Toxoplasma gondii Infection Promotes Neuroinflammation Through Cytokine Networks and Induced Hyperalgesia in BALB/c Mice.
We hypothesized that in Toxoplasma gondii infection, communication among immune cells promotes neuroinflammation through cytokine networks and induces pain sensitivity under conditions of neuropathic pain. The animal model of Toxoplasma infection was established by the intraperitoneal inoculation of 20-25 tissue cysts from Tehran strain of T. gondii to BALB/c mice. Amitriptyline (20 mg/kg, i.p., 1/day) administrated to animals for 7 days before behavioral tests. Pain behavioral tests including tail flick, hot plate, and formalin test were evaluated in all the groups. The mRNA levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 were examined by real-time PCR. Results revealed that T. gondii induce hyperalgesia in the infected mice, whereas amitriptyline showed a promising effect against the hyperalgesia induced by Toxoplasma infection. The mRNA levels of the aforementioned cytokines significantly (P < 0.05) increased in the infected mice compared to the uninfected ones. Obtained findings suggested that T. gondii infection could promote neuroinflammation through cytokine networks and induced hyperalgesia in BALB/c mice, whereas amitriptyline as an analgesic drug reverses them.
Research Center for Tropical and Infectious Diseases, Kerman University of Medical Sciences, Kerman, Iran.
Hossein
H
Mahmoudvand
Research Center for Tropical and Infectious Diseases, Kerman University of Medical Sciences, Kerman, Iran.
Naser
N
Ziaali
Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran.
Hamed
H
Ghazvini
Department of Medical Parasitology & Mycology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Saeideh
S
Shojaee
Department of Medical Parasitology & Mycology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Hossein
H
Keshavarz
Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran.
Khadijeh
K
Esmaeilpour
Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran. vsheibani2@yahoo.com.
Vahid
V
Sheibani
D000639:Amitriptyline / Q000627:therapeutic use*; D018712:Analgesics, Non-Narcotic / Q000627:therapeutic use*; D000818:Animals; D016207:Cytokines / Q000276:immunology; D004195:Disease Models, Animal; D006930:Hyperalgesia / Q000188:drug therapy* / Q000469:parasitology*; D007249:Inflammation / Q000276:immunology; D053583:Interleukin-1beta / Q000235:genetics; D015850:Interleukin-6 / Q000235:genetics; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009437:Neuralgia / Q000188:drug therapy* / Q000469:parasitology*; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D014122:Toxoplasma / Q000276:immunology; D014123:Toxoplasmosis / Q000469:parasitology / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
D018712:Analgesics, Non-Narcotic; D016207:Cytokines; C000594089:IL1B protein, rat; D053583:Interleukin-1beta; D015850:Interleukin-6; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D000639:Amitriptyline
Toxoplasma gondii; amitriptyline; cytokine; neuroinflammation; pain