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Open AccessReview

Streptococcus pneumoniae and Its Virulence Factors H2O2 and Pneumolysin Are Potent Mediators of the Acute Chest Syndrome in Sickle Cell Disease

1
Department of Medicine, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA
2
Institute for Medical Microbiology, Justus-Liebig-University, Biomedical Research Centre Seltersberg, 35392 Giessen, Germany
3
Vascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA
4
Department of Pharmacology and Toxicology, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA
5
Department of Pediatrics, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA
*
Author to whom correspondence should be addressed.
Received: 5 January 2021 / Revised: 8 February 2021 / Accepted: 11 February 2021 / Published: 17 February 2021
(This article belongs to the Special Issue Toxins and Lung Infection)
Sickle cell disease (SCD) is one of the most common autosomal recessive disorders in the world. Due to functional asplenia, a dysfunctional antibody response, antibiotic drug resistance and poor response to immunization, SCD patients have impaired immunity. A leading cause of hospitalization and death in SCD patients is the acute chest syndrome (ACS). This complication is especially manifested upon infection of SCD patients with Streptococcus pneumoniae (Spn)—a facultative anaerobic Gram-positive bacterium that causes lower respiratory tract infections. Spn has developed increased rates of antibiotics resistance and is particularly virulent in SCD patients. The primary defense against Spn is the generation of reactive oxygen species (ROS) during the oxidative burst of neutrophils and macrophages. Paradoxically, Spn itself produces high levels of the ROS hydrogen peroxide (H2O2) as a virulence strategy. Apart from H2O2, Spn also secretes another virulence factor, i.e., the pore-forming exotoxin pneumolysin (PLY), a potent mediator of lung injury in patients with pneumonia in general and particularly in those with SCD. PLY is released early on in infection either by autolysis or bacterial lysis following the treatment with antibiotics and has a broad range of biological activities. This review will discuss recent findings on the role of pneumococci in ACS pathogenesis and on strategies to counteract the devastating effects of its virulence factors on the lungs in SCD patients. View Full-Text
Keywords: sickle cell disease; acute chest syndrome; Streptococcus pneumoniae; pneumolysin; H2O2 sickle cell disease; acute chest syndrome; Streptococcus pneumoniae; pneumolysin; H2O2
MDPI and ACS Style

Gonzales, J.; Chakraborty, T.; Romero, M.; Mraheil, M.A.; Kutlar, A.; Pace, B.; Lucas, R. Streptococcus pneumoniae and Its Virulence Factors H2O2 and Pneumolysin Are Potent Mediators of the Acute Chest Syndrome in Sickle Cell Disease. Toxins 2021, 13, 157. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13020157

AMA Style

Gonzales J, Chakraborty T, Romero M, Mraheil MA, Kutlar A, Pace B, Lucas R. Streptococcus pneumoniae and Its Virulence Factors H2O2 and Pneumolysin Are Potent Mediators of the Acute Chest Syndrome in Sickle Cell Disease. Toxins. 2021; 13(2):157. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13020157

Chicago/Turabian Style

Gonzales, Joyce; Chakraborty, Trinad; Romero, Maritza; Mraheil, Mobarak A.; Kutlar, Abdullah; Pace, Betty; Lucas, Rudolf. 2021. "Streptococcus pneumoniae and Its Virulence Factors H2O2 and Pneumolysin Are Potent Mediators of the Acute Chest Syndrome in Sickle Cell Disease" Toxins 13, no. 2: 157. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13020157

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Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

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