present the immune system's natural defense system is impaired and secondary bacterial infections are promoted by sTREM-1. The role of phagocytosis in it is unclear. However, it could have important implications for neuronal degeneration. TREM2 is also a member of the TREM-1 family and is expressed specifically in microglia. It is believed to regulate CNS homeostasis.

The TREM1 gene is expressed by neutrophils as well as macrophages. TREM1 has been proven to enhance phagocytosis through increasing the production of neutrophil-derived macrophages. TREM1 is also essential for the proper functioning of the phagocytic cells. Therefore, it is crucial to study the role of TREM1 in phagocytosis as well as to find the ligands that trigger this gene.

TREM-1 is essential for the immune response, non-infectious diseases , and autoimmune diseases. It has been proven to be a valuable biomarker for the detection of certain infectious and inflammatory diseases. Doctors can determine TREM-1 in order to check the immune function and determine if patients have any symptomatic diseases. There are no commercially available antibodies that detect TREM-1.

TREM-1 was identified in human RASF during co-culture tests. It reached its highest expression after 24 hours of coculture. Similar results were observed in mice treated with PTSF and OSF. However, a-TREM-1 didn't exhibit in PTSF and the OASF. This indicates that RASF is necessary to increase TREM-1 expression.

It blocks the microglia transition's proinflammatory subtype.

Researchers have recently discovered that TREM1 inhibitors can hinder the proinflammatory subtype transformation of microglia. They were able block TREM1 signaling and reduce neuroinflammation. They also discovered that TREM1 inhibits Card9-NFKB-mediated signaling and interacts with PAD4-NETs. This study suggests that TREM1 may be a potential therapeutic target for SAH.

TREM1 blocks PGF2I-stimulated IL-6 release. TREM1 also phosphorylates the p38 MAP kinase, and enhances PAD4NETs-induced production of IL-6. 17-AAG and Onalespib did not affect the phosphorylation p44/p42MAP kinase MYPT-1 or Rho-kinase. HSP90-siRNA triggered the activation of p38 Kinase.

TREM1 was first discovered in peripheral blood neutrophils. It was later confirmed to be present in macrophages, microglia and endothelial cells. It plays a major role in inflammation and causes the release of various chemokines. It was found that TREM1 inhibitors block the proinflammatory subtype transition of microglia as well as the crosstalk between central and peripheral immunity.

A recent single-cell sequencing study discovered 34 genes that were highly enriched in microglia. There were 73 genes enriched in monocytes and neutrophils. These genes could represent microglia that are resident and have an impact on immune response to disease. However, this information is incomplete and further studies are required to confirm these findings. The possibility of these inhibitors in clinical trials must be evaluated with care.

It inhibits neuronal synapses

An inhibition synapse is a kind of neuronal cell. Synapses are located close to the neuronal synapse, and are distinguished by the particularization and release of vesicles and receptors. They are typically elliptical in shape. The cell types responsible for IPSPs are still being studied by researchers, but their roles in the development of synaptic plasticity are becoming apparent.

The process of communication between neurons requires that signals can pass through these synapses. This gap must be crossed by signals, and then the neuron needs to release a chemical compound known as a neurotransmitter. Neurotransmitters release chemicals from a neuron's terminal axon to transmit information to another cell. These chemical messengers may be positive or negative and may have a stimulating or inhibitory impact. Serotonin for instance is a neurotransmitter inhibitor. This chemical helps calm the mind and induce sleep.

There are two primary circuit configurations for synaptic inhibition. In feedback inhibition, excitatory primary neurons synapse to inhibitory interneurons. Feedforward inhibition is when the Axons of the downstream principal neurons connect directly to inhibitory interneurons. GABA, an amino acid that is not a part of a protein, is the most abundant inhibitory neurotransmitter that is found in the brain. GABAA receptors and GABA receptors are the two kinds of receptors it binds. Its loss of GABA results in the development of neurological/psychiatric disorders.

It protects against LPS-induced shock

A new study has shown that GENT, an antimicrobial drug, blocks Septic shock induced by LPS in mice. The mortality rate of mice was measured frequently following LPS injection. Before and after LPS injection mice were also given 50 mg/kg GENT. After the LPS injection, lung tissues were collected and analyzed by H&E staining. In comparison to mice not treated with GENT, mice treated with LPS exhibited significantly lower mortality.

In the LPS model, two-dose LPS also showed that hRetn has protective effects. The levels of hRetn in the bloodstream were higher in mice that had been injecting with the bacterial substance as compared to those in the control. The mice treated with hRetn showed lower levels of eosinophils, neutrophils, and eos which protected them from the fatal dose of LPS. The protective effect was linked with a higher T helper 2 response in mice treated with hRETNTg.

In vivo, GENT inhibited macrophage inflammatory response expression in mice. It also blocked the expression of F4/80 (a antigen that is specific to macrophages). Macrophages also express iNOS which is a pro-inflammatory mediator that is activated by LPS induction. When cytokine levels rise and macrophages get activated iNOS and F4/80 are both positive.

The protective effect of hRetn on Nb-infected mice was further supported by a flow cytometric analysis of the peritoneal cavity. Although increased neutrophil influx wasn't the cause of Nb's protective effects, hRetn did enhance the effects of Nb-induced shock. Previous studies have shown that neutrophils in mice infected with Nb exhibited marked distinctions from LPS-infected mice. They also showed a shift in cytokine responses from type I to type II.