Role of Clostridium Perfringens in Neonatal Necrotizing Enterocolitis and the Utility of Anaerobic Blood Cultures

C, Alejandra Sandoval; O, María Paz Romero; E, Carolina Guerra; B, Carolina Riquelme; C, Giannina Izquierdo

doi:10.47363/jprrr/2021(3)133

Cited by 1 publication

(2 citation statements)

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“…This pathogen secretes more than 20 virulent toxins and is associated with several serious enteric illnesses and soft tissue injuries, including necrotizing enterocolitis, food poisoning, and gas gangrene. 1 For animal husbandry, necrotizing enterocolitis linked with C. perfringens is responsible for an estimated economic loss between USD$2 and $6 billion annually. 2 What is worse, the cost for treating necrotizing enterocolitis clinically caused by C. perfringens in preterm infants is conservatively estimated at around £13.5 million in the UK per year.…”

Section: ■ Introductionmentioning

confidence: 99%

“…Clostridium perfringens is a Gram-positive and spore-forming anaerobe, as well as a gut commensal bacterium. This pathogen secretes more than 20 virulent toxins and is associated with several serious enteric illnesses and soft tissue injuries, including necrotizing enterocolitis, food poisoning, and gas gangrene . For animal husbandry, necrotizing enterocolitis linked with C.…”

Section: Introductionmentioning

confidence: 99%

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G Protein-Coupled Receptor 120 Mediates Host Defense against Clostridium perfringens Infection through Regulating NOD-like Receptor Family Pyrin Domain-Containing 3 Inflammasome Activation

Liu

Lei

et al. 2023

J. Agric. Food Chem.

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Clostridium perfringens is a major cause of infectious foodborne disease, frequently associated with the consumption of raw and undercooked food. Despite intensive studies on clarifying C. perfringens pathogenesis, the molecular mechanisms of host− pathogen interactions remain poorly understood. In soft tissue and mucosal infection models, Gpr120 -/mice, G protein-coupled receptor 120 (GPR120), are more susceptible to C. perfringens infection. Gpr120 deficiency leads to a low survival rate (30 and 10%, p < 0.01), more bacterial loads in the muscle (2.26 × 10 8 ± 2.08 × 10 8 CFUs/g, p < 0.01), duodenum (2.80 × 10 7 ± 1.61 × 10 7 CFUs/g, p < 0.01), cecum (2.50 × 10 8 ± 2.05 × 10 8 CFUs/g, p < 0.01), and MLN (1.23 × 10 6 ± 8.06 × 10 5 CFUs/g, p < 0.01), less IL-18 production in the muscle (8.54 × 10 3 ± 1.20 × 10 3 pg/g, p < 0.01), duodenum (3.34 × 10 3 ± 2.46 × 10 2 pg/g, p < 0.01), and cecum (3.81 × 10 3 ± 5.29 × 10 2 pg/g, p < 0.01), and severe organ injury. Obviously, GPR120 facilitates IL-18 production and pathogen control via potassium efflux-dependent NOD-like receptor family pyrin domain-containing 3 (NLRP3) signaling. Mechanistically, GPR120 interaction with NLRP3 potentiates the NLRP3 inflammasome assembly. Thus, this study uncovers a novel role of GPR120 in host protection and reveals that GPR120 may be a potential therapeutic target for limiting pathogen infection.

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Section: ■ Introductionmentioning

confidence: 99%