Understanding the Entanglement: Neutrophil Extracellular Traps (NETs) in Cystic Fibrosis

نویسندگان

  • Saira R. Martínez-Alemán
  • Lizbeth Campos-García
  • José P. Palma-Nicolas
  • Romel Hernández-Bello
  • Gloria M. González
  • Alejandro Sánchez-González
چکیده

Cystic fibrosis (CF) is an autosomal recessive disorder caused by mutations in the gene that codes for the CF trans-membrane conductance regulator. These mutations result in abnormal secretions viscous airways of the lungs, favoring pulmonary infection and inflammation in the middle of neutrophil recruitment. Recently it was described that neutrophils can contribute with disease pathology by extruding large amounts of nuclear material through a mechanism of cell death known as Neutrophil Extracellular Traps (NETs) into the airways of patients with CF. Additionally, NETs production can contribute to airway colonization with bacteria, since they are the microorganisms most frequently found in these patients. In this review, we will discuss the implication of individual or mixed bacterial infections that most often colonize the lung of patients with CF, and the NETs role on the disease.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Does NETosis Contribute to the Bacterial Pathoadaptation in Cystic Fibrosis?

Significant advances in our understanding of neutrophil biology were made in the past several years. The exciting discovery that neutrophils deploy neutrophil extracellular traps (NETs) to catch pathogens paved the way for a series of additional studies to define the molecular mechanisms of NET generation and the biological significance of NETosis in acute and chronic pathologic conditions. Thi...

متن کامل

Role of MicroRNAs in BCG Therapy by the Induction of Neutrophil Extracellular Traps in Bladder Cancer

The treatment of bladder cancer is usually performed by Bacillus Calmette-Guerin (BCG) instillation. BCG therapy is a common therapeutic method with fewer side effects compared with chemotherapy, radiotherapy, etc. BCG can also inhibit the progression and recurrence of bladder cancer by inducing apoptosis pathways, arrest cell cycle, autophagy, and neutrophil extracellular traps (NETs) formatio...

متن کامل

Neutrophil extracellular traps promote lipopolysaccharide-induced airway inflammation and mucus hypersecretion in mice

Bacterial lipopolysaccharide (LPS) contributes to airway inflammation and mucus hypersecretion in chronic airway inflammatory diseases, such as chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF). Neutrophil extracellular traps (NETs) are extracellular meshworks composed of DNA fibers and antimicrobial proteins. Although NET formation has been detected in COPD and CF patients,...

متن کامل

Evasion of Neutrophil Extracellular Traps by Respiratory Pathogens.

The release of neutrophil extracellular traps (NETs) is a major immune mechanism intended to capture pathogens. These histone- and protease-coated DNA structures are released by neutrophils in response to a variety of stimuli, including respiratory pathogens, and have been identified in the airways of patients with respiratory infection, cystic fibrosis, acute lung injury, primary graft dysfunc...

متن کامل

Neutrophil extracellular traps (NETs) - formation and implications.

Neutrophils are cells of the immune system which freely circulate in blood vessels and are recruited to the inflammation sites when the human organism responds to microbial infections. One of the mechanisms of neutrophil action is the formation of neutrophil extracellular traps (NETs) The process of NET generation, called netosis, is a specific type of cell death, different from necrosis and ap...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 7  شماره 

صفحات  -

تاریخ انتشار 2017