2. Academic Validation
  3. TRPV4 is not the molecular sensor for bacterial lipopolysaccharides-induced calcium signaling

TRPV4 is not the molecular sensor for bacterial lipopolysaccharides-induced calcium signaling

  • Cell Immunol. 2023 Jan:383:104651. doi: 10.1016/j.cellimm.2022.104651.
Yuhui Wang 1,  Yanping Hao 2,  Jinhua Jin 1,  Zhihua Yi 3,  Yifei Liu 4,  Huan Zhou 2,  Guodun Zhao 5,  Lu Wen 2,  Huiqing Dong 5,  Yun Zhang 5,  Menghui Zhang 6,  Yuxin Jia 7,  Lei Han 2,  Heng Xu 7,  Ting Wang 8,  Jing Feng 9
Affiliations

Affiliations

  • 1 Department of Anesthesiology, Plastic Surgery Hospital, Chinese Academy of Medical Scicences and Peking Union Medical College, Beijing, China.
  • 2 Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China; University of Chinese Academy of Sciences, Beijing, China.
  • 3 Medical College of Nanchang University, School of Nursing, Nanchang, China.
  • 4 Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
  • 5 Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China; School of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing, China.
  • 6 Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China; School of Pharmacy, Henan University, Kaifeng, China.
  • 7 Division of Reconstructive Microsurgery, Department of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine (China), Shanghai, China.
  • 8 Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China. Electronic address: [email protected].
  • 9 Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China; University of Chinese Academy of Sciences, Beijing, China; School of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing, China; School of Pharmacy, Henan University, Kaifeng, China. Electronic address: [email protected].
PMID: 36493524 DOI: 10.1016/j.cellimm.2022.104651
Abstract

Lipopolysaccharides (LPS) is one of the most potent pathogen-associated signals for the immune system of vertebrates. In addition to the canonical pathway of LPS detection mediated by Toll-like Receptor 4 (TLR4) signaling pathway, TRP channel-mediated pathways endow sensory neurons and epithelial cells with the ability to detect and react to Bacterial endotoxins. Previous work revealed that LPS triggers TRPV4-dependent calcium influx in urothelial cells (UCs) and mouse tracheobronchial epithelial cells (mTEC). In marked contrast, here we show that most subtypes of LPS could not directly activate TRPV4 channel. Although LPS from Salmonella enterica serotype Minnesota evoked a [CA2+]i response in freshly isolated human bronchial epithelial cells (ECs), freshly isolated mouse ear skin single-cell suspensions, or HEK293T cells transiently transfected with mTRPV4, this activation occurred in a TRPV4-independent manner. Additionally, LPS from either E. coli strains or Salmonella enterica serotype Minnesota did not evoke significant difference in inflammation and pain hyperalgesia between wild type and TRPV4 deficient mice. In summary, our results demonstrate that in vitro and in vivo effects induced by LPS are independent of TRPV4, thus providing a clarity to the questioned role of LPS in TRPV4 activation.

Keywords

Calcium influx; Inflammation; LPS; Pain; TRPV4; Whole cell current.

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