# Interleukins in community-acquired pneumonia: from biomarkers to precision medicine

## TL;DR

This paper reviews interleukins in pneumonia, exploring their role in inflammation and potential for precision medicine.

## Contribution

The paper proposes a shift to immunological endotyping and AI models for precision CAP management.

## Key findings

- Interleukins like IL-2, IL-6, and IL-10 play key roles in CAP inflammation.
- Combining cytokines with organ dysfunction markers improves treatment decisions.
- Multi-omics and AI could enable precision medicine for pneumonia.

## Abstract

Community-acquired pneumonia (CAP) is still a leading cause of death due to infection globally, yet precise severity assessment remains a significant clinical problem. More than any other group of cytokines, interleukins are central to the regulation of inflammation and shed light on this intricate pathology. In the present review we summarize the biological and clinical characteristics of some of the principal interleukins (ILs) in CAP, classified primarily according to their physiological activity as pro-inflammatory (IL-2, IL-6, IL-8 and IL-12), anti-inflammatory (IL-7, IL-10 and IL-37), dual-action (IL-4 and IL-17), and emerging factors (IL-3, IL-27 and IL-33). Additionally, recent multimodal approaches are discussed such as combining cytokines with organ dysfunction parameters (MR-proADM) or revealing host-response patterns to inform antibiotic and corticosteroid management. We propose that the field needs to transition to immunological endotyping, multi-omics (integrating genetics and lung microbiome), and artificial intelligence (AI) models based on dynamic patient data to achieve precision medicine in CAP management.