Neutrophils are often exclusively considered as a first-line innate immune defence, able to rapidly kill or trap pathogens and causing in case of over-activation tissue damage. In the female reproductive tract, however, the presence and activity of neutrophils seems to be tightly regulated. Major players in orchestrating this regulation are cyclical steroid sex hormones present during the menstrual cycle and pregnancy. This review describes the role of sex hormones in regulating directly or indirectly the functionality of neutrophils, the role of neutrophils during fertilization and pregnancy and in controlling viral, fungal and bacterial infection. This review also discusses the consequence of overt neutrophil activation in pregnancy pathologies.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6718280 | PMC |
http://dx.doi.org/10.1111/cei.13278 | DOI Listing |
J Leukoc Biol
January 2025
Department of Molecular and Cellular Biology, The Scripps Research Institute, La Jolla, CA.
Regulated sequential exocytosis of neutrophil granules is essential in orchestrating the innate immune response, while uncontrolled secretion causes inflammation. We developed and characterized Nexinhib20, a small-molecule inhibitor that targets azurophilic granule exocytosis in neutrophils by blocking the interaction between the small GTPase Rab27a and its effector JFC1. Its therapeutic potential has been demonstrated in several pre-clinical models of inflammatory disease.
View Article and Find Full Text PDFFront Public Health
January 2025
Second Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, China.
Background: Inflammation is a critical component in the process of resolved hepatitis B virus (HBV) infection. The neutrophil-to-lymphocyte ratio (NLR) serves as a sensitive indicator of systemic inflammation and immune activation. Our study aimed to investigate the correlation between elevated NLR levels and the risk of all-cause mortality in patients with resolved HBV infection.
View Article and Find Full Text PDFBiochem Pharmacol
January 2025
Division of Pharmacodynamics, Faculty of Pharmacy, Keio University, Tokyo, Japan. Electronic address:
Sepsis is a life-threatening condition caused by severe infection and often complicates acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) due to the collapse of the oxidative and inflammatory balance induced by microbial pathogens, including lipopolysaccharides (LPS). In sepsis-related ARDS/ALI, NADPH oxidase (NOX) and toll-like receptors (TLR) in neutrophils and macrophages are key players in initiating oxidative and inflammatory imbalances. Although NOX and TLR activation has been linked to carbon monoxide (CO), the mechanism by which CO affects sepsis-related ARDS/ALI through NOX and TLR remains unknown.
View Article and Find Full Text PDFCytokine
January 2025
Department of Gastroenterology, General Hospital of Ningxia Medical University (The First Clinical Medical College of Ningxia Medical University), 750004 Yinchuan, China.
Background: Sepsis is an infection-related systemic inflammation with high mortality rates. Activation of formyl peptide receptor 1 (FPR1) in immune cells can promote their chemotaxis and inflammatory response, which imbalances immune response during the process of sepsis. FPR1 blockade did diminish systemic inflammatory response during bacterial infection.
View Article and Find Full Text PDFFront Pharmacol
January 2025
Laboratory of Pharmacology, Key Laboratory of Ethnomedicine of Ministry of Education, School of Pharmacy, Minzu University of China, Beijing, China.
Background: (Lanata) is generally used to treat pustule infection in Inner Mongolia folk medicine and is called "the holy medicine for pustule." However, the pharmacological mechanism of Lanata in treating pustule infection is still unclear.
Aims: This study aimed to investigate the therapeutic effects of Lanata on skin infection and explore the underlying mechanisms.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!