PMID- 36335442
OWN - NLM
STAT- MEDLINE
DCOM- 20221108
LR  - 20221108
IS  - 1578-1267 (Electronic)
IS  - 0301-0546 (Linking)
VI  - 50
IP  - 6
DP  - 2022
TI  - High throughput virtual screening strategy to develop a potential treatment for 
      bronchial asthma by targeting interleukin 13 cytokine signaling.
PG  - 22-31
LID - 10.15586/aei.v50i6.573 [doi]
AB  - Chronic inflammation in the airway passage leads to the clinical syndrome of 
      pediatric asthma. Allergic reactions caused by bacterial, viral, and fungal 
      infection lead to the immune dis-balance which primes T helper cells (Th2), a 
      specific cluster of differentiation 4 (CD4) T cell differentiation. This favors 
      the Th2-specific response by activating the inter-leukin 4/interleukin 13 
      (IL-4/IL-13) cytokine signaling and further activates the secretion of 
      immunoglobulin E (IgE). IL-13 develops bronchial asthma by elevating bronchial 
      hyperresponsiveness and enables production of immunoglobulin M (IgM) and IgE. The 
      present study aims to target IL-13 signaling using molecular docking and 
      understanding molecular dynamic simulation (MDS) to propose a compelling 
      candidate to treat asthma. We developed a library of available allergic drugs 
      (n=20) and checked the binding affinity against IL-13 protein (3BPN.pdb) through 
      molecular docking and confirmed the best pose binding energy of -3.84 and -3.71 
      for epinephrine and guaifenesin, respectively. Studying the interaction of 
      hydrogen bonds and Van der Walls, it is estimated that electrostatic energy is 
      sufficient to interact with the active site of the IL-13 and has shown to inhibit 
      inflammatory signaling. These computational results confirm epinephrine and 
      guaifenesin as potential ligands showing potential inhibitory activity for IL-13 
      signaling. This study also suggests the designing of a new ligand and screening 
      of a large cohort of drugs, in the future, to predict the exact mechanism to 
      control the critical feature of asthma.
FAU - Ma, Qin
AU  - Ma Q
AD  - Department of Respiratory and Critical Care, Tianjin Fourth Central Hospital, 
      Hebei District, Tianjin, PR China.
FAU - Tong, Huimin
AU  - Tong H
AD  - Department of Respiratory and Critical Care, Tianjin Fourth Central Hospital, 
      Hebei District, Tianjin, PR China.
FAU - Jing, Junhu
AU  - Jing J
AD  - Department of Respiratory and Critical Care, Tianjin Fourth Central Hospital, 
      Hebei District, Tianjin, PR China; j15922220402@163.com.
LA  - eng
PT  - Journal Article
DEP - 20221101
PL  - Singapore
TA  - Allergol Immunopathol (Madr)
JT  - Allergologia et immunopathologia
JID - 0370073
RN  - 0 (Interleukin-13)
RN  - 495W7451VQ (Guaifenesin)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - YKH834O4BH (Epinephrine)
RN  - 0 (Cytokines)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Humans
MH  - Child
MH  - Animals
MH  - Mice
MH  - Interleukin-13/metabolism
MH  - Th2 Cells
MH  - Molecular Docking Simulation
MH  - *Guaifenesin/metabolism/therapeutic use
MH  - *Asthma
MH  - Immunoglobulin E
MH  - *Hypersensitivity
MH  - Epinephrine/therapeutic use
MH  - Cytokines/metabolism
MH  - Mice, Inbred BALB C
MH  - Ovalbumin
MH  - Disease Models, Animal
OTO - NOTNLM
OT  - epinephrine
OT  - guaifenesin
OT  - interleukin
OT  - molecular dynamic simulation
EDAT- 2022/11/07 06:00
MHDA- 2022/11/09 06:00
CRDT- 2022/11/06 05:12
PHST- 2021/12/26 00:00 [received]
PHST- 2022/07/02 00:00 [accepted]
PHST- 2022/11/06 05:12 [entrez]
PHST- 2022/11/07 06:00 [pubmed]
PHST- 2022/11/09 06:00 [medline]
AID - 10.15586/aei.v50i6.573 [doi]
PST - epublish
SO  - Allergol Immunopathol (Madr). 2022 Nov 1;50(6):22-31. doi: 
      10.15586/aei.v50i6.573. eCollection 2022.