Lactoferrin Reduces Mycobacterial Trehalose 6,6'-dimycolate Induced M1-type Inflammation and Permits Fluoroquinolone Entry to Granulomas.

Lactoferrin Reduces Mycobacterial Trehalose 6,6'-dimycolate Induced M1-type Inflammation and Permits Fluoroquinolone Entry to Granulomas. Biochem Cell Biol. 2020 May 13;: Authors: Nguyen TKT, Niaz Z, d'Aigle J, Hwang SA, Kruzel ML, Actor JK Abstract Primary Mycobacterium tuberculosis (Mtb) infection results in the formation of a densely packed granulomatous response that essentially limits entry and efficacy of immune effector cells. Furthermore, the physical nature of the granuloma does not readily permit entry of therapeutic agents to sites where organisms reside. The Mtb cell wall mycolic acid, trehalose 6,6'-dimycolate (TDM), is a physiologically-relevant molecule to model macrophage mediated events during establishment of the tuberculosis-induced granuloma pathogenesis. No current therapeutic modalities focus to modulate host immune responses to ameliorate tuberculosis disease. Previous studies identified lactoferrin (LF), a natural iron-binding protein proven to modulate inflammation, as able to ameliorate granuloma cohesiveness. Therefore, a series of studies were enabled to further examine the effect of recombinant human LF (rHLF) on histological progression of the TDM-induced pathology. Treatment with rHLF demonstrated significant reduction in size and number of inflammatory foci following TDM injection, with reduced pulmonary pro-inflammatory cytokines TNF-α and IL-1β. LF allowed greater penetration of fluoroquinolone the...
Source: Biochemistry and Cell Biology - Category: Biochemistry Authors: Tags: Biochem Cell Biol Source Type: research