PMID- 28025466
OWN - NLM
STAT- MEDLINE
DCOM- 20170815
LR  - 20181113
IS  - 1884-8796 (Electronic)
IS  - 0916-8737 (Print)
IS  - 0916-8737 (Linking)
VI  - 52
IP  - 0
DP  - 2016
TI  - Deterioration of epithelium mediated mechanisms in diabetic-antigen sensitized 
      airways of guinea pigs.
PG  - 93-104
LID - 10.1540/jsmr.52.93 [doi]
AB  - BACKGROUND: The onset of diabetes causes disruption of respiratory epithelial 
      mediators. The present study investigates whether diabetes modifies the 
      epithelium mediated bronchial responses in hyper-reactive airway smooth muscle 
      (ASM) primarily through nitric oxide (NO), cyclooxygenase (COX), and epithelium 
      derived hyperpolarizing factor (EpDHF) pathways. METHODS: Experimental model of 
      guinea pigs having hyper-reactive airways with or without diabetes were 
      developed. The responses of tracheal rings to cumulative concentrations of 
      acetylcholine (ACh) and isoproterenol (IP) in the presence and absence of 
      epithelium and before and after incubation with NO, K(+)(ATP) and COX inhibitors, 
      N-(omega)-Nitro-L-arginine methyl ester (L-NAME; 100 muM), glybenclamide (10 muM) and 
      indomethacin (100 muM) were assessed. RESULTS: In diabetic guinea pigs with 
      hyper-reactive airways, a decrease in ACh induced bronchoconstriction was 
      observed after epithelium removal and after incubation with L-NAME/indomethacin, 
      suggesting damage to NO/COX pathways. Hyper-reactivity did not alter the response 
      of trachea to ACh but affected the response to IP which was further reduced in 
      hyper-reactive animals with diabetes. The ASM response to IP after glybenclamide 
      treatment did not alter in hyper-reactive guinea pigs and diabetic guinea pigs 
      with hyper-reactive airways, suggesting damage to the EpDHF pathway. Treatment 
      with indomethacin reduced IP response in the hyper-reactive model, and did not 
      produce any change in diabetic model with hyper-reactive airways, indicating 
      further disruption of the COX pathway. CONCLUSION: EpDHF pathway is damaged in 
      hyper-reactive guinea pigs and in diabetic guinea pigs with hyper-reactive 
      airways. Diabetes further aggravates the NO and COX mediated pathways in diabetic 
      guinea pigs with hyper-reactive airways.
FAU - Bano, Saidullah
AU  - Bano S
AD  - Department of Physiology, VP Chest Institute, University of Delhi, Delhi, India.
FAU - Swati, Omanwar
AU  - Swati O
FAU - Kambadur, Muralidhar
AU  - Kambadur M
FAU - Mohammad, Fahim
AU  - Mohammad F
LA  - eng
PT  - Journal Article
PL  - Japan
TA  - J Smooth Muscle Res
JT  - Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi
JID - 9211664
RN  - 0 (Antigens, Bacterial)
RN  - 0 (Bacterial Proteins)
RN  - 0 (invJ protein, Salmonella typhimurium)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 5W494URQ81 (Streptozocin)
RN  - EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases)
RN  - L628TT009W (Isoproterenol)
RN  - N9YNS0M02X (Acetylcholine)
RN  - SX6K58TVWC (Glyburide)
RN  - XXE1CET956 (Indomethacin)
SB  - IM
MH  - Acetylcholine/immunology
MH  - Animals
MH  - Antigens, Bacterial
MH  - Bacterial Proteins
MH  - Bronchial Hyperreactivity/*immunology/*pathology
MH  - Bronchoconstriction/immunology
MH  - Diabetes Complications/*immunology/*pathology
MH  - Diabetes Mellitus, Experimental/*immunology/*pathology
MH  - Female
MH  - Glyburide/pharmacology
MH  - Guinea Pigs
MH  - Humans
MH  - Indomethacin/pharmacology
MH  - Isoproterenol/immunology
MH  - Male
MH  - Muscle, Smooth/immunology/pathology
MH  - Nitric Oxide
MH  - Prostaglandin-Endoperoxide Synthases
MH  - Respiratory Mucosa/*immunology/*pathology
MH  - Streptozocin
MH  - Trachea/*immunology/*pathology
PMC - PMC5321855
EDAT- 2016/12/28 06:00
MHDA- 2017/08/16 06:00
PMCR- 2016/01/01
CRDT- 2016/12/28 06:00
PHST- 2016/12/28 06:00 [entrez]
PHST- 2016/12/28 06:00 [pubmed]
PHST- 2017/08/16 06:00 [medline]
PHST- 2016/01/01 00:00 [pmc-release]
AID - 0467 [pii]
AID - 10.1540/jsmr.52.93 [doi]
PST - ppublish
SO  - J Smooth Muscle Res. 2016;52(0):93-104. doi: 10.1540/jsmr.52.93.