Iba1-expressing microglia respond to herpes simplex virus infection in the mouse trigeminal ganglion
Isamu Mori1, Fumi Goshima, Tetsuo Koshizuka
1Department of Microbiology and Immunology, Research Center for Infectious Disease, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan.
Abstract:
Microglial response in the trigeminal ganglion of mice corneally inoculated with herpes simplex virus (HSV) was investigated. Virus-infected neurons of the trigeminal ganglion did not exhibit apoptotic signal, while those of the trigeminal sensory brainstem nucleus did. Cells expressing ionized calcium binding adapter molecule 1 (Iba1), a specific marker of microglia/macrophages, increased in number in the virally infected region of the trigeminal ganglion, with morphological transformation to an activated phenotype, frequently detected as perineural satellites. Further microglial transformation to macropahges was not evident. Iba1-immunopositive perineural satellites also appeared in the vicinity of virally infected region. Such activated microglia expressed basic fibroblast growth factor (bFGF) molecules. The reverse transcription-polymerase chain reaction (RT-PCR) detected upregulated synthesis of mRNA for bFGF in the trigeminal ganglion. In contrast, in the trigeminal sensory brainstem nucleus, a small number of bFGF-producing cells appeared only in the vicinity of virally infected area. Collectively, Iba1-bearing microglia exist in the mouse trigeminal ganglion and respond to herpes simplex virus infection, most likely conferring neuroprotective functions upon the trigeminal ganglion.
Insights
Microglia in the mouse trigeminal ganglion activate during herpes simplex virus (HSV) infection, expressing basic fibroblast growth factor (bFGF) and potentially offering neuroprotection.
Area of Science:
- Neuroscience
- Immunology
- Virology
Background:
- Herpes simplex virus (HSV) can infect the trigeminal ganglion, a key site for viral latency.
- Understanding the host immune response within the trigeminal ganglion is crucial for managing HSV infections.
Purpose of the Study:
- To investigate the microglial response within the trigeminal ganglion following corneal HSV inoculation in mice.
- To characterize the activation state and molecular expression of microglia in response to viral infection.
Main Methods:
- Corneal inoculation of mice with HSV.
- Immunohistochemistry to detect ionized calcium binding adapter molecule 1 (Iba1)-positive cells and basic fibroblast growth factor (bFGF).
- Reverse transcription-polymerase chain reaction (RT-PCR) to assess mRNA expression of bFGF.
Main Results:
- Increased numbers of activated microglia (Iba1-positive) were observed in the HSV-infected trigeminal ganglion, often appearing as perineural satellites.
- Activated microglia expressed bFGF, and trigeminal ganglion tissue showed upregulated bFGF mRNA synthesis.
- Unlike the trigeminal ganglion, apoptotic signals were observed in the trigeminal sensory brainstem nucleus, and bFGF expression was limited.
Conclusions:
- Microglia in the trigeminal ganglion mount a distinct response to HSV infection, characterized by activation and bFGF expression.
- The observed microglial activation and bFGF production suggest a potential neuroprotective role in the trigeminal ganglion during HSV infection.
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