Contribution of Interleukin-6 (IL-6) to Body Defense and Healing in Pulmonary Tuberculosis

To examine the contribution of IL-6 to host defense and healing in pulmonary tuberculosis (TB). Pulmonary tuberculosis continues to pose a significant global health challenge, with disease outcomes determined by complex host-pathogen interactions. Interleukin-6 (IL-6), a multifunctional cytokine, has been implicated in immune regulation and tissue recovery during TB, but its specific role is not fully established. This review aimed to examine the contribution of IL-6 to host defense and healing in pulmonary TB.

A comprehensive literature search was performed across PubMed, Scopus, Web of Science, ScienceDirect, and Medline following PRISMA guidelines, covering publications from 2015 to 2025. Search terms included "pulmonary tuberculosis," "IL-6," "Immune response," and "Healing." Eligible studies were human-based, published in English, and provided full-text access. Data extraction focused on study design, population, IL-6 sample type, and findings related to immune response and healing.

Evidence consistently demonstrated IL-6 as a key modulator of TB immunity. IL-6 supports macrophage activation, T-cell differentiation, and granuloma formation, enhancing host defense against Mycobacterium tuberculosis. Additionally, IL-6 regulates inflammation and promotes tissue repair, contributing to recovery. However, dysregulated or excessive IL-6 activity was linked to heightened inflammation and lung pathology, indicating a dual role in both protection and potential tissue damage.

Interleukin-6 is central to immune defense and healing in pulmonary TB, exerting protective effects while requiring precise regulation to prevent pathological outcomes. Future research should clarify underlying mechanisms and explore IL-6-targeted strategies for improved TB treatment.