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Acidic mammalian chitinase tuning after enteric helminths eradication in inflammatory respiratory disease patients
Author(s) -
Hasby Saad Marwa A.,
Watany Mona,
Tomoum Mohamed,
ElMehy Dalia,
Elsheikh May,
Sharshar Ragia
Publication year - 2018
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/pim.12583
Subject(s) - biology , immunology , helminths , enterobius , respiratory system , immune system , protozoa , microbiology and biotechnology , anatomy
Summary Aim This study aimed at investigating the presence of intestinal parasitic infections in inflammatory respiratory diseases patients during the disease attack, and measuring the acidic mammalian chitinase (AMCase) gene expression in blood before and after infection eradication. Methodology This case‐control study included 123 inflammatory respiratory diseases patients and 120 apparently healthy individuals. Repeated stool examination was done, while total and specific IgE were measured. AMC ase gene expression was analysed by real time‐polymerase chain reaction ( RT ‐ PCR ). Results Infection was detected in 32.5% of the diseased and 23.25% of the healthy individuals. Higher rate of the helminthic infection was detected (23.57) in comparison to the protozoal (12.19%) in the patients. A significantly higher rate of infection with the chitin‐rich helminths “Enterobius vermicularis & Hymenolepis nana” and level of anti‐Dermatophagoide‐IgE were reported in the patients (14.63%, 6.5% and 23.57%, respectively). AMC ase expression was significantly higher in helminths‐infected patients than the noninfected, or protozoa infected. After infection eradication, AMC ase expression significantly declined in the previously helminth‐infected patients (mean ± SD = 13.9 ± 3.918 before and 4.515 ± 1.93 after), but insignificantly affected in the protozoa infected (mean ± SD = 2.095 ± .285 before and 2.675 ± 1.181 after). Conclusion Chitin‐rich intestinal helminths are suspected to precipitate Th2‐immune response in remote tissues by enhancing systemic AMC ase expression through intestinal mucosa and macrophages irritation.