This 2023 human cell study investigated sulforaphane’s effects on tuberculosis infections:
“Basic research efforts on tuberculosis (TB) immunotherapy are currently only the tip of the iceberg. This study highlights the association between autophagy-related genes and immune infiltration in TB, an infectious pathogen that has been around for tens of thousands of years.
Sulforaphane (SFN) is readily absorbed into the bloodstream by the intestine due to its lipophilic nature. Experiments in this study TB patient cells showed that SFN could promote autophagy in macrophages infected with Mycobacterium abscessus (Mab). Intracellular bacterial load of macrophages was associated with SFN-enhanced cellular autophagic processes.
The relationship between autophagy and immune cells is complex, and recurrence of tuberculosis is significantly influenced by intracellular mycobacteria of macrophages. Macrophages have longer lifespans than neutrophils, and provide shelter for mycobacteria as they are better suited than neutrophils to establish strategies for targeting autophagy.
This is one of the reasons why autophagy in macrophages was the focus of this study. Appropriate autophagy is beneficial for the body and controls Mtb replication, but autophagic programmed cell death can activate tissues to produce an excessive inflammatory response, resulting in severe damage to lung tissues.
Autophagy-related genes regulated by SFN have good diagnostic potential, with FOXO1 potentially serving as a target for TB immunotherapy. Downstream targets of FOXO1 include important pro-inflammatory signaling molecules such as IL-1β and TNF-α, which are important for control of mycobacterium.”
https://www.sciencedirect.com/science/article/pii/S156757692300276X “Identifying autophagy-related genes as potential targets for immunotherapy in tuberculosis”
Take yeast cell wall β-glucan, too, and train your immune system.