Opposite effects of M. leprae or M. bovis BCG delipidation on cellular accumulation into mouse pleural cavity. Distinct accomplishment of mycobacterial lipids in vivo

Abstract

Intact M. leprae and its lipids did not incite any cell recruitment. Apolar external cell wall lipids from M. leprae and BCG induce different cellular responses. They seem to have a crucial importance at the first contact of mycobacteria with the host cell, modulating the influx of neutrophils/macrophages in the early (4/24 h) onset of the inflammatory reaction.

A Novel Treatment for Ocular Tumors Using Membrane FasL Vesicles to Activate Innate Immunity and Terminate Immune Privilege

“…This biphasic infiltration was similar to that observed after Mycobacterium bovis BCG (bacillus of Calmette and Guérin) infection, in which the first wave of neutrophils was dependent on activated resident macrophages and the second wave of neutrophils was dependent on activated T cells. [35][36][37] Our previous tumor studies revealed a similar pattern in which tumors cells expressing membrane-only FasL induce an early infiltration of neutrophils, followed later by a more sustained influx of neutrophils that remain present until the tumor is rejected completely. Complete tumor rejection is ultimately dependent on T cells, suggesting T cells may be important in sustaining the influx of neutrophils.…”

Mycobacterium aviumComplex Promotes Recruitment of Monocyte Hosts for HIV-1 and Bacteria

“…as well as differences in receptor use (51), cytokine and chemokine induction may not be comparable (52,53). Previous reports indicate that M. tuberculosis can induce neutrophil, eosinophil, monocyte, and lymphocyte migration (46,48,49,52), as well as chemokine up-regulation in infected monocytes/macrophages (47,49,50). Mycobacterial infections have been shown to activate NF-B via Toll-like receptors, resulting in the enhanced expression of TNF-␣, CCR5, and IL-8 (25, 54 -57).…”

Spotlight on mycobacterial lipid exploitation using nanotechnology for diagnosis, vaccines, and treatments

“… 24 While the mechanisms linked to biological effects of mycobacterial lipids on host cells are poorly understood, growing evidence highlights their importance in pathogenicity (see Box 1 ). For instance, the delipidation of mycobacterial cells has been associated with both immune activation and suppression 25 ; from gene manipulation experiments, we know that the impairment of biosynthetic lipid pathways may lead to a tremendous decline in virulence of mycobacterial strains 26. , 27.…”