Administration to mouse of endotoxin from gram-negative bacteria leads to activation and apoptosis of T lymphocytes

Castro, Ana; Bemer, Véronique; Nóbrega, Alberto; Coutinho, António; Truffa‐Bachi, Paolo

doi:10.1002/(sici)1521-4141(199802)28:02<488::aid-immu488>3.0.co;2-r

Cited by 74 publications

(39 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This is in line with several reports that LPS stimulates murine CD8 1 T activation in vivo via an indirect pathway involving APC [17,18,26]. The reason for the failure of murine CD8 1 T cells, in contrast to human CD8 1 T cells, to respond to LPS is not fully understood.…”

Section: Discussionsupporting

confidence: 79%

Direct recognition of LPS by human but not murine CD8⁺ T cells via TLR4 complex

Komai-Koma¹,

Gilchrist²,

Xu³

2009

Eur J Immunol

View full text Add to dashboard Cite

LPS comprises a major PAMP and is a key target of the immune system during bacterial infection. While LPS can be recognised by innate immune cells via the TLR4 complex, it is unknown whether T lymphocytes, especially CD8 1 T cells are also capable of doing so. We report here that naïve human CD8 1 T cells, after activation by TCR stimulation, express surface TLR4 and CD14. These activated CD8 1 T cells can then secrete high concentrations of IFN-c, granzyme and perforin in response to LPS. These effects can be specifically inhibited using siRNA for TLR4. Furthermore, LPS can synergise with IL-12 to polarise the CD8 1 T cells into cytotoxic T-cell 1 (Tc1) that produce IFN-c but not IL-4, with or without TCR activation. Moreover, CD8 1 CD45RO 1 memory T cells constitutively expressed TLR4 and markedly enhanced IFN-c production when stimulated with LPS. In contrast, activated murine CD8 1 T cells lack TLR4 and CD14 expression and fail to respond to LPS for proliferation and cytokine production. Thus, human but not murine CD8 1 T cells are able to directly recognise bacterial LPS via LPS receptor complex and TLR4 provides a novel signal for the activation of effector and memory human CD8 1 T cells.Key words: CD14 . CD8 1 T cells . Tc1 . LPS . TLR Supporting Information available online IntroductionLPS is an abundant glycolipid in the outer-membrane of Gramnegative bacteria [1][2][3]. It consists of hydrophobic lipid A, the o-polysaccharide chain and a core oligosaccharide [3][4][5]. LPS is perhaps the most well-studied microbial molecule due to its powerful immune activating properties, extremely stable nature and wide distribution in the environment [1][2][3]. It is the key molecule responsible for the bacteria-triggered inflammatory response resulting in organ failure and death [1][2][3]. LPS is also closely associated with pathogenesis of many inflammatory diseases [1][2][3][4]. Despite this, the proinflammatory effects of LPS when harnessed may be beneficial; its powerful effect on both innate and adaptive immunity may provide a new generation of immune adjuvants for vaccine development against infection and cancer [2-4]. Therefore, a clearer understanding of how host recognises LPS is fundamentally important.TLR are a group of evolutionarily developed pathogen-pattern recognition receptors that are widely distributed on immune cells [3,5]. At least ten members of the TLR family in humans have been identified. These recognise different microbial products from bacteria, virus, fungi and parasites [2][3][4]. Host cells recognise LPS via a receptor complex consisting of TLR4, CD14 and MD2 in which LPS only signals through TLR4 and triggers cellular activation and expression of inflammatory genes [2][3][4]. Since TLR was originally identified in Drosophila, which lacks an adaptive immune system, the initial belief was that recognition of pathogen products was a characteristic of innate cells bearing 1564TLR [5,6]. However, the role of T cells bearing TLR in pathogen recognition is less well understood.Growing evide...

show abstract

Section: Discussionsupporting

confidence: 79%

Direct recognition of LPS by human but not murine CD8⁺ T cells via TLR4 complex

Komai-Koma¹,

Gilchrist²,

Xu³

2009

Eur J Immunol

View full text Add to dashboard Cite

show abstract

“…In the present study, the periarterial lymphatic sheath of the spleen of the LPS group showed aggregation and thinning in shape, with a decrease in the quantity of lymphocytes. The histological changes of spleen demonstrate that the number of T lymphocytes in the inner periarterial lymphatic sheath decreases markedly after LPS injection, which is consistent with the results of previous studies (Groeneveld et al, 1985;Castro et al). The reduction of intrasplenic T cells may be due to the increase of apoptosis which was related to LPS-activated B cells.…”

Section: Discussioncontrasting

confidence: 68%

“…However, Castro and his colleagues have reported that administration of LPS to spleen activated all B cells and most T cells (CD4 and CD8 T cells), and increased the expression of the activation marker CD69. Massive T cells apoptosis was seen following LPS exposure in the spleen (Castro et al, 1998). In the present study, the periarterial lymphatic sheath of the spleen of the LPS group showed aggregation and thinning in shape, with a decrease in the quantity of lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

