Expression of the α7 nAChR Subunit Duplicate Form (CHRFAM7A) Was Down-Regulated in Patients with Intracranial Infection and Reduced Inflammation in in vitro Model by p38 MAPK

Abstract

<b><i>Objective:</i></b> In this study, we investigated that the effects and possible mechanisms of the α7 nAChR subunit duplicate form (CHRFAM7A) affected inflammation in the model of intracranial infection. <b><i>Methods:</i></b> Mice of the model group were injected (intracranial injection) with <i>Staphylococcus aureus</i>. Mouse microglial BV2 cell was exposed with 200 ng of LPS for 4 h. <b><i>Results:</i></b> CHRFAM7A mRNA expressions were reduced in patients with intracranial infection. CHRFAM7A mRNA and protein expressions were suppressed in mice with intracranial infection in a time-dependent manner. CHRFAM7A reduced inflammation in mice with intracranial infection. The inhibition of CHRFAM7A reduced inflammation in mice with intracranial infection. CHRFAM7A suppressed p38 MAPK in mice with intracranial infection. The inhibition of p38 MAPK shows the effects of CHRFAM7A in intracranial infection. <b><i>Conclusion:</i></b> Our data demonstrate that the expression of the CHRFAM7A was down-regulated in patients with intracranial infection and reduced inflammation in in vitro model by p38 MAPK, which suggests the potential role of CHRFAM7A as a diagnostic biomarker for intracranial infection.