The propolis produced by bees are used in alternative medicine for treating inflammation, and infections, presumably due to its antioxidant properties. In this context, five propolis from México were investigated to determine their inhibitory lipid peroxidation properties. The ethyl acetate extract from a red propolis from Chiapas State (4-EAEP) was the most potent (IC₅₀ = 1.42 ± 0.07 μg/mL) in the TBARS assay, and selected for further studies. This extract afforded two new compounds, epoxypinocembrin chalcone (6), and an ε-caprolactone derivative (10), as well as pinostrobin (1), izalpinin (2), cinnamic acid (3), pinocembrin (4), kaempherol (5), 3,3-dimethylallyl caffeate in mixture with isopent-3-enyl caffeate (7a + 7b), 3,4-dimethoxycinnamic acid (8), rhamnetin (9) and caffeic acid (11). The HPLC profile, anti-mycobacterial, and antioxidant properties of this extract was also determined. Most of the isolated compounds were also tested by inhibition of reactive oxygen species (ROS) in challenged mouse bone marrow-derived mast cells (BMMCs), and DPPH. Their anti-inflammatory activity was evaluated by TPA, and MPO (myeloperoxidase) activity by ear edema test in mice. The most potent compounds were 7a + 7b in the TBARS assay (IC₅₀ = 0.49 ± 0.06 μM), and 2 which restored the ROS baseline (3.5 μM). Our results indicate that 4-EAEP has anti-oxidant, and anti-inflammatory properties due to its active compounds, suggesting it has anti-allergy and anti-asthma potential.

Tuberculosis (TB), caused primarily by Mycobacterium tuberculosis (Mtb), remains a major global health challenge and the leading cause of death worldwide from a single infectious agent. In developed countries, TB is a prototypical re-emerging infectious disease, while in developing nations, it is a devastating health issue. In humans and mice, cell-mediated immunity, driven by T lymphocytes, plays a crucial role in coordinating and regulating the immune response to eliminate Mtb. Significant evidence indicates that CD4+ T helper lymphocytes (Th-1 cells) and Th-17 cells are vital to the protective immune response against Mtb. CD4+ Th-1 cells activate macrophages, enhancing their ability to eliminate mycobacteria. They also recruit additional immune cells to infection and inflammation sites and promote the cytotoxicity of CD8+ T lymphocytes, which are essential for killing infected cells through apoptosis. Indeed, the immune response to Mtb involves a carefully balanced interaction between protective inflammation and tissue-damaging pathology. Therefore, the involvement of anti-inflammatory cells, such as Th-2 lymphocytes and T regulatory cells, is also critical in modulating and controlling inflammation that can cause tissue damage. In this chapter, the roles of various T-lymphocyte subtypes in the immune response to Mtb are discussed, along with the different T-cell immune evasion strategies Mtb employs to prevent clearance. Additionally, novel immunotherapeutic approaches aimed at enhancing protective T-cell activity or suppressing harmful T-cell effects are explored, providing potential methods to facilitate pathogen eradication and reduce the lengthy chemotherapy required for this significant infectious disease.