Production of tumor necrosis factor by human cells in vitro and in vivo, induced by group B streptococci

Williams, Phillip; Bohnsack, John F.; Augustine, Nancy H.; Drummond, Wendi K.; Rubens, Craig E.; Hill, Harry R.

doi:10.1016/s0022-3476(05)81706-8

Cited by 72 publications

(54 citation statements)

References 33 publications

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“…Because of the critical role of cytokines in determining the effector functions of both phagocytic cells and lymphocytes, it is likely that the outcome of GBS disease could, at least in part, depend on cytokines induced during infection, as shown in several other experimental models of infectious diseases [43][44][45][46][47]. Recent reports have shown that GBS, both during natural [12,16] and experimental infections [13][14][15], induce high levels of TNFa, IL-1b, IL-6 and IFN-g. However, these studies focused on defining the role of inflammatory cytokines in the pathogenesis of disease.…”

Section: Discussionmentioning

confidence: 99%

Cytokine Response to Group B Streptococcus Infection in Mice

et al. 1998

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This study was undertaken to better understand the complex relationship between specific and non‐specific host defence mechanisms and group B streptococci (GBS). A comprehensive kinetics analysis of cytokine mRNA expression was performed, by Northern blot assay, in peritoneal exudate cells (PEC) and spleen cells (SC) recovered from CD‐1 mice at various times during the course of an intraperitoneal infection with a lethal dose (5 × 103 microorganisms/mouse) of type Ia GBS, reference strain 090 (GBS‐Ia). Analysis of cytokines involved in the development of a specific TH response shows that GBS‐Ia in PEC induce only a weak increase of IL‐2 mRNA expression and in SC a cytokine pattern characterized by IL‐2, IFN‐γ and IL‐12 in the absence of IL‐4, IL‐5 and IL‐10. This selected cytokine pattern could provide appropriate conditions for the development of a TH1 response. Analysis of inflammatory cytokines, which are usually induced early during an in vivo infection, shows that there is a significant expression of mRNA specific for IL‐1β, TNFα and IL‐6, both in PEC and SC only at 24 h which persists at a high level until 36 h. This delayed cytokine induction, accompanied by the contemporary activation of splenic phagocytic cells, occurs only when the number of GBS‐Ia is extremely high. In fact, at 24 h GBS‐Ia have heavily colonized all organs. In vitro infection of thioglycollate‐elicited peritoneal macrophages confirms that the ability of GBS‐Ia to induce a strong inflammatory cytokine response depends strictly on the number of infecting microorganisms. Indeed, macrophages respond to GBS‐Ia with a very rapid induction of IL‐1β and TNFα mRNA when infected at a ratio of 1:10, but not at 100:1. Two major observations emerged from this study: (1) GBS‐Ia, by inducing a cytokine pattern which seems to favour development of a TH1 response, could evade antibody production essential for resistance to GBS; and (2) inflammatory cytokine response is induced when a heavy microbial invasion of the host has already occurred. These novel features of GBS‐Ia could contribute to the development and progression of lethal infection in mice.

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Section: Discussionmentioning

confidence: 99%

Cytokine Response to Group B Streptococcus Infection in Mice

et al. 1998

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“…Here we show that the p38 and p42/44 MAPK pathways are involved in COX-2 expression in human monocytes. Secretion of TNF-␣ by human monocytes after exposure to GBS [9] is also likely regulated through the p38 MAPK pathway [35,42]. Furthermore, the production of COX-2 in zymosan-stimulated human monocytes is regulated through p38 [43].…”

Section: Discussionmentioning

confidence: 99%

“…GBS were isolated and heat-killed organisms prepared as previously described [9,32]. Briefly, the bacteria were grown overnight in Todd-Hewitt broth (Difco Laboratories, Inc., Detroit, MI) for 18 h at 37°C.…”

Section: Gbs Strain Isolationmentioning

confidence: 99%

“…Recent in vitro experiments demonstrated that exposure of clinically isolated strains of GBS to human amniotic or decidual cells causes production of both chemokines and cytokines [7,8]. We first reported that human mixed mononuclear cells and isolated macrophages produce tumor necrosis factor ␣ (TNF-␣) after exposure to GBS [9]. In addition to TNF-␣ secretion, human mononuclear leukocytes and macrophages secrete interleukin (IL)-1 and IL-6 after exposure to GBS [9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

“…We first reported that human mixed mononuclear cells and isolated macrophages produce tumor necrosis factor ␣ (TNF-␣) after exposure to GBS [9]. In addition to TNF-␣ secretion, human mononuclear leukocytes and macrophages secrete interleukin (IL)-1 and IL-6 after exposure to GBS [9][10][11][12]. Rowen and colleagues reported that exposure of human monocytes to GBS induced secretion of leukotriene B 4 [13].…”

Section: Introductionmentioning

confidence: 99%

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Induction of cyclooxygenase-2 by human monocytes exposed to group B streptococci

Maloney

Thompson

Hill

et al. 2000

Journal of Leukocyte Biology

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Group B streptococcal (GBS) infections are associated with high morbidity and mortality. The molecular pathways mediating the pathophysiological events in GBS infection are not fully delineated. Cyclooxygenases (COX) are the enzymes that convert arachidonate to active eicosanoids. To identify the effects of GBS on eicosanoid metabolism and regulatory mechanisms, we exposed human monocytes to GBS and found that they secreted prostaglandin E 2 , prostacyclin, and thromboxane A 2 . Exposure to GBS caused monocytes to express COX-2 mRNA and protein in both a time-and concentration-dependent manner that correlated with eicosanoid production. COX-1 protein was unchanged. Addition of the anti-inflammatory cytokines interleukin (

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Molekulare Mechanismen der neonatalen Abwehr von bakteriellen Infektionen

Berner

Molekulare Medizin

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Production of tumor necrosis factor by human cells in vitro and in vivo, induced by group B streptococci

Cited by 72 publications

References 33 publications

Cytokine Response to Group B Streptococcus Infection in Mice

Cytokine Response to Group B Streptococcus Infection in Mice

Induction of cyclooxygenase-2 by human monocytes exposed to group B streptococci

Molekulare Mechanismen der neonatalen Abwehr von bakteriellen Infektionen

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