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Microbiology: Current Research 2017 | Volume 1, Issue 2

Joint Conference

GLOBAL APPLIED MICROBIOLOGY CONFERENCE

MICROBIAL & BIOCHEMICAL RESEARCH AND TECHNOLOGIES

October 18-19, 2017

Toronto, Canada

International Congress on

&

Detection of ER stress after infection of human macrophages by

Mycobacterium tuberculosis

Samuel Eguasi Inkabi

Linköping University, Sweden

P

ost infection, macrophages, the first cells in the lungs that

propel defense against pathogen invasion and play crucial

activity in the onset and maintenance of immune responses

against Mtb. The macrophages play this crucial defense role

by phagocytosis, which have the macrophages ‘‘eat’’ up the

Mtb

bacilli

. Macrophages therefore become infected with

mycobacteria and may undergo apoptosis (programmed cell

death) to destroy pathogens and prevent further spreading.

Apoptosis, which results in the elimination of Mtb can be

triggered by endoplasmic reticulum (ER) stress which is

the physiological or pathological processes that disturb

protein folding in the endoplasmic reticulum caused by

the phagocytosis of the Mtb

bacilli

by the macrophages.

The dysregulation of ER homeostasis can cause chronic

diseases in humans and it is crucial to study ER stress using

mammalian cells to understand ER-stress related diseases

such as Tuberculosis. Here, we studied the ER stress

induction and the extent of ER stress induction using human

monocytes derived macrophages (hMDMs). We used the

ER stress inducers tunicamycin and thapsigargin, and also

infecting the macrophages with different doses of Mtb and

analysing CHOP and ATF6-alpha expression by western blot.

This indicated that both inducers triggered CHOP activation,

that a low dose of Mtb suppressed the expression of these

ER-stress markers in most donors, and that infection with a

higher dose of Mtb stimulated expression of both markers

in 4 out of 6 donors. Alternatively, live microscopy was also

performed on Raw macrophages and 16HBE epithelial cells

after transfection with the ER stress plasmid sensor pEGFP-

XBP1dDBD-STOP-tagRFPt and stimulation with tunicamycin

and purified protein derivative of tuberculin (PPD). We

have here confirmed the detection of ER-stress in human

monocyte derived macrophages using positive inducers,

and shown that low doses of Mtb decreases induction of ER-

stress whereas, high dose of Mtb induces ER- stress

Speaker Biography

Samuel Eguasi Inkabi has completed his MSc in Medical Biology from Linkoping

University, Sweden. He also holds a Bachelor’s in Biochemistry from Kwame Nkrumah

University of Science and Technology, Ghana. His research focuses on infectious

diseases, cancer and avian genetics. He has co-authored a publication and authored

peer review papers in reputed journals.

e:

samin711@student.liu.se