PMID- 34245822
OWN - NLM
STAT- MEDLINE
DCOM- 20210818
LR  - 20210818
IS  - 1096-1208 (Electronic)
IS  - 0882-4010 (Linking)
VI  - 158
DP  - 2021 Sep
TI  - Role of resuscitation promoting factors in reactivation of latent tuberculosis 
      during high glucose conditions employing human granuloma in vitro model.
PG  - 105068
LID - S0882-4010(21)00340-5 [pii]
LID - 10.1016/j.micpath.2021.105068 [doi]
AB  - BACKGROUND: Diabetes aggravates the risk of tuberculosis (TB) through impairment 
      of immunity which may lead to the activation of latent tuberculosis (LTBI). LTBI 
      serves as a homeostatic state where host does not develop any symptoms of the 
      disease as host immune system assist in the containment of infection leading to 
      granuloma formation. However, the compromised immunity imbalances this 
      equilibrium which further leads to reactivation of LTBI. The aim of this study 
      was to assess if hyperglycemia like conditions contribute towards activation of 
      latent tuberculosis. MATERIAL/METHODS: In vitro granuloma model was developed 
      using peripheral blood monocytic cells (PBMCs) under normal and high glucose 
      conditions and the characteristics of dormancy i.e. tolerance towards rifampicin, 
      loss of acid fastness were monitored. Further, activation was assessed by 
      expression analysis of various resuscitation promoting factors rpfA-E. RESULTS: 
      Granuloma formation was not observed in the presence of high glucose. The gene 
      expression of hspX was downregulated whereas the expression of rpfA-E genes was 
      upregulated under high glucose conditions after 48 h of glucose treatment. The 
      expression of rpfD gene remained upregulated till 72 h of glucose treatment. 
      CONCLUSION: High glucose concentrations impede the granuloma formation and may 
      lead to activation of latent tubercle bacilli through resuscitation promoting 
      factors. Thus, rpfs represent an important targets for new interventions that can 
      abate the burden from co-pathogenesis of tuberculosis and diabetes.
CI  - Copyright (c) 2021. Published by Elsevier Ltd.
FAU - Verma, Arpana
AU  - Verma A
AD  - Department of Biochemistry, Postgraduate Institute of Medical Education and 
      Research, Chandigarh, India. Electronic address: arpana.verma88@gmail.com.
FAU - Radotra, Bishan D
AU  - Radotra BD
AD  - Department of Histopathology, Postgraduate Institute of Medical Education and 
      Research, Chandigarh, India. Electronic address: bishanradotra@gmail.com.
FAU - Sharma, Sadhna
AU  - Sharma S
AD  - Department of Biochemistry, Postgraduate Institute of Medical Education and 
      Research, Chandigarh, India. Electronic address: sadhnabiochem@gmail.com.
LA  - eng
PT  - Journal Article
DEP - 20210707
PL  - England
TA  - Microb Pathog
JT  - Microbial pathogenesis
JID - 8606191
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Glucose
MH  - Granuloma
MH  - Humans
MH  - *Latent Tuberculosis
MH  - *Mycobacterium tuberculosis
MH  - *Tuberculosis
OTO - NOTNLM
OT  - Diabetes
OT  - Granuloma
OT  - Hyperglycemic conditions
OT  - LTBI
OT  - Resuscitation
OT  - Tuberculosis
EDAT- 2021/07/11 06:00
MHDA- 2021/08/19 06:00
CRDT- 2021/07/10 20:09
PHST- 2020/10/15 00:00 [received]
PHST- 2021/05/01 00:00 [revised]
PHST- 2021/06/21 00:00 [accepted]
PHST- 2021/07/11 06:00 [pubmed]
PHST- 2021/08/19 06:00 [medline]
PHST- 2021/07/10 20:09 [entrez]
AID - S0882-4010(21)00340-5 [pii]
AID - 10.1016/j.micpath.2021.105068 [doi]
PST - ppublish
SO  - Microb Pathog. 2021 Sep;158:105068. doi: 10.1016/j.micpath.2021.105068. Epub 2021 
      Jul 7.