LTB4R Membrane Protein Introduction

Introduction of LTB4R

LTB4R, encoded by LTB4R gene, is a member of G-protein coupled receptor family and couples to pertussis toxin-sensitive Gi-like G proteins. It is one of two receptors for leukotriene B4 (LTB4), with far higher affinity than the other LTB4 receptor 2 (LTB4R2). Moreover, the pattern expression of the two receptors is different. LTB4R1 is predominantly restricted to peripheral leukocytes, while LTB4R2 is expressed more ubiquitously, with the highest level in the skin, spleen, bone marrow and lymphocytes. The two receptors are both associated with pathologic inflammation.

Function of LTB4R Membrane Protein

LTB4R is a receptor for leukotriene B4, a potent chemotactic receptor for inflammatory cells. The activated receptor by its ligands stimulates the activation of G proteins, resulting in the activation of phosphatidylinositol-calcium second messenger system. BLT1-LTB4 pathway regulates inflammation and immune response, involving lymphocyte activation, antigen presenting, chemotaxis of eosinophils and recruitment of lymphocytes. Studies have shown that mice deficient in BLT1 could exhibit a significant decrease in neutrophil recruitment and results in inflammation responses. Hence, the inhibition of BLT1 may be an effective therapeutic approach for the treatment of various inflammatory diseases, such as bronchial asthma, inflammatory bowel diseases, rheumatoid arthritis, atopic dermatitis and postmenopausal osteoporosis. Besides, BLT1 is also the cardiac P2Y receptor and the interaction of them regulates L-type calcium currents thereby mediating cardiac muscle contraction. And BLT1-LTB4 axis also regulates the migration of vascular smooth muscle cells and is involved in the pathological process of atherogenesis.

Fig.1 Inhibition of leukotriene B4 receptor 1 attenuates LPS-induced cardiac dysfunction: role of AMPK-regulated mitochondrial function. (Stoddard, 2015)

Application of LTB4R Membrane Protein in Literature

1. Miyabe Y., et al. LTB4 and BLT1 in inflammatory arthritis. Seminars in Immunology. 2017, 33:52-57. PubMed ID: 29042029
   
   

   The findings show that LTB4 and BLT1 may be involved in the pathogenesis of human rheumatoid arthritis (RA), indicating a novel therapeutic target for LTB4-BLT1 pathway for the treatment of RA.

2. Gelfand E W. Importance of the leukotriene B4-BLT1 and LTB4-BLT2 pathways in asthma. Seminars in Immunology. 2017, 33:44-51. PubMed ID: 29042028
   
   

   The study reveals that the LTB4-BLT1 pathway plays an essential role in asthma pathogenesis. However, the function of BLT2 in asthma remains is unclear. It is suggested that LTB4-BLT1 pathway is a novel therapeutic target for asthma patients that remain uncontrolled despite intensive corticosteroid treatment.

3. Subramanian B.C., et al. The role of the LTB4-BLT1 axis in chemotactic gradient sensing and directed leukocyte migration. Seminars in Immunology. 2017, 33:16-29. PubMed ID: 29042024
   
   

   In this review, authors propose that LTB4-BLT1 axis mediates signal-relay between chemotaxing neutrophils and a range of inflammatory conditions including tumor progression and metastasis.

4. Jala V.R., et al. The yin and yang of leukotriene B4 mediated inflammation in cancer. Seminars in Immunology. 2017, 33:58-64. PubMed ID: 28982616
   
   

   The article shows that BLT1 blockage could attenuate neutrophilic inflammation and tumor promotion. And BTL1 plays a critical role in initiating anti-tumor immunity by mediating CD8⁺ T cell recruitment in a number of xenograft models.

5. Jala V.R., et al. Leukotriene B4-receptor-1 mediated host response shapes gut microbiota and controls colon tumor progression. Oncoimmunology. 2017, 6(12):e1361593. PubMed ID: 29209564
   
   

   The findings identify a novel interplay between the Toll-like receptor-mediated microbial sensing mechanisms and BLT1-mediated host response in the control of colon tumor development.

LTB4R Preparation Options

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Reference

1. Sun M, et al. (2017). Inhibition of leukotriene B4 receptor 1 attenuates lipopolysaccharide-induced cardiac dysfunction: role of AMPK-regulated mitochondrial function. Scientific Reports. 7, 44352

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