Endogenous gamma interferon-independent host resistance against Listeria monocytogenes infection in CD4+ T cell- and asialo GM1+ cell-depleted mice

Nakane, Akio; Numata, Atsushi; Chen, Y.; Minagawa, Tomonori

doi:10.1128/iai.59.10.3439-3445.1991

Cited by 40 publications

(28 citation statements)

References 18 publications

(22 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…IFN-Q production ceased just before mice died. IFN-Q is reportedly produced mainly by natural killer (NK) cells early in L. monocytogenes infection [11,35,36]. We con¢rmed that endogenous IFN-Q production induced by lethal L. monocytogenes infection in C57BL/6 mice was abolished when the mice were pretreated with anti-asialo GM1 antibody or anti-NK1.1 mAb (data not shown), presuming that NK cells might be dysfunctional or might be depleted before death from listeriosis.…”

Section: Discussionmentioning

confidence: 90%

Endogenous cytokines during a lethal infection with Listeria monocytogenes in mice

Nakane¹

1999

FEMS Microbiology Letters

Self Cite

View full text Add to dashboard Cite

It has been demonstrated that endogenous cytokines including Q interferon (IFN-Q), tumour necrosis factor-K (TNF-K), and interleukin-6 (IL-6) play protective roles but that IL-4 and IL-10 play detrimental roles in nonlethal Listeria monocytogenes infection in mice. In this paper, we studied the roles of endogenous cytokines in a lethal infection with L. monocytogenes in mice. TNF-K and IL-6 titres in the bloodstreams, spleens and livers paralleled bacterial numbers in the organs, and both these cytokines and the bacterial numbers peaked just before the mice died. The high titres of TNF-K notably detected in the circulation in lethal infection were different from those in nonlethal infection. The maximum production of IFN-Q was observed before the peaks of TNF-K and IL-6, and IFN-Q almost disappeared from the bloodstreams and organs just before the mice died. No notable difference of IFN-Q titres between lethal infection and nonlethal infection in the specimens obtained from mice was observed. IL-10 was also detected in the bloodstreams earlier than the peaks of TNF-K and IL-6 during lethal infection, while IL-4 was never detected in the sera. The administration of monoclonal antibodies (mAbs) against TNF-K, IFN-Q, IL-6, IL-4 or IL-10 failed to rescue mice from lethal L. monocytogenes infection, whereas anti-TNF-K mAb and anti-IFN-Q mAb prevented mice from lethality by high-dose endotoxin shock. These results suggest that lethality in L. monocytogenes infection might not be determined solely by these cytokines. z

show abstract

Section: Discussionmentioning

confidence: 90%

Endogenous cytokines during a lethal infection with Listeria monocytogenes in mice

Nakane¹

1999

FEMS Microbiology Letters

Self Cite

View full text Add to dashboard Cite

show abstract

“…In a sublethal infection with L. monocytogenes, conversion from the sublethal infection to the lethal infection was not observed in CD8 + cell-depleted mice, although antilisterial resistance was markedly suppressed in these animals [21,28,29]. Alternatively, depletion of CD4 + cells showed little effect on antilisterial resistance [21,28,29]. Furthermore, studies using severe combined immunodeficiency mutant mice showed that host resistance to L. monocytogenes infection could be expressed in the presence of endogenous cytokines such as TNF and IFN-y [30,31].…”

Section: Anti-tcrmentioning

confidence: 99%

A monoclonal antibody against T-cell receptor αβ induces endogenous cytokines and prevents mice from a lethal infection with Listeria monocytogenes

Nakane¹

1995

FEMS Immunology and Medical Microbiology

Self Cite

View full text Add to dashboard Cite

In vivo induction of cytokines by a monoclonal antibody (mAb) against T-cell receptor (TCR) cyp and the protective effect induced by the mAb on a lethal infection with Listeria monocytogenes were studied. Injection of anti-TCR (YP mAb induced rapid production of endogenous tumour necrosis factor in the spleens, and gamma interferon and interleukin-6 in the bloodstreams and spleens of mice. Administration of anti-CD4 mAb, anti-CD8 mAb, or anti-Thyl.2 mAb resulted in suppression of anti-TCR cr/3 mAb-induced endogenous cytokine production. Mice were protected against lethal L. monocytogenes infection when treated with anti-TCR cwp mAb. The protective effect was not demonstrated in CD4 + cellor CD8 + cell-depleted mice. These results suggest that anti-TCR ap mAb shows a protective effect on a lethal infection with L. monocytogenes in mice and that the mAb-induced endogenous cytokines might be involved in the effect of anti-TCR rub mAb. factor (TNF), gamma interferon (IFN-71, interleukin-1 (IL-l), IL-6, and colony-stimulating factors has been reported for L. monocytogenes-infected mice [3-71. Studies including in vivo administration of monoclonal antibodies (mAbs) against cytokines and gene knockout technology demonstrated that TNF and IFN-y are crucial in antilisterial resistance [8-141. We previously reported that an anti-CD3 mAb protected mice against a lethal infection with L. monocytogenes through induction of endogenous 092%8244/95/$09.50 0 1995 Federation of European Microbiological Societies. All rights reserved SSDI 0928-8244(95)00040-2

