Bruton's Tyrosine Kinase Deficiency Ameliorates Antimicrobial Host Defense during Peritonitis Induced by Pathogenic Escherichia coli.
Zhe LiuCornelis van 't VeerRudi W HendriksJoris J T H RoelofsTom van der PollAlex F de VosPublished in: Infection and immunity (2022)
Peritonitis and abdominal sepsis remain major health problems and challenge for clinicians. Bruton's tyrosine kinase (Btk) is a versatile signaling protein involved in the regulation of B cell development and function, as well as innate host defense. In the current study, we aimed to explore the role of Btk in the host response during peritonitis and sepsis in mice induced by a gradually growing pathogenic strain of Escherichia coli bacteria. We found that Btk deficiency ameliorated antibacterial host defense during the late stage of E. coli-induced peritonitis. Btk was not required for cytokine and chemokine release in response to either E. coli or lipopolysaccharide and did not impact organ damage evoked by E. coli. Btk deficiency also did not alter neutrophil influx to the primary site of infection. However, the absence of Btk modestly enhanced phagocytosis of E. coli by neutrophils. These results indicate that Btk-mediated signaling is superfluous for inflammatory responses and remarkably detrimental for antibacterial defense during E. coli-induced peritonitis.
Keyphrases
- tyrosine kinase
- escherichia coli
- epidermal growth factor receptor
- mental health
- acute kidney injury
- intensive care unit
- healthcare
- high glucose
- diabetic rats
- immune response
- staphylococcus aureus
- biofilm formation
- klebsiella pneumoniae
- oxidative stress
- palliative care
- replacement therapy
- septic shock
- inflammatory response
- mouse model
- adipose tissue
- metabolic syndrome
- climate change
- insulin resistance
- small molecule
- wound healing
- candida albicans