Listeria Infections of the Eye

2016 ◽  
Vol 27 (2) ◽  
pp. 115-121 ◽  
Author(s):  
Herbert Hof
Keyword(s):  
Listeria Monocytogenes ◽  
Anterior Chamber ◽  
Causative Agent ◽  
Guinea Pigs ◽  
Specific Therapy ◽  
Ocular Infections ◽  
Exact Diagnosis

The bacterium Listeria monocytogenes resides originally in the environment. Infections of the eye have been induced experimentally; for example, in rabbits and guinea pigs. Natural ocular infections occur in various animals; in most instances, they are induced exogenously; for example, by contaminated silage affecting primarily the conjunctiva, cornea, or the anterior chamber. Sporadic infections as well as outbreaks have been described. In humans, besides exogenous infections, endogenous infections also occur, inducing mainly endophthalmitis. Since an exact diagnosis of the causative agent is often delayed, specific therapy starts too late, so that the outcome is often poor. The antibiotics of primary choice would be ampicillin or a quinolone such as moxifloxacin or levofloxacin. The role of fosfomycin for therapy of ocular infections is discussed.

scholarly journals Actin assembly-inducing protein ActA promotes FcγRIa-mediatedListeriainternalization

2017 ◽  
Author(s):  
Sofya S. Perelman ◽  
Michael E. Abrams ◽  
Neal M. Alto
Keyword(s):  
Listeria Monocytogenes ◽  
Causative Agent ◽  
Cell Invasion ◽  
Immune Defense ◽  
Human Immunoglobulin ◽  
Type I ◽  
Actin Assembly ◽  
Gene Target ◽  
Immunoglobulin Receptor

AbstractListeria monocytogenesis a Gram-positive intracellular pathogen and the causative agent of human listeriosis. While the ability ofL. monocytogenesto enter and survive in professional phagocytes is critical to establish a successful infection, mechanisms of invasion are poorly understood. Our previous investigation into the role of type I interferon-stimulated genes in bacterial infection revealed that the human immunoglobulin receptor FcγRIa served as aL. monocytogenesinvasion factor. FcγRIa-mediatedL. monocytogenesentry occurred independently of immunoglobulin interaction or bacterial internalins. However, the bacterial determinants that mediate FcγRIa interaction remain unclear. Using a comparative genomics approach, we identify actin assembly-inducing protein ActA as a pathogen specific ligand of FcγRIa. FcγRIa enhanced entry of pathogenicL. monocytogenesandL. ivanoviistrain but not non-pathogenicL. innocua. We found that the major virulence regulator PrfA is required for pathogen entry into FcγRIa-expressing cells and identify its gene targetactAas the criticalListerialigand. ActA alone was sufficient to promote entry into FcγRIa-expressing cells, and this function is independent of its actin nucleating activity. Together, these studies present an unexpected role of ActA beyond its canonical function in actin-based motility and expand our understanding ofListeriastrategies for host cell invasion.ImportanceListeria monocytogenesis a food-borne bacterial pathogen and a causative agent of listeriosis with up to 50% mortality rate in immunocompromised individuals. While the mechanisms ofListeriaentry into non-phagocytic cells have been extensively characterized, the details of phagocytic cell invasion are still poorly understood. We have recently discovered that human immunoglobulin receptor FcγRIa mediatesListeriauptake by monocytic cells. This process occurred independently of canonical immunoglobulin interactions as well as classicListeriainternalization factors. Importantly, molecular determinants ofListeria-FcγRIa interaction leading to bacterial entry, remained unknown. In this study, we demonstrate thatListeriavirulence factor actin-assembly inducing protein ActA is required for FcγRIa-mediated entry. Further, ActA was found to be sufficient for the internalization, suggesting its role as a bacterial ligand of FcγRIa. Together, these findings expand our knowledge of mechanisms thatListeriahas evolved to exploit cellular signaling pathways and immune defense of the host.

Listeria monocytogenes strains encoding premature stop codons in inlA invade mice and guinea pig fetuses in orally dosed dams

2013 ◽  
Vol 62 (12) ◽  
pp. 1799-1806 ◽  
Author(s):  
Anne Holch ◽  
Hanne Ingmer ◽  
Tine Rask Licht ◽  
Lone Gram
Keyword(s):  
Listeria Monocytogenes ◽  
Guinea Pig ◽  
Food Processing ◽  
Guinea Pigs ◽  
Stop Codon ◽  
Fetal Liver ◽  
Fatal Case ◽  
Premature Stop Codon ◽  
Tissue Samples ◽  
Pregnant Mice

Listeria monocytogenes is an important food-borne bacterial pathogen and listeriosis can result in abortions in pregnant women. The bacterium can colonize food-processing environments, where specific molecular subtypes can persist for years. The purpose of this study was to determine the virulence potential of a group of food-processing persistent L. monocytogenes strains encoding a premature stop codon in inlA (encoding internalin A) by using two orally dosed models, pregnant mice and pregnant guinea pigs. A food-processing persistent strain of L. monocytogenes invaded placentas (n = 58; 10 % positive) and fetuses (3 % positive) of pregnant mice (n = 9 animals per strain), similar to a genetically manipulated murinized strain, EGD-e InlA m* (n = 61; 3 and 2 %, respectively). In pregnant guinea pigs (n = 9 animals per bacterial strain), a maternofetal strain (from a human fetal clinical fatal case) was isolated from 34 % of placenta samples (n = 50), whereas both food-processing persistent strains were found in 5 % of placenta samples (n = 36 or 37). One of the food-processing persistent strains, N53-1, was found in up to 8 % of guinea pig fetal liver and brain samples, whereas the maternofetal control was found in 6 % of fetal tissue samples. As the food-processing persistent strains carry a premature stop codon in inlA but are invasive in orally dosed pregnant mice and guinea pigs, we hypothesize that listerial crossing of the placental barrier can occur by a mechanism that is independent of an interaction between E-cadherin and InlA.

Paradoxical effect of salbutamol in a model of acute organophosphates intoxication in guinea pigs: role of substance P release

2007 ◽  
Vol 292 (4) ◽  
pp. L915-L923 ◽  
Author(s):  
Jaime Chávez ◽  
Patricia Segura ◽  
Mario H. Vargas ◽  
José Luis Arreola ◽  
Edgar Flores-Soto ◽  
...  
Keyword(s):  
Substance P ◽  
Guinea Pigs ◽  
Smooth Muscle Contraction ◽  
In Vivo Experiments ◽  
Intracellular Ca ◽  
Neurokinin 1 ◽  
Substance P Release

Organophosphates induce bronchoobstruction in guinea pigs, and salbutamol only transiently reverses this effect, suggesting that it triggers additional obstructive mechanisms. To further explore this phenomenon, in vivo (barometric plethysmography) and in vitro (organ baths, including ACh and substance P concentration measurement by HPLC and immunoassay, respectively; intracellular Ca2+ measurement in single myocytes) experiments were performed. In in vivo experiments, parathion caused a progressive bronchoobstruction until a plateau was reached. Administration of salbutamol during this plateau decreased bronchoobstruction up to 22% in the first 5 min, but thereafter airway obstruction rose again as to reach the same intensity as before salbutamol. Aminophylline caused a sustained decrement (71%) of the parathion-induced bronchoobstruction. In in vitro studies, paraoxon produced a sustained contraction of tracheal rings, which was fully blocked by atropine but not by TTX, ω-conotoxin (CTX), or epithelium removal. During the paraoxon-induced contraction, salbutamol caused a temporary relaxation of ∼50%, followed by a partial recontraction. This paradoxical recontraction was avoided by the M2- or neurokinin-1 (NK1)-receptor antagonists (methoctramine or AF-DX 116, and L-732138, respectively), accompanied by a long-lasting relaxation. Forskolin caused full relaxation of the paraoxon response. Substance P and, to a lesser extent, ACh released from tracheal rings during 60-min incubation with paraoxon or physostigmine, respectively, were significantly increased when salbutamol was administered in the second half of this period. In myocytes, paraoxon did not produce any change in the intracellular Ca2+ basal levels. Our results suggested that: 1) organophosphates caused smooth muscle contraction by accumulation of ACh released through a TTX- and CTX-resistant mechanism; 2) during such contraction, salbutamol relaxation is functionally antagonized by the stimulation of M2 receptors; and 3) after this transient salbutamol-induced relaxation, a paradoxical contraction ensues due to the subsequent release of substance P.