Distribution and Expression of Visfatin-Positive Cells in the Spleen of Lipopolysaccharide-Stimulated Piglets

et al. 2014

View full text Add to dashboard Cite

SUMMARY:The histological changes in the spleen and the immunohistochemical expression of visfatin in lipopolysaccharidestimulated piglets are reported to examine the relation between visfatin and inflammation. The results are as follows: (1) After LPS treated, the spleen displayed thicker capsules and trabecula, the thinner periarterial lymphatic sheath, and the more expandable splenic sinusoid, with an increase in the number of splenic nodules, lymphocytes, ellipsoids of the marginal zone, red blood cells and macrophagocytes. (2) Visfatinpositive cells were mainly distributed in the red pulp of the spleen, with less in splenic nodules and periarterial lymphatic sheath. In the LPStreated group, the signal intensity and quantity of the visfatin-positive cells were significantly higher in the red pulp and the ellipsoids of the spleen (P<0.01), whereas lower in the periarterial lymphatic sheath. These results indicate that LPS stimulation induces inflammation, causing the histological changes of the piglet spleen and activating humoral immune response. Moreover, variation of visfatin in the spleen suggests that lymphocytes and macrophages are the potent source of visfatin which participates in the humoral immune response in the inflammation.

show abstract

“…Recently, Salmonella spp. were shown to trigger apoptosis of monocyte-macrophages and apoptosis or anergy in T cells, whereas PMN spontaneous apoptosis can be delayed by interaction with the bacteria [219][220][221][222]. Modulation of this mechanism in the cells encountered in the various tissues of the RES may provide an excellent strategy to evade the immune system.…”

Section: Extraintestinal Infection : Interaction With the Reticulo-enmentioning

confidence: 99%

Host adapted serotypes of Salmonella enterica

et al. 2000

View full text Add to dashboard Cite

Salmonella constitutes a genus of zoonotic bacteria of worldwide economic and health importance. The current view of salmonella taxonomy assigns the members of this genus to two species: S. enterica and S. bongori. S. enterica itself is divided into six subspecies, enterica, salamae, arizonae, diarizonae, indica, and houtenae, also known as subspecies I, II, IIIa, IIIb, IV, and VI, respectively [1]. Members of Salmonella enterica subspecies enterica are mainly associated with warm-blooded vertebrates and are usually transmitted by ingestion of food or water contaminated by infected faeces. The pathogenicity of most of the distinct serotypes remains undefined, and even within the most common serotypes, many questions remain to be answered regarding the interactions between the organism and the infected host.Salmonellosis manifests itself in three major forms: enteritis, septicaemia, and abortion, each of which may be present singly or in combination, depending on both the serotype and the host involved. Although currently over 2300 serovars of Salmonella are recognized, only about 50 serotypes are isolated in any significant numbers as human or animal pathogens [2, 3] and they all belong to subspecies enterica. Of these, most cause acute gastroenteritis characterized by a short incubation period and a severe systemic disease in man or animals, characterized by septicaemia, fever and/or abortion, and such serotypes are often associated with one or few host species [4–6].It is the intention of this review to present a summary of current knowledge of these host-adapted serotypes of S. enterica. The taxonomic relationships between the serotypes will be discussed together with a comparison of the pathology and pathogenesis of the disease that they cause in their natural host(s). Since much of our knowledge on salmonellosis is based on the results of work on Typhimurium, this serotype will often be used as the baseline in discussion. It is hoped that an appreciation of the differences that exist in the way these serotypes interact with the host will lead to a greater understanding of the complex host–parasite relationship that characterizes salmonella infections.

show abstract

Administration to mouse of endotoxin from gram-negative bacteria leads to activation and apoptosis of T lymphocytes

Cited by 74 publications

References 36 publications

Direct recognition of LPS by human but not murine CD8⁺ T cells via TLR4 complex

Direct recognition of LPS by human but not murine CD8⁺ T cells via TLR4 complex

Distribution and Expression of Visfatin-Positive Cells in the Spleen of Lipopolysaccharide-Stimulated Piglets

Host adapted serotypes of Salmonella enterica

Contact Info

Product

Resources

About

Administration to mouse of endotoxin from gram-negative bacteria leads to activation and apoptosis of T lymphocytes

Cited by 74 publications

References 36 publications

Direct recognition of LPS by human but not murine CD8+ T cells via TLR4 complex

Direct recognition of LPS by human but not murine CD8+ T cells via TLR4 complex

Distribution and Expression of Visfatin-Positive Cells in the Spleen of Lipopolysaccharide-Stimulated Piglets

Host adapted serotypes of Salmonella enterica

Contact Info

Product

Resources

About

Direct recognition of LPS by human but not murine CD8⁺ T cells via TLR4 complex

Direct recognition of LPS by human but not murine CD8⁺ T cells via TLR4 complex