Very recently, only 2 days ago, Pitts and D’Orazio [1] reported an interesting outcome on PGE2, a lipid-signaling compound with multiplex tasks in both homeostasis and inflammation. Depending on the cellular context, it may suppress certain immune responses. In their research, they tested whether PGE2 could inhibit bacterial killing by polymorphonuclear neutrophils (PMN) by means of a mouse model of foodborne listeriosis. They found that PGE2 pretreatment dropped-off the aptitude of PMN harvested from the bone marrow of either BALB/cByJ or C57BL/6J mice to kill Listeria monocytogenes in vitro. PGE2 treatment supported the migration of PMN toward the chemoattractant leukotriene B4, declined uptake of Listeria monocytogenes by PMN, and inhibited the respiratory burst of PMN compared with vehicle-treated cells. When immune cells were isolated from the livers of infected mice and tested directly ex vivo for the presence of PGE2, BALB/cByJ cells produced remarkably more than C57BL/6J cells. Thus, these results suggest that robust PGE2 production can suppress PMN effector functions, leading to decreased bacterial killing, which may contribute to the innate susceptibility of BALB/cByJ mice to infection with the facultative intracellular bacterial pathogen Listeria monocytogenes. Thus, these important data, have caught my attention given that during my youth, as researcher, I have carried out studies on Listeria monocytogenes - see references [2-8] and latterly on bacteriocins as reported in [9] and dairy products like source of beneficial microorganism able to survival in GIT[10-13]

Listeriosis Patients by Listeria monocytogenes Infection: A Resurgent Foodborne Disease in Immune-Compromised Subjects

Maria Luigia Pallotta
Primo
2019-01-01

Abstract

Very recently, only 2 days ago, Pitts and D’Orazio [1] reported an interesting outcome on PGE2, a lipid-signaling compound with multiplex tasks in both homeostasis and inflammation. Depending on the cellular context, it may suppress certain immune responses. In their research, they tested whether PGE2 could inhibit bacterial killing by polymorphonuclear neutrophils (PMN) by means of a mouse model of foodborne listeriosis. They found that PGE2 pretreatment dropped-off the aptitude of PMN harvested from the bone marrow of either BALB/cByJ or C57BL/6J mice to kill Listeria monocytogenes in vitro. PGE2 treatment supported the migration of PMN toward the chemoattractant leukotriene B4, declined uptake of Listeria monocytogenes by PMN, and inhibited the respiratory burst of PMN compared with vehicle-treated cells. When immune cells were isolated from the livers of infected mice and tested directly ex vivo for the presence of PGE2, BALB/cByJ cells produced remarkably more than C57BL/6J cells. Thus, these results suggest that robust PGE2 production can suppress PMN effector functions, leading to decreased bacterial killing, which may contribute to the innate susceptibility of BALB/cByJ mice to infection with the facultative intracellular bacterial pathogen Listeria monocytogenes. Thus, these important data, have caught my attention given that during my youth, as researcher, I have carried out studies on Listeria monocytogenes - see references [2-8] and latterly on bacteriocins as reported in [9] and dairy products like source of beneficial microorganism able to survival in GIT[10-13]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11695/92924
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