Background and Aims::
Pathogenic bacteria and host cells counteract or neutralize
each other's effect in two fundamental ways: Direct invasion and secretion of various substances.
Among these, lipases secreted by pathogenic bacteria and host cell lysozyme are key actors.
Secreted lipases from pathogenic bacterial are suggested as a key player in the pathogen-host
interaction. Among the gut microbial energy sources, glucose and fats have been referred to as
one of the best inducers and substrates for bacterial lipases. Enrichment of bacterial growth
medium with extra glucose or oil has been shown to induce lipase production in pathogenic
bacteria. More recently, research has focused on the role of human gut phage alterations in the
onset of dysbiosis because the bacteria-phage interactions can be dramatically affected by the
nutrient milieu of the gut. However, the reciprocal role of bacterial lipases and phages in this
context has not been well studied and there is no data available about how high glucose
or fat availability might modulate the cellular milieu of the pathogenic bacteria-phageeukaryotic
host cell interface. The purpose of this study was to evaluate the immunologic outcome
of pathogenic bacteria-phage interaction under normal, high glucose, and high butter oil
conditions to understand how nutrient availability affects lipase activity in pathogenic bacteria
and, ultimately, the eukaryotic host cell responses to pathogenic bacteria-phage interaction.
Materials and Methods::
10 groups of co-cultured T84 and HepG2 cells were treated with Pseudomonas
aeruginosa strain PAO1 (P.a PAO1) in the presence and absence of its KPP22 phage
and incubated in three different growth media (DMEM, DMEM + glucose and DMEM + butter
oil). Structural and physiological (barrier function and cell viability), inflammatory (IL-6 and
IL-8), metabolic (glucose and triglycerides), and enzymatic (lipases and lysozyme) parameters
were determined.
Results::
Excess glucose or butter oil enhanced additively extracellular lipase activity of P.a
PAO1. Excess glucose or butter oil treatments also magnified P. a PAO1- induced secretion of
inflammatory signal molecules (IL-1β, IL-6) from co-cultured cells, concomitant with the enhancement
of intracellular triglycerides in co-cultured HepG2 cells, these effects being abolished
by phage KPP22.
Conclusion::
The results of the present study imply that KPP22 phage influences the interplay
between food substances, gut bacterial lipases, and the gut cellular milieu. This can be applied
in two-way interaction: by affecting the microbial uptake of excess free simple sugars and fats
from the gut milieu leading to decreased bacterial lipases and by modulating the immune system
of the intestinal -liver axis cells. Further studies are needed to see if the biological consequences
of these effects also occur in vivo.
result:
Excess glucose or butter oil enhanced additively extracellular lipase activity of P.a PAO1. Excess glucose or butter oil treatments also magnified P. a PAO1- induced secretion of inflammatory signal molecules (IL-1β, IL-6) from co-cultured cells, concomitant with the enhancement of intracellular triglycerides in co-cultured HepG2 cells, these effects being abolished by phage KPP22.