show abstract

“…Evaluation of in vivo cell depletion has been shown previously (Nakane and Minagawa, 1984;Nakane et al, 1991;Hiromatsu et al, 1992).…”

Section: In Vivo Depletion Of Cd3 + Cells Cd4 + Cells Cd8 + Cells mentioning

confidence: 99%

“…helping immune reaction, cytotoxicity to infected cells, and secretion of cytokines (Ertl et al, 1989;Lindsley et al, 1991;Nakane et al, 1991). CD4 ÷ T lymphocytes secrete cytokines (Nakane et al, 1991) and show helper activities (Ertl et al, 1989). CD8 ÷ lymphocytes act as cytotoxic T lymphocytes (CTL) and destroy virus-infected cells (Lindsley et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

“…In our observation on Theiler's virus GD VII strain, endogenous interferon gamma (IFN-y) was produced in the brains and spinal cords of the infected mice (Kohanawa et al, 1993). IFN-T which is secreted by natural killer (NK) cells and T lymphocytes (Klavinskis et al, 1989;Taylor et al, 1989;Nakane et al, 1991) is an important cytokine in viral infections (Klavinskis et al, 1989;Leist et al, 1989;Smith et al, 1991;Lucin et al, 1992). In lymphocytic choriomeningitis virus infection, CD8 + lymphocytes and CD4 + lymphocytes which are protective against this virus produce endogenous IFN-y (Gessner et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Theiler's virus is eliminated by a gamma-interferon-independent mechanism in the brain

Kohanawa¹,

Nakane²,

Asano³

et al. 1994

Journal of Neuroimmunology

Self Cite

View full text Add to dashboard Cite

The intravenous infection of Theiler's virus GD VII strain causes acute encephalomyelitis in infected mice. To determine the cellular mechanism of resistance and interferon (IFN)-gamma-producing cell populations, mononuclear cells isolated from tissues of the brain were analyzed by the flow cytometry method. Antibodies specific for CD3, CD4, CD8, T cell receptor (TCR)-alpha beta, and Asialo GM1 were used to deplete the corresponding cell populations in Theiler's virus-infected mice. CD4+ lymphocytes and CD8+ lymphocytes infiltrated in the brains of infected mice from 5 days postinfection (p.i.). The number of CD3+/TCR-gamma delta+ lymphocytes increased in the brains on Day 6 p.i. The elimination of CD3+ lymphocytes or CD4+ lymphocytes augmented viral replication and suppressed the production of IFN-gamma. The suppression of IFN-gamma production by anti-CD3 monoclonal antibody (mAb) persisted, although the suppression by anti-CD4 mAb was observed only on Day 6 p.i. The depletion of CD8+ lymphocytes as well as TCR-alpha beta+ lymphocytes also augmented the viral replication; however, it did not alter the production of IFN-gamma. Anti-Asialo GM1 antibody had no effect on viral replication and IFN-gamma production. These results indicate that T lymphocytes are important for eliminating Theiler's virus from the brain, CD3+/CD4+/CD8- lymphocytes and CD3+/TCR alpha beta-/CD4-/CD8- lymphocytes would produce IFN-gamma in brain. However, from the result on the experiment of the depletion of TCR-alpha beta+ lymphocytes, the defence mechanisms by T lymphocytes against Theiler's virus would be independent of endogenous IFN-gamma production.

show abstract

Endogenous gamma interferon-independent host resistance against Listeria monocytogenes infection in CD4+ T cell- and asialo GM1+ cell-depleted mice

Cited by 40 publications

References 18 publications

Endogenous cytokines during a lethal infection with Listeria monocytogenes in mice

Endogenous cytokines during a lethal infection with Listeria monocytogenes in mice

A monoclonal antibody against T-cell receptor αβ induces endogenous cytokines and prevents mice from a lethal infection with Listeria monocytogenes

Theiler's virus is eliminated by a gamma-interferon-independent mechanism in the brain

Contact Info

Product

Resources

About