# Role of Myeloid Cell Glucose Transporter 1 in the Host Response During Pneumonia Caused by Streptococcus pneumoniae

## TL;DR

This study explores how glucose transporter 1 (GLUT1) affects immune responses in pneumonia caused by Streptococcus pneumoniae.

## Contribution

The novel contribution is the investigation of GLUT1's role in myeloid cells during pneumonia and the discovery that its absence does not impair host response.

## Key findings

- GLUT1 gene expression is upregulated in monocytes from CAP patients compared to controls.
- Myeloid-specific GLUT1-deficient mice show an unaltered host response during pneumococcal pneumonia.
- GLUT1 mRNA levels are increased in neutrophils from CAP patients, but protein levels remain unchanged.

## Abstract

During infection, myeloid cells are subjected to a fast increase in energy demand. Glucose transporter 1 (GLUT1) is a key mediator of glucose metabolism, especially for glycolysis. The present study aimed to investigate GLUT1 expression in monocytes and neutrophils from patients with community-acquired pneumonia (CAP) and to determine the functional role of GLUT1 in the responsiveness during pneumonia evoked in mice by Streptococcus (S.) pneumoniae, the most common causative pathogen in CAP. GLUT1 expression in monocytes and neutrophils of patients and controls was determined by RNA sequencing and flow cytometry analysis. Myeloid cell-specific GLUT1-deficient mice and controls were intranasally infected with S. pneumoniae, after which bacterial loads, lung pathology, and cytokine levels were analyzed. GLUT1 gene expression was upregulated in monocytes from CAP patients in comparison to matched subjects without infection, and protein expression was increased upon ex vivo activation. In neutrophils, GLUT1 mRNA levels were significantly upregulated in CAP patients, but protein levels were not altered. Surprisingly, myeloid-specific GLUT1-deficient mice displayed an unaltered host response during pneumococcal pneumonia. These data suggest that GLUT1 may contribute to immune responses of myeloid cells during CAP, but that its role may be superseded by other mechanisms during pneumococcal pneumonia.