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Neurokinin 1 receptor signaling affects the local innate immune defense against genital herpes virus infection.

Artikel i vetenskaplig tidskrift
Författare Alexandra Svensson
Joanna Kaim
Carina Mallard
Annika Olsson
Ernst Brodin
Tomas Hökfelt
Kristina Eriksson
Publicerad i Journal of immunology (Baltimore, Md. : 1950)
Volym 175
Nummer/häfte 10
Sidor 6802-11
ISSN 0022-1767
Publiceringsår 2005
Publicerad vid Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning
Institutionen för medicinsk mikrobiologi och immunologi
Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi
Sidor 6802-11
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Central Nervous System, pathology, virology, Female, Herpes Genitalis, immunology, metabolism, prevention & control, virology, Herpes Simplex Virus Vaccines, pharmacology, Herpesvirus 2, Human, drug effects, immunology, physiology, Immunity, Natural, Killer Cells, Natural, immunology, Mice, Mice, Inbred C57BL, Mice, Knockout, Receptors, Neurokinin-1, deficiency, genetics, immunology, Signal Transduction, Substance P, metabolism, pharmacology, Vaccines, Attenuated, pharmacology, Vagina, immunology, metabolism, virology, Virus Replication, drug effects
Ämneskategorier Mikrobiologi inom det medicinska området

Sammanfattning

We show that genital infection with neurotropic HSV type 2 (HSV-2) induced a significant increase of the neuropeptide substance P (SP) within the genital tract of mice. SP was shown to weakly interfere with the HSV-2 replication. Furthermore, lack of SP signaling through the use of mice deficient in the SP receptor, neurokinin 1 receptor (NK1R), revealed an important role for SP in the innate defense against HSV-2. NK1R-deficient mice had significantly enhanced levels of HSV-2 in the genital tract and in the CNS following infection and a significantly accelerated disease progression, which was associated with an impaired NK cell activity locally in the vagina. Lack of NK1R signaling did, however, not impair the animals' ability to mount a protective immune response to HSV-2 following vaccination with an attenuated virus. Both NK1R+/+ and NK1R-/- mice developed strong HSV-2-specific Th1 T cell responses following vaccination. No genital viral replication was observed in either vaccinated NK1R-deficient or NK1R+/+ control animals following a genital HSV-2 challenge, and all of these animals survived without any symptoms of disease. In conclusion, the present results indicate that SP and NK1R signaling contributes to the innate resistance against HSV-2 infection in mice.

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