scholarly journals Role of Branched-Chain Fatty Acids in pH Stress Tolerance in Listeria monocytogenes

2006 ◽  
Vol 73 (3) ◽  
pp. 997-1001 ◽  
Author(s):  
Efstathios S. Giotis ◽  
David A. McDowell ◽  
Ian S. Blair ◽  
Brian J. Wilkinson
Keyword(s):  
Fatty Acids ◽  
Listeria Monocytogenes ◽  
Stress Tolerance ◽  
Ph Sensitive ◽  
Branched Chain Fatty Acids ◽  
Alkaline Conditions ◽  
Branched Chain ◽  
Ph Adaptation ◽  
Chain Fatty Acids

ABSTRACT In alkaline conditions, Listeria monocytogenes cells develop higher proportions of branched-chain fatty acids (FAs), including more anteiso forms. In acid conditions, the opposite occurs. Reduced growth of pH-sensitive mutants at adverse pH (5.0/9.0) was alleviated by the addition of 2-methylbutyrate (an anteiso-FA precursor), suggesting that anteiso-FAs are important in adaptation to adverse pH. The balance between anteiso- and iso-FAs may be more important than changes in the amounts and/or degrees of saturation of FAs in pH adaptation.

Putative antihyperpyretic factor induced by LPS in spleen of guinea pigs

2005 ◽  
Vol 289 (3) ◽  
pp. R680-R687 ◽  
Author(s):  
Carlos Feleder ◽  
Vit Perlik ◽  
Ying Tang ◽  
Clark M. Blatteis
Keyword(s):  
Kupffer Cells ◽  
Guinea Pigs ◽  
Collateral Circulation ◽  
Splenic Vein ◽  
Inhibitory Factor ◽  
Febrile Response ◽  
Temperature Changes ◽  
The Core ◽  
Temporally Correlated

We reported previously that the onset of LPS-induced fever, irrespective of its route of administration, is temporally correlated with the appearance of LPS in the liver and that splenectomy significantly increases both the febrile response to LPS and the uptake of LPS by Kupffer cells (KC). To further evaluate the role of the spleen in LPS fever production, we ligated the splenic vein and, 7 and 30 days later, monitored the core temperature changes over 6 h after intraperitoneal (ip) injection of LPS (2 μg/kg). Both the febrile response and the uptake of LPS by KC were significantly augmented. Like splenectomy, splenic vein ligation (SVL) increased the febrile response and LPS uptake by KC until the collateral circulation developed, suggesting that the spleen may normally contribute an inhibitory factor that limits KC uptake of LPS and thus affects the febrile response. Subsequently, to verify the presence of this factor, we prepared splenic extracts from guinea pigs pretreated with LPS (8 μg/kg ip) or pyrogen-free saline, homogenized and ultrafiltered them, and injected them intravenously into splenectomized (Splex) guinea pigs pretreated with LPS (8 μg/kg ip). The results confirmed our presumption that the splenic extract from LPS-treated guinea pigs inhibits the exaggerated febrile response and the LPS uptake by the liver of Splex guinea pigs, indicating the presence of a putative splenic inhibitory factor, confirming the participation of the spleen in LPS-induced fever, and suggesting the existence of a novel antihyperpyretic mechanism. Preliminary data indicate that this factor is a lipid.

scholarly journals Role of PGE2 in Neurotransmission from Pre- to Post-Ganglionic Hypogastric Nerves of Guinea Pigs.

1992 ◽  
Vol 58 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Akikazu Fujita ◽  
Tadayoshi Takeuchi ◽  
Fumiaki Hata ◽  
Osamu Yagasaki
Keyword(s):  
Guinea Pigs
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