Abortion, Stillbirth, Early Death of Young in Rabbits by Listeria monocytogenes. II. Oral Exposure.

Gray, M. L.; Singh, Chintamani; Thorp, F.

doi:10.3181/00379727-89-21747

Cited by 26 publications

(13 citation statements)

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“…Abortion and stillbirth due to Listeria spp. have been reproduced experimentally by intravenous, oral, and respiratory inoculation in naturally susceptible gestating animal hosts, such as sheep, cattle, rabbits, and guinea pigs, as well in pregnant mice and rats (1,238,239,329,450,487,488,586). This shows that L. monocytogenes gains access to the fetus by hematogenous penetration of the placental barrier (Fig.…”

Section: Pathogenesismentioning

confidence: 99%

ListeriaPathogenesis and Molecular Virulence Determinants

et al. 2001

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The gram-positive bacterium Listeria monocytogenes is the causative agent of listeriosis, a highly fatal opportunistic foodborne infection. Pregnant women, neonates, the elderly, and debilitated or immunocompromised patients in general are predominantly affected, although the disease can also develop in normal individuals. Clinical manifestations of invasive listeriosis are usually severe and include abortion, sepsis, and meningoencephalitis. Listeriosis can also manifest as a febrile gastroenteritis syndrome. In addition to humans, L. monocytogenes affects many vertebrate species, including birds. Listeria ivanovii, a second pathogenic species of the genus, is specific for ruminants. Our current view of the pathophysiology of listeriosis derives largely from studies with the mouse infection model. Pathogenic listeriae enter the host primarily through the intestine. The liver is thought to be their first target organ after intestinal translocation. In the liver, listeriae actively multiply until the infection is controlled by a cell-mediated immune response. This initial, subclinical step of listeriosis is thought to be common due to the frequent presence of pathogenic L. monocytogenes in food. In normal indivuals, the continual exposure to listerial antigens probably contributes to the maintenance of anti-Listeria memory T cells. However, in debilitated and immunocompromised patients, the unrestricted proliferation of listeriae in the liver may result in prolonged low-level bacteremia, leading to invasion of the preferred secondary target organs (the brain and the gravid uterus) and to overt clinical disease. L. monocytogenes and L. ivanovii are facultative intracellular parasites able to survive in macrophages and to invade a variety of normally nonphagocytic cells, such as epithelial cells, hepatocytes, and endothelial cells. In all these cell types, pathogenic listeriae go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. In this way, listeriae disseminate in host tissues sheltered from the humoral arm of the immune system. Over the last 15 years, a number of virulence factors involved in key steps of this intracellular life cycle have been identified. This review describes in detail the molecular determinants of Listeria virulence and their mechanism of action and summarizes the current knowledge on the pathophysiology of listeriosis and the cell biology and host cell responses to Listeria infection. This article provides an updated perspective of the development of our understanding of Listeria pathogenesis from the first molecular genetic analyses of virulence mechanisms reported in 1985 until the start of the genomic era of Listeria research

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Section: Pathogenesismentioning

confidence: 99%

ListeriaPathogenesis and Molecular Virulence Determinants

et al. 2001

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“…Whether these conditions are present in the intrauterine environment and specifically in the placenta and amniotic fluid during pathological pregnancies, however, needs to be further elucidated. It is plausible that the pregnant uterus might represent a favorable environment for the replication of certain pathogens and might regulate the balance of lipopeptides expression of PTB‐related bacteria, thus directly impacting the type of inflammatory responses by both immune and nonimmune cells . Of note, L. monocytogenes and Mycoplasma fermentans , pathogens correlated with PTB in humans, exclusively contains/expresses diacylated lipoproteins, structurally similar to Pam2Cys, in its cell wall .…”

Section: Resultsmentioning

confidence: 99%

Differential outcomes of TLR2 engagement in inflammation-induced preterm birth

Cappelletti

Lawson

Chan

et al. 2017

Journal of Leukocyte Biology

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Preterm birth (PTB) is the leading cause of neonatal mortality worldwide. Infection and inflammation are considered main causes of PTB. Among multiple pathogens, Gram‐positive bacteria are commonly linked with induction of PTB. Although activation of innate immune responses, via TLR2 engagement, by Gram‐positive bacteria is a likely cause, whether induction of PTB depends on the potency of specific microbial components to induce Toll‐like receptor (TLR)2‐driven inflammation has not been elucidated. Here, we show that TLR2 activation by synthetic lipopeptides, Pam2Cys, and Pam3Cys specifically, variably influenced inflammation and subsequent induction of PTB. Pam2Cys challenge, compared to Pam3Cys, induced PTB and promoted significantly higher expression of inflammatory cytokines, specifically IL‐6 and IFN‐β, both in vivo and in vitro. Notably, antibody‐mediated neutralization of IL‐6 or genetic deletion of type I IFN receptor (IFNAR) was sufficient to protect from Pam2Cys‐driven PTB and to temper excessive proinflammatory cytokine production. Conversely, IFN‐β or IL‐6 was not sufficient to promote induction of PTB by Pam3Cys. In summary, our data implies a divergent function of TLR2‐activating lipopeptides in the magnitude and type of ligand‐driven inflammatory vigor in induction of PTB.

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“…There is little doubt that the infants in group 'A' were infected before birth and this precipitated delivery. Experimental evidence (Gray, Singh and Thorp, 1955) also suggests that those in group 'B' became infected shortly before or at the time of delivery.…”

Section: Discussionmentioning

confidence: 99